<%BANNER%>

Effect of Dietary n-3 Fatty Acid Source on Plasma, Red Blood Cell and Milk Composition and Immune Status of Mares and Foals

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EFFECT OF DIETARY n-3 FATTY AC ID SOURCE ON PLASMA, RED BLOOD CELL AND MILK COMPOSITION AND IMMUNE STATUS OF MARES AND FOALS By ELIZABETH LINDSAY STELZLENI A THESIS PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLOR IDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE UNIVERSITY OF FLORIDA 2006

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Copyright 2006 by Elizabeth Lindsay Stelzleni

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This document is dedicated to my mother a nd step-father, Melanie and Jim Eisenhour, for their unconditional love and support even when they had no idea what I was doing, and to my husband Alex, who I could not have survived graduate school without.

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iv ACKNOWLEDGMENTS First and foremost I want to thank my husband Alex for his never ending patience, love and understanding through these first years of our marriage. His faith in me has oftentimes exceeded the faith I have in myse lf, and without his constant encouragement I could not have completed this work. I am so proud of him for completing his doctoral degree this summer, while at the same time wa lking me through my first experiences of graduate school. I am extremely lucky to have a husband who is also my best friend. I owe great gratitude to Dr. Lori Warre n, my committee chair. Her guidance and wisdom have been invaluable to me, both in side the classroom and out. She has been instrumental in my choices of future paths, and I thank her for this direction. I would also like to thank Drs. Lokenga Badinga and Steeve Giguere, who served on my committee and dedicated their time to improving my project and thesis. Joel McQuagge also deserves my appreciation for his encouragement, humor and friendship. My sample analysis could not have b een completed had it not been for the supervision and instruction of Jan Kivipelto. Jan also receives my de bt of gratitude for being a shoulder to lean on a nd an open ear to talk to. I owe thanks as well to Steve Vargas and the employees of the University of Florida Horse Research Center, especially Cher Jackson. Their help, both in taking samp les and organizing data, was crucial to this project. I would also like to thank the horses of the Horse Research Center and Horse Teaching Unit. Without their cooperation and patience I could not have completed this work. A special thank you goes to “Buste r Buckley,” who always made me smile.

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v I am fortunate enough to have friends th roughout the department willing to offer help and smiles during the past few years. Many thanks go to Sarah Dilling, Kelly Spearman, Drew Cotton, Aimee Holton, Sarah White and Liz Greene for their assistance. I also appreciate the support of the crew at the Horse Teach ing Unit, especially Justin Calahan and Kristin Detweiler. Last, but most definitely not least, I w ould like to thank my grandmother, Lois VanNatta; my “Baba,” Dena Lovacheff; my sisterand brother-inlaw, Jennifer and Todd Schwent; and the rest of Alex’s and my fam ily. I would like to le nd a special thank you to my in-laws, Lynne and Michael Stelzlen i, for their unconditional love, support and encouragement of Alex and me. Most importa ntly, I want to thank my mother, Melanie Eisenhour, for showing me the kind of woman I want to be and my step-father, Jim Eisenhour, for taking me in and loving me lik e his own daughter. They have offered me nothing but undying love and support and have been my biggest fans. I am forever indebted to them for all they have done.

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vi TABLE OF CONTENTS page ACKNOWLEDGMENTS.................................................................................................iv LIST OF TABLES...............................................................................................................x LIST OF FIGURES........................................................................................................xvii ABSTRACT.....................................................................................................................xi x CHAPTER 1 INTRODUCTION........................................................................................................1 2 REVIEW OF LITERATURE.......................................................................................3 Fatty Acid Structure, Di gestion and Metabolism.........................................................3 Fatty Acid Structure..............................................................................................3 Fatty Acid Digestion..............................................................................................4 De novo Fatty Acid Synthesis...............................................................................7 Fatty Acid Degradation.........................................................................................8 Polyunsaturated Fatty Acids.........................................................................................9 n-6 and n-3 Polyunsatur ated Fatty Acids..............................................................9 Elongation of and Competition Be tween n-6 and n-3 Families..........................13 Eicosanoid Production and Function...................................................................16 The Immune System...................................................................................................17 Acquired Immunity.............................................................................................17 Immunoglobulins.................................................................................................17 Passive Immunity in the Foal..............................................................................20 Failure of Passive Transfer..................................................................................22 Innate Immunity..................................................................................................24 Inflammation.......................................................................................................24 Effects of Dietary PUFA Supplemen tation on Inflammation and Immune Function..................................................................................................................26 Blood and Tissue Responses to Experimental Feeding of n-3 PUFA.................26 Effects of PUFA supplementation on th e acquisition of passive immunity in the foal..................................................................................................30 Effects of PUFA supplementation on the inflammatory response...............33 Effects of PUFA supplementation on disease resistance and survival.........35 Characteristics of Mare Milk......................................................................................39

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vii Mare Colostrum...................................................................................................39 Factors Affecting Mare Colostrum IgG Content.................................................39 Composition of Mare Milk..................................................................................41 Effect of Diet on Fat and Fatty Acid Composition of Milk................................43 Fatty Acid Transfer across the Placenta.....................................................................46 Conclusions.................................................................................................................49 3 MATERIALS AND METHODS...............................................................................51 Animals.......................................................................................................................5 1 Diets and Treatments..................................................................................................52 Bodyweights...............................................................................................................54 Blood Sample Collection and Processing...................................................................54 Colostrum and Milk Collection and Processing.........................................................56 Fatty Acid Analysis....................................................................................................57 Intradermal Skin Test.................................................................................................58 Supplement and Feed Sample Analysis......................................................................59 Statistical Analysis......................................................................................................59 4 RESULTS...................................................................................................................61 Feed and Supplement Analysis...................................................................................61 Mare Fatty Acid Intake...............................................................................................62 Mare and Foal Bodyweight........................................................................................63 Mare Plasma Fatty Acid Composition........................................................................63 Omega-6 Fatty Acids...........................................................................................63 Omega-3 Fatty Acids...........................................................................................64 Omega-6:Omega-3 Fatty Acid Ratios.................................................................98 Mare Colostrum and Milk Fatty Acid Composition...................................................65 Foal Plasma Fatty Acid Composition.........................................................................66 Omega-6 Fatty Acids...........................................................................................66 Omega-3 Fatty Acids...........................................................................................67 Omega-6:Omega-3 Fatty Acid Ratios.................................................................68 Fatty Acid Correlations...............................................................................................68 Fatty Acid Composition of Red Blood Cells..............................................................69 Mare Red Blood Cell Fatty Acids.......................................................................69 Foal Red Blood Cell Fatty Acids.........................................................................69 Mare Serum, Colostrum and Milk IgG.......................................................................70 Foal Serum IgG...........................................................................................................71 Mare and Foal Responses to the Intradermal Skin Test.............................................71 Mare Response to PHA.......................................................................................71 Foal Response to PHA.........................................................................................72 Comparing Mare and Foal Responses to PHA....................................................72 5 DISCUSSION...........................................................................................................105 Fatty Acid Composition of Feeds and Supplements.................................................105

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viii Mare and Foal Bodyweight......................................................................................108 Mare Plasma Fatty Acid Content..............................................................................109 Mare Milk Fatty Acid Content.................................................................................111 Foal Plasma Fatty Acid Content...............................................................................112 Mare and Foal Red Blood Cell Fatty Acid Content.................................................114 Effect of n-3 Supplementation on IgG......................................................................116 Mare and Foal Inflammatory Response....................................................................119 6 IMPLICATIONS......................................................................................................121 APPENDIX A RAW DATA.............................................................................................................123 Mare Expected and Actual Foaling Dates and Dates Started on Trial.....................123 Fatty Acid Composition of Monthly Pasture Samples.............................................126 Mare Fatty Acid Intake.............................................................................................127 Mare Bodyweight.....................................................................................................128 Foal Bodyweight.......................................................................................................131 Mare Serum IgG.......................................................................................................134 Mare Colostrum and Milk IgG.................................................................................136 Foal Serum IgG.........................................................................................................139 Fatty Acid Composition of Pl asma from FISH Mares.............................................142 Fatty Acid Composition of Plasma from FLAX Mares............................................147 Fatty Acid Composition of Plasma from CON Mares..............................................152 Fatty Acid Composition of Colostru m and Milk from FISH Mares........................157 Fatty Acid Composition of Colostru m and Milk from FLAX Mares.......................163 Fatty Acid Composition of Colost rum and Milk from CON Mares.........................169 Fatty Acid Composition of Pl asma from FISH Foals...............................................175 Fatty Acid Composition of Plasma from FLAX Foals.............................................180 Fatty Acid Composition of Plasma from CON Foals...............................................185 Fatty Acid Composition of Red Blood Cells from FISH Mares..............................190 Fatty Acid Composition of Red Blood Cells from FLAX Mares.............................195 Fatty Acid Composition of Re d Blood Cells from CON Mares...............................200 Fatty Acid Composition of Red Blood Cells from FISH Foals................................205 Fatty Acid Composition of Red Blood Cells from FLAX Foals..............................210 Fatty Acid Composition of Re d Blood Cells from CON Foals................................215 Response of Mares during an Intradermal Skin Test................................................220 Response of Foals during an Intradermal Skin Test.................................................223 B PROCEDURE FOR IMMUNOGLOBULIN G ANALYSIS...................................226 C PROCEDURE FOR FATTY ACID ANALYSIS....................................................228

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ix LIST OF REFERENCES.................................................................................................232 BIOGRAPHICAL SKETCH...........................................................................................243

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x LIST OF TABLES Table page 2-1 Fatty acid composition of common feed s and fat supplements fed to horses.....12 2-2 Fatty acid composition of common forages fed to horses...................................13 2-1 Immunoglobulin concentrations of serum and milk in mature horses................18 3-1 Nutrient composition of the grain mix concentrate and the milled flaxseed and encapsulated fish oil supplements................................................................53 3-2 Nutrient composition of the bahiag rass pasture (by month) and Coastal bermudagrass hay................................................................................................54 4-1 Fatty acid composition of the grain mix concentrate and the milled flaxseed and encapsulated fish oil supplements................................................................73 4-2 Fatty acid composition of winter an d spring bahiagrass pasture and Coastal bermudagrass hay................................................................................................74 4-3 Mare average daily fatty aci d intake from December-March..............................75 4-4 Mare average daily fatty acid intake from April-June.........................................76 4-5 Mare bodyweights..............................................................................................77 4-6 Foal bodyweights................................................................................................77 4-7 Overall effect of treatment on th e fatty acid composition of mare plasma........78 4-8 Omega-6 fatty acid content of mare plasma........................................................79 4-9 Omega-3 fatty acid content of mare plasma........................................................80 4-10 Omega-6:omega-3 fatty acid ratios in mare and foal plasma and mare milk......81 4-11 Overall effect of treatment on the total fat content of mare colostrum and milk......................................................................................................................82 4-12 Overall effect of treatment on the fatty acid composition of mare colostrum and milk...............................................................................................................82

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xi 4-13 Omega-6 fatty acid content of mare colostrum and milk....................................83 4-14 Omega-3 fatty acid content of mare colostrum and milk....................................84 4-15 Overall effect of treatment on th e fatty acid composition of foal plasma..........85 .4-16 Omega-6 fatty acid content of foal plasma..........................................................86 4-17 Omega-3 fatty acid content of foal plasma..........................................................87 4-18 Correlations between mare milk and mare plasma fatty acid concentrations and mare milk and foal plasma fatty acid concentrations...................................88 4-19 Overall effect of treatment on the fa tty acid content of mare red blood cells....89 4-20 Linoleic acid content of mare red blood cells.....................................................90 4-22 Linoleic and alpha-linolenic acid contents of foal red blood cells......................91 4-21 Overall treatment effect on the fatty acid composition of foal red blood cells..92 4-23 Overall effect of treatment on mare serum and colostrum IgG content at foaling..................................................................................................................93 4-24 IgG content of mare milk....................................................................................93 4-25 Correlations between IgG content of mare and foal serum, colostrum, and mare age...............................................................................................................94 4-26 IgG content of foal serum....................................................................................95 4-27 Skin thickness of mares in res ponse to an intradermal injection of phytohemagglutinin.............................................................................................95 4-28 Skin thickness of foals in res ponse to an intradermal injection of phytohemagglutinin.............................................................................................96 4-29 Skin response of mares and foals pool ed across treatments to an intradermal skin test using phytohemagglutinin as the stimulant...........................................97 A-1 FISH mare expected foaling dates, ac tual foaling dates and dates started on trial.....................................................................................................................123 A-2 FLAX mare expected foaling dates, ac tual foaling dates and dates started on trial.....................................................................................................................124 A-3 CON mare expected foaling dates, ac tual foaling dates and dates started on trial.....................................................................................................................125

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xii A-4 Fatty acid composition of bahiagra ss pasture (by month) and Coastal bermudagrass hay..............................................................................................126 A-5 Mare daily intake of forage grain and supplement by month...........................127 A-6 FISH mare bodyweights....................................................................................128 A-7 FLAX mare bodyweights..................................................................................129 A-8 CON mare bodyweights....................................................................................130 A-9 FISH foal bodyweights......................................................................................131 A-10 FLAX foal bodyweights....................................................................................132 A-11 CON foal bodyweights......................................................................................133 A-12 Serum IgG content of FISH mares at foaling...................................................134 A-13 Serum IgG content of FLAX mares at foaling.................................................134 A-14 Serum IgG content of CON mares at foaling...................................................135 A-15 IgG content of colostrum and milk from FISH mares.......................................136 A-16 IgG content of colostrum and milk from FLAX mares.....................................137 A-17 IgG content of colostrum and milk from CON mares.......................................138 A-18 IgG content of seru m from FISH foals..............................................................139 A-19 IgG content of seru m from FLAX foals............................................................140 A-20 IgG content of serum from CON foals..............................................................141 A-21 Fatty acid composition of FISH mare pl asma at 28 d prior to expected foaling date....................................................................................................................142 A-23 Fatty acid composition of FISH mare plasma at 28 d post-foaling...................144 A-24 Fatty acid composition of FISH mare plasma at 56 d post-foaling...................145 A-26 Fatty acid composition of FLAX mare plasma at 28 d before expected foaling date....................................................................................................................147 A-27 Fatty acid composition of FL AX mare plasma at foaling.................................148 A-28 Fatty acid composition of FLAX mare plasma at 28 d post-foaling.................149

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xiii A-29 Fatty acid composition of FLAX mare plasma at 56 d post-foaling.................150 A-30 Fatty acid composition of FLAX mare plasma at 84 d post-foaling.................151 A-31 Fatty acid composition of CON mare pl asma at 28 d before expected foaling date....................................................................................................................152 A-32 Fatty acid composition of CO N mare plasma at foaling...................................153 A-33 Fatty acid composition of CON ma re plasma at 28 d post-foaling...................154 A-34 Fatty acid composition of CON ma re plasma at 56 d post-foaling...................155 A-35 Fatty acid composition of CON ma re plasma at 84 d post-foaling...................156 A-36 Fatty acid composition of FISH mare colostrum..............................................157 A-37 Fatty acid composition of FISH mare milk at 36 h post-foaling.......................158 A-38 Fatty acid composition of FISH mare milk at 14 d post-foaling.......................159 A-39 Fatty acid composition of FISH mare milk at 28 d post-foaling.......................160 A-40 Fatty acid composition of FISH mare milk at 56 d post-foaling.......................161 A-41 Fatty acid composition of FISH mare milk at 84 d post-foaling.......................162 A-42 Fatty acid composition of FLAX mare colostrum.............................................163 A-43 Fatty acid composition of FLAX mare milk at 36 h post-foaling.....................164 A-44 Fatty acid composition of FLAX mare milk at 14 d post-foaling.....................165 A-45 Fatty acid composition of FLAX mare milk at 28 d post-foaling.....................166 A-46 Fatty acid composition of FLAX mare milk at 56 d post-foaling.....................167 A-47 Fatty acid composition of FLAX mare milk at 84 d post-foaling.....................168 A-48 Fatty acid composition of CON mare colostrum...............................................169 A-49 Fatty acid composition of CON mare milk at 36 h post-foaling.......................170 A-50 Fatty acid composition of CON mare milk at 14 d post-foaling.......................171 A-51 Fatty acid composition of CON mare milk at 28 d post-foaling.......................172 A-52 Fatty acid composition of CON mare milk at 56 d post-foaling.......................173 A-53 Fatty acid composition of CON mare milk at 84 d post-foaling.......................174

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xiv A-54 Fatty acid composition of FI SH foal plasma at birth........................................175 A-55 Fatty acid composition of FISH foal plasma at 14 d of age..............................176 A-56 Fatty acid composition of FISH foal plasma at 28 d of age..............................177 A-57 Fatty acid composition of FISH foal plasma at 56 d of age..............................178 A-58 Fatty acid composition of FISH foal plasma at 84 d of age..............................179 A-59 Fatty acid composition of FL AX foal plasma at birth.......................................180 A-60 Fatty acid composition of FLAX foal plasma at 14 d of age............................181 A-61 Fatty acid composition of FLAX foal plasma at 28 d of age............................182 A-62 Fatty acid composition of FLAX foal plasma at 56 d of age............................183 A-63 Fatty acid composition of FLAX foal plasma at 84 d of age............................184 A-64 Fatty acid composition of CON foal plasma at birth.........................................185 A-65 Fatty acid composition of CON foal plasma at 14 d of age..............................186 A-66 Fatty acid composition of CON foal plasma at 28 d of age..............................187 A-67 Fatty acid composition of CON foal plasma at 56 d of age..............................188 A-68 Fatty acid composition of CON foal plasma at 84 d of age..............................189 A-69 Fatty acid composition of FISH mare red blood cells at 28 d before expected foaling date........................................................................................................190 A-70 Fatty acid composition of FISH mare red blood cells at foaling.......................191 A-71 Fatty acid composition of FISH mare red blood cells at 28 d post-foaling.......192 A-72 Fatty acid composition of FISH mare red blood cells at 56 d post-foaling.......193 A-73 Fatty acid composition of FISH mare red blood cells at 84 d post-foaling.......194 A-74 Fatty acid composition of FLAX mare red blood cells at 28 d before expected foaling date........................................................................................................195 A-75 Fatty acid composition of FLAX mare red blood cells at foaling.....................196 A-76 Fatty acid composition of FLAX mare red blood cells at 28 d post-foaling.....197 A-77 Fatty acid composition of FLAX mare red blood cells at 56 d post-foaling.....198

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xv A-78 Fatty acid composition of FLAX mare red blood cells at 84 d post-foaling.....199 A-79 Fatty acid composition of CON mare red blood cells at 28 d before expected foaling date........................................................................................................200 A-80 Fatty acid composition of CON mare red blood cells at foaling.......................201 A-81 Fatty acid composition of CON mare red blood cells at 28 d post-foaling.......202 A-82 Fatty acid composition of CON mare red blood cells at 56 d post-foaling.......203 A-83 Fatty acid composition of CON mare red blood cells at 84 d post-foaling.......204 A-84 Fatty acid composition of FISH foal red blood cells at birth............................205 A-85 Fatty acid composition of FISH fo al red blood cells at 14 d of age..................206 A-86 Fatty acid composition of FISH fo al red blood cells at 28 d of age..................207 A-87 Fatty acid composition of FISH fo al red blood cells at 56 d of age..................208 A-88 Fatty acid composition of FISH fo al red blood cells at 84 d of age..................209 A-89 Fatty acid composition of FLAX foal red blood cel ls at birth..........................210 A-90 Fatty acid composition of FLAX fo al red blood cells at 14 d of age................211 A-91 Fatty acid composition of FLAX fo al red blood cells at 28 d of age................212 A-92 Fatty acid composition of FLAX fo al red blood cells at 56 d of age................213 A-93 Fatty acid composition of FLAX fo al red blood cells at 84 d of age................214 A-94 Fatty acid composition of CON foal red blood cells at birth............................215 A-95 Fatty acid composition of CON fo al red blood cells at 14 d of age..................216 A-96 Fatty acid composition of CON fo al red blood cells at 28 d of age..................217 A-97 Fatty acid composition of CON fo al red blood cells at 56 d of age..................218 A-98 Fatty acid composition of CON fo al red blood cells at 84 d of age..................219 A-99 Skin thickness values of FISH ma res during an intradermal skin test..............220 A-100 Skin thickness values of FLAX ma res during an intradermal skin test............221 A-101 Skin thickness values of CON ma res during an intradermal skin test..............222 A-102 Skin thickness values of FISH fo als during an intradermal skin test................223

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xvi A-103 Skin thickness values of FLAX fo als during an intradermal skin test..............224 A-104 Skin thickness values of CON fo als during an intradermal skin test................225

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xvii LIST OF FIGURES Figure page 2-1 Essential fatty acid metabolism...........................................................................14 4-1 Total omega-6 fatty acid content in mare plasma from 28 d pre-partum to 84 d post-foaling.......................................................................................................97 4-2 Total omega-3 fatty acid content in mare plasma from 28 d pre-partum to 84 d post foaling.......................................................................................................98 4-3 Total omega-6 fatty acid content of ma re milk from foaling (d0) through 84 d post-foaling..........................................................................................................98 4-4 Total omega-3 FA content of mares milk from foaling (d0) through 84 d postfoaling..................................................................................................................99 4-5 Total omega-6 fatty acid content of fo al plasma from birth (d0) through 84 d of age...................................................................................................................99 4-6 Total omega-3 fatty acid content of fo al plasma from birth (d0) through 84 d of age.................................................................................................................100 4-7 Linoleic acid content of mare red blood cells from 28 d pre-partum to 84 d post-foaling........................................................................................................100 4-8 Linoleic acid content of foal red bloo d cells from birth ( d0) to 84 d of age.....101 4-9 Alpha-linolenic acid content of foal red blood cells from birth (d0) to 84 d of age......................................................................................................................101 4-10 Correlation between mare serum IgG c oncentration at foaling (d0) and foal serum IgG concentration 36 h post-foaling.......................................................102 4-11 Foal serum IgG concentrati on at birth and before nursing................................102 4-12 Foal serum IgG content after colostrum ingestion from 36 h to 84 d postfoaling................................................................................................................103 4-13 Skin thickness of mares in res ponse to an intradermal injection of phytohemagglutinin...........................................................................................103

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xviii 4-14 Skin thickness of foals in res ponse to an intradermal injection of phytohemagglutinin...........................................................................................104 4-15 Skin thickness of mares and foals in response to an intradermal injection of phytohemagglutinin...........................................................................................104

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xix Abstract of Thesis Presen ted to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Master of Science EFFECT OF DIETARY n-3 FATTY AC ID SOURCE ON PLASMA, RED BLOOD CELL AND MILK COMPOSITION AND IMMUNE STATUS OF MARES AND FOALS By Elizabeth Lindsay Stelzleni August 2006 Chair: Lori K. Warren Major Department: Animal Sciences Supplementing the diets of horses with fat is a popular trend in today’s equine industry. However, little focus has been given to the effect of supplementing with omega-3 fatty acids (FA) in the broodmare and her suckling foal. To study these effects, 36 Thoroughbred and Quarter Horse mares w ith an average bodyweight of 580.9 3.5 kg (mean SE) were randomly assigned to one of three treatment groups: 1) basal diet with no supplementation (CON, n = 12); 2) basal di et plus milled flaxseed supplementation (FLAX, n = 12); or 3) basal diet plus encap sulated fish oil supplementation (FISH, n = 12) from 28 days prior to expected foaling date until 84 days after foaling. The flaxseed and fish oil supplements were fed to mares in amounts to provide 6 g total n-3 FA/100 kg BW per day. The basal diet consisted of a commercial grain-based concentrate, Coastal bermudagrass hay and bahiagrass pasture.

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xx Blood samples were obtained from mares at 28 d pre-partum and milk and blood samples were obtained from mares and fo als at foaling, 36 h and 14, 28, 56 and 84 d post-partum to determine FA and IgG conten t. On d 84, mares and foals received paired intradermal injections of phytohemagluttini n (PHA) and skin thickness was determined over a 48 h period as a measure of the in flammatory response. Bodyweights were obtained from mares and foals at 14 d intervals throughout the trial. Treatment had no effect on gestation le ngth (P = 0.84), mare bodyweight (P = 0.80) or foal bodyweight (P = 0.76). Mares fed FLAX had higher plasma alpha-linolenic acid (ALA) (P=0.06) than mares fed FISH or CON mares. Mares fed FISH had higher plasma eicosapentaenoic acid (EPA), docosahexanoi c acid (DHA) and total n-3 (P=0.03) than FLAX and CON mares. Across treatments, tota l milk n-3 increased (P=0.0005) and total n-6 decreased (P=0.0001) from foaling to d 84. Milk from FLAX mares had higher ALA (P=0.01) than milk from FISH and CON mare s. Milk from FISH mares had higher EPA and DHA and a lower n-6:n-3 ratio (P=0.007) than milk from FLAX and CON mares. Foals suckling FLAX mares had higher plasma ALA (P=0.04) than foals suckling FISH and CON mares. Foals suckling FISH mares had higher plasma EPA, DHA and total n-3 and a lower plasma n-6:n-3 ratio (P=0.002) than FLAX and CON foals. Treatment did not affect colostrum, milk or foal serum IgG. Response to PHA injection was greater (P=0.0001) in mares compared to foals but similar between treatments. Although the addition of n-3 FA to the mare’s diet altere d the FA content of mare milk and mare and foal plasma, changes in total IgG and PHA intradermal responses were not detected..

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1 CHAPTER 1 INTRODUCTION Supplementing the diet with fat is a popular trend in the hors e industry. Fat is commonly fed to horses to improve the hair coat, improve body condition and increase the energy density of the diet. However, mo st of the research that has examined fat supplementation of the horse has been performed with little regard to the type of fatty acids (FA) provided. In a ddition, most of this research has focused on mature performance horses; relatively little inform ation is available on fat supplementation of mares and the effects on the suckling foal. Corn oil, soybean oil, and rice bran ar e common sources of fat added to horse rations; however, these feeds are high in omeg a-6 FA. High levels of n-6 FA have been associated with more pronounced inflammatory responses in humans (Meydani et al., 1993; Simopoulos, 1999); therefore, potential exis ts for such diets to also have negative biological effects in the horse. Based on the immunomodulatory effects of n-3 FA in humans and other animals (Simopoulos, 1999; Anderson and Fritsche, 2002), there is interest in determining whether n-3 FA supplementation can modify inflammatory and immune responses in horses. In addition, the diet ary source of n-3 FA may be important for eliciting the desired health benefits. Flax seed is an excellent source of alpha-linolenic acid (ALA), whereas fish oil is a good source of eico sapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Although both are rich in total n-3 FA, fish oil may be a more effective means of providing biologically active n-3 FA than flax.

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2 The immune status of foals is a vital c oncern for horse breeders, as suckling foals are susceptible to many health problems incl uding diarrhea and septicemia. These health problems can cause significant veterinary e xpense, as well as e ndanger the life of the foal. Previous research has shown that suppl ementation of broodmares with linseed oil or a mix of corn and linseed oil increases the n3 content of her milk and the n-3 content of her foal’s blood (Duvaux-Ponter et al, 2004; Spea rman et al., 2005). Therefore, it seems possible to enhance the concentr ation of n-3 FA in the foal by manipulation of the mare’s diet. The objectives of this research were to 1) examine the effect of dietary n-3 supplementation on the FA composition of mare milk and mare and foal plasma; 2) examine the efficiency with which ground flaxseed or encapsulated fish oil augment the presence of EPA and DHA in the mare and foal; 3) examine the effects of supplementation with flaxseed vs. fish oil on increasing colostrum, m ilk and foal plasma IgG; and 4) examine the effects of feeding flaxseed vs. fish oil on the inflammatory response in the mare and foal. We hypothesize that supplementing the mare with fish oil will increase the EPA and DHA c oncentrations in mare milk and mare and foal blood to a higher extent than will flaxseed, will increase the IgG in mare colostrum and foal blood, and will decrease the inflammatory response in mares and foals.

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3 CHAPTER 2 REVIEW OF LITERATURE Fatty Acid Structure, Digestion and Metabolism Fatty Acid Structure Fatty acids (FA) consist of carbon (C), hydrogen (H) and oxyge n (O) arranged in a carbon chain with a carboxyl group (-COOH) at one end and a methyl group (-CH3) at the other. FA are classified and named by their chain lengths and their degree of unsaturation, or number of double bonds. Unsa turated FA can be m onounsaturated (only one double bond) or polyunsaturated (two or mo re double bonds), whereas saturated fatty acids have no double bonds. Fatty acids are al so classified as short, medium or long chain, with short chain FA having less than 8 carbons, medium chain FA having 8 to 16 carbons and long chain FA having greater th an 16 carbons. The numbering sequence of the carbons in a fatty acid chain begins at the carboxyl end, with the carboxyl carbon being C1. An older system used Greek letter s to identify carbon atoms. In this system, C2 (the first carbon after the carboxyl carbon) was the -carbon, C3 was the -carbon and so on, ending with the last carbon in the chain at the methyl end as the -carbon (Gurr et al., 2002). Currently, the numbering system is the pr eferred method of naming individual FA. In this system, the number of carbon atoms in the FA chain is given followed by a colon and the number of double bonds. For example, stearic acid, a saturated FA of 18C, is identified as C18:0. Linol eic acid, a polyunsaturated FA of 18C with two double bonds, is identified as C18:2. While the current numbering system is preferred, the older system

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4 is used to identify -6 and -3 fatty acids, where the last double bond in the fatty acid chain is six and three carbons away from the -carbon, respectively (Greene, 2006). Newer research may substitute the with an n but the meaning does not change. The presence of double bonds in a fatty acid chain also allows for positional and geometric isomerism. Positional isomerism refers to a different location of double bonds in the carbon chain. Geometric isomeris m refers to the orientation of the hydrogen atoms around the carbon-carbon double bond. A cis configuration results when both hydrogen atoms are on the same side of the bond, while a trans configurations results when hydrogen atoms are on opposite sides of th e bond. Most natural unsaturated FA are in the cis configuration (Spa llholz et al., 1999). Fatty Acid Digestion Dietary fats exist mostly as triglyceri des (TG) which are made up of three FA attached to a glycerol backbone (Mu and H oy, 2004). The digestion of these TG begins in the stomach by the action of gastric lipase released from the gastric mucosa. In humans and rats, lingual lipase from the von E bner glands, a group of serous glands on the tongue, also aids in FA digestion in the stomach. This lipase is transferred with the food bolus into the stomach where its activity begins (Mu and Hoy, 2004). Secretion of the lingual lipase occurs continuously but is stimulated by dietary (high fat) and mechanical (suckling) factor s (Carey et al., 1983; Tso, 1989). Digestion by both lipases produces free FA and diglycerides (Carey et al., 1983; Tso, 1989). The lingual lipase is especially important in the newborn, as pancr eatic lipase activity is not fully developed at birth. In addition, the short and medium-cha in TG present in milk fat are readily hydrolyzed by the lingual lipase (Tso, 1989) Horse saliva, however, does not possess

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5 this lingual lipase (Frape, 1998; Ellis and Hill, 2005). In fact, it is currently thought that equine saliva does not contain any enzyme ac tivity (Ellis and Hill, 2005). Therefore, equine saliva is not as importa nt in beginning digestion but is vital in providing feed lubrication (Frape, 1998) and buffering of the f eed-saliva mixture (Ellis and Hill, 2005). While only 10-30% of dietary fat is hydrolyzed in the stomach, the majority of FA digestion takes places in the small intestine, especially in the duodenum. In animals with a gall bladder, the action of the food bolus entering the duodenum stimulates gall bladder emptying, secretion of pancreatic lipase and th e release of cholecystok inin (CCK). Bile acids are also released from the gall bladder or directly from the liver to emulsify the fat (Mu and Hoy, 2004). The horse, however, does not have a gall bladder, but this does not seem to affect the digestion of fat (Cunha, 1991). In the horse, bile continuously drains from the liver into the small intestine to facilitate the em ulsion of fat (Frape, 1998). Furthermore, the peristaltic and segmental c ontractions present in the intestine supply mechanical energy to reduce the fat particle size and increase the inte rfacial area of the fat droplets (Carey et al., 1983). The acti on of pancreatic lip ase on a triglyceride molecule releases two free FA and a 2-m onoglyceride. These compounds, along with biliary salts, form micelles that are absorbed into the intestinal mucosal cells by passive diffusion (Doreau and Chilliard, 1997). In the ho rse, pancreatic lipase is secreted in high amounts and increases as fat is added to the di et (Frank et al., 2004). Therefore, the horse is able to digest high amounts of fat in the di et. Horses have been fed diets with 20% of the DE provided by oil with good results and no negative effect on digestibility (Cunha, 1991).

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6 Once the monoglycerides and free FA are abso rbed into the intestinal cell, the longchain fatty acids (LCFA) must be transporte d to the endoplasmic reticulum, the major site of absorbed lipid metabolism. One explan ation for how the LCFA reach the endoplasmic reticulum is by the action of fatty acid-binding protein (FABP). FABP is present in the intestinal mucosa, liver, kidney, and adipos e tissue and has no affinity for short or medium-chain FA (Tso, 1985). It has been pos tulated that FABP ma y be responsible for removing LCFA acids from their binding to the cytosolic side of the luminal membrane and transferring them to the endoplasmic re ticulum (Carlier et al ., 1991). Unlike LCFA, short and medium-chain FA are transferred direc tly from the intestinal cell into the portal blood as free FA bound to albumin (Carlier et al., 1991). Once inside the endoplasmic reticulum, LC FA and monoglycerides are recombined into triglycerides by the m onoglyceride pathway. The enzyme complex that makes up this pathway is known as “triglyceride synthe tase.” This complex consists of three enzymes: acyl-CoA synthetase, MG transacyla se and diglyceride transacylase. The acylCoA synthetase, in the presence of CoA, ac tivates the LCFA to form acyl-CoA. The acyl-CoA is then used for the reacylation of mo noglyceride to diglycerides and finally to triglycerides (Tso, 1985). The re sulting triglyceride s are then packaged with cholesterol esters and phospholipids into chylomicrons, which are large lipoproteins that act as carriers of dietary triglycerides. Chylomic ron formation is activated by the addition of apoproteins, which are proteins that play an important role in the formation and secretion of chylomicrons by the enterocytes. Once c hylomicrons are formed, they are released by exocytosis into the lymphatic system wher e they can enter the blood stream via the thoracic duct and be trans ported to the rest of the body (Carlier et al., 1991).

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7 De novo Fatty Acid Synthesis There are two primary sources of FA in the body: FA provided by the diet and FA made by the animal via de novo synthesis (Lehner and Kuksis, 1996). The pathways for de novo FA synthesis exist in the animal duri ng the well-fed state and in monogastrics occur primarily in the liver. Most of the carbon used for de novo FA formation is supplied through the pyruvate pool and from th e end product of glycolysis. There are three substances needed for FA synthesis: acetyl CoA, malonyl CoA and NADPH. The first step in the synthesis of FA is the formation of acetyl CoA from pyruvate in the mitochondrial matrix by the action of pyruva te dehydrogenase. The acetyl CoA must then be moved out of the mitochondria and into the cytosol wher e FA synthesis takes place. Because the inner mitochondrial membrane is not permeable to acetyl CoA, the acetyl CoA is combined with oxaloacetate to form citrate. Citrate is then translocated to the cytosol where it is cleaved back to oxaloacetate and a cetyl CoA by ATP:citrate lyase (Gurr et al., 2002). This mechan ism of moving acetyl CoA into the cytosol in the form of citrate is called th e citrate shuttle. Once acetyl CoA reaches the cytosol, de novo FA synthesis begins. The first reaction of this mechanism, which is al so the rate limiting reaction, involves the formation of malonyl CoA by the enzyme acetyl-CoA carboxylase (ACC) (Knowles, 1989). The malonyl CoA forms the source of th e vast majority of the carbons of a FA chain. The enzyme complex that synthesi zes LCFA from acetyl and malonyl CoA is fatty acid synthase (FAS). This enzyme complex has synthase, reductase and dehydrase actions. The typical end product of animal FAS action is palmitic acid (C16:0) (Greene, 2006).

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8 Once produced, palmitic acid can be elongated and desaturated. Type III synthases (commonly called elongases) lengthen FA prefor med in the animal 2C at a time. The principal elongation reactions occur in the endoplasmic reticulum membranes and involve acyl-CoA as a primer, malonyl-CoA as a donor of 2C units and NADPH as the reducing coenzyme. This system is capable of producing FA chain with an excess of 20 carbons (Suneja et al., 1990). Desaturati on, or the addition of double bonds, occurs mainly by oxidative desaturation, a process by which a double bond is introduced directly into the LCFA with O2 and NADH as cofactors (Scheu erbrandt and Bloch, 1962). Mammalian desaturases are only able to introduce double bonds in the 9, 6 and 5 positions. Plant desaturases can introduce additional double bonds at the 12 and 15 positions, therefore creating n-6 and n-3 FA. All double bonds introduced by the process of oxidative desaturation are in the cis configuration (Lehner and Kuksis, 1996). Fatty Acid Degradation The mobilization and oxidation of FA o ccur primarily during fasting, physical exercise and stress in the animal in order to break down dietary or st ored TG into FA to provide energy. The mobilization of FA occurs via lipolysis in the adipose tissue, in which FA are cleaved from their glycerol backbone mainly by hor mone sensitive lipase (HSL) and released into circulation (Johns on and Greenwood, 1998). The main forms of FA oxidation are termed alpha ( ), beta ( ) and omega ( ), referring to which carbon on the acyl chain is attacked. Of these three, -oxidation is the most prevalent. In oxidation, there is a stepwise removal of 2C units from the carboxyl end of the FA (Greene, 2006).

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9 The mitochondria and microbodies (peroxi somes and glyoxysomes) are capable of performing -oxidation. The process begins by conve rting the FA into fatty acyl-CoA as soon as it enters the cy tosol of the cell. The inner m itochondrial membrane, however, is impermeable to fatty acyl-CoA. In order to move this molecule across the membrane, the enzyme carnitine:palmitoyl transferase (CPT1), located on the outer mitochondrial membrane, combines the fatty acyl-CoA with carnitine. The resulting acyl carnitine is then transported across the membrane crossing the inner membrane by a carnitine:acylcarnitine transloc ase (Pande, 1975). Once the acy l carnitine is inside the mitochondrial matrix, CPT2 transfers the acy l group from carnitine to CoA, therefore reforming acyl-CoA as a substrate for further -oxidation (Bieber, 1988). The process of -oxidation involves a repeated seque nce of four reactions resulting in the removal of 2C from the acyl chai n. First, acyl-CoA dehydrogenase acts on the acyl-CoA to form trans-3,3-enoyl-CoA. Enoyl hydratase then acts on the product of the first reaction to form 3-hydroxy acyl-CoA. Th e third reaction is catalyzed by the enzyme 3-hydroxy acyl-CoA dyhyrogenase which works with NAD+ to form 3-oxoacyl-CoA. The final reaction involves 3-oxoacyl-CoA thiola se which produces a shorter fatty acylCoA and acetyl-CoA (Bieber, 1988). The resulting acyl-CoA is recycled back into oxidation for the removal of additional 2 car bon units, while the acetyl-CoA can be used in the TCA cycle to produ ce energy (Gurr et al., 2002). Polyunsaturated Fatty Acids n-6 and n-3 Polyunsaturated Fatty Acids By definition, n-6 polyunsatured fatty acids (PUFA) have the last double bond in the FA chain six carbons from the methyl (omega) end. The two most physiologically

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10 import n-6 PUFA are linoleic aci d (LA; C18:2) and arachidonic acid (AA; C20:4). Of these, LA is considered a dietary essential fatty acid because it cannot be synthesized by mammals. Sources of LA include vegetable oils such as corn, sunflower, peanut, and soy oils (Carlier et al., 1991). Li noleic acid can be elongated and desaturated in the body to produce AA in a mechanism that is discussed la ter in this chapter. Omega-6 PUFA, with AA as the principal component, predominate in organs and tissues performing storage functions (adipose tissue), chemical processing (liver), excretion (kidney) and mechanical work (muscle) (Innis, 1991). In addition, plasma lipoproteins contain high amounts of LA in triglycerides, cholesterol esters and phospho lipids (Innis, 1992a). A very important feature of n-6 PUFA is their eff ect on the body. In general, n-6 PUFA have proinflammatory, prothrombotic and proaggregat ory effects, characterized by increases in blood viscosity, vasospasm, vasoconstr iction and decreases in bleeding time (Simopoulos, 1999). Omega-3 PUFA have the last double bond in their carbon chains three carbons from the methyl end. The dietary esse ntial PUFA from the n-3 family is -linolenic acid (ALA; 18:3), but other physio logically important n-3 PUFA include eicosapentaenoic acid (EPA; 20:5) and docosahexaenoic acid (DHA; 22:6) (Innis, 1992a ). Using elongase and desaturase actions similar to those in n-6 PUFA, ALA can be transformed into EPA, which can be further transformed into DHA. Alpha-linolenic acid is found primarily in the chloroplast of green leafy ve getables and in seeds of fla x, linseed and walnuts. Fatty fish and fish oils, however, are the main s ources of EPA and DHA (Benatti et al., 2004). The primary sites of n-3 PUFA accumulati on in the body include the nervous tissue, reproductive organs and retina membra nes (Innis, 1991). Unlike the plasma

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11 concentrations of LA, tissue and plasma trig lyceride and cholesterol ester levels of ALA are usually quite low (<1-2% FA) (Innis, 1992a). Polyunsaturated FA of the n-3 family are known to have anti-inflammatory, antith rombotic, antiarrhythm ic, hypolipidemic and vasodilatory effects on the body (Simopoulos, 1999). To obtain optimal health, it is important to have adequate dietary amounts of PUFA of both the n-6 and n-3 families, but it may also be important to have a proper ratio between the two. A ratio of 4-5:1 of n-6:n-3 has been suggested as most beneficial for humans, but most investigation in this area has been conducted in lab animals (Wiseman, 1997). The efficiency at which the horse conve rts ALA to EPA and DHA is unknown. In addition, while a recommendation for a benefici al n-6:n-3 ratio exists for humans, the optimal ratio for horses is unknown. Most horse feeds today are high in n-6 FA, with the horse’s major n-3 FA intake obtained from forages. The FA composition of common grains and fat supplements fed to horses are presented in Table 2-1 and the FA composition of common forages fed to horses are presented in Table 2-2.

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12 Table 2-1. Fatty acid composition of common feeds and fat supplements fed to horses Feed Fatty acid1 Textured Grain2 Oats3 Corn Oil4 Flaxseed Oil5 Fish Oil4 Rice Bran Oil6 Soybean Meal3 C14:0 0.14 Trace 0.2 0.1 5.6 0.43 Trace C16:0 NA7 22.1 10.8 5.4 21.6 16.27 10.7 C18:0 NA 1.3 20.6 3.6 9.0 1.84 1.5 C18:1 NA 38.1 10.2 0.0 15.5 41.92 21.4 C18:2n-6 38.82 24.9 54.8 15.2 1.5 35.44 14.2 C18:3n-3 3.72 2.1 1.1 53.6 1.4 1.24 7.0 C20:4n-6 0.03 NA NA 0.1 NA NA NA C20:5n-3 0.08 NA 0.3 0.0 13.5 NA NA C22:6n-3 0.06 NA 0.2 0.0 11.5 NA NA 1 Presented as g fatty acid/100 g fat 2 Commercial grain mix (Hallway Feeds, Lexington, KY) contai ning barley, corn, soybean meal, molasses, oats and suppl emental pellet; 14.8% CP, 6.5% fat; from O’Connor et al., 2004. 3 From Ellis and Hill, 2005. 4 From Chen et al., 2006. 5 From Francois et al., 2003. 6 From Sierra et al., 2005. 7 NA = information not available.

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13 Table 2-2. Fatty acid composition of common forages fed to horses Forage Fatty acid1 Fresh Bahiagrass2 Fresh Perennial Rye Grass3 Bermudagrass Hay2 Timothy Hay4 C14:0 0.00 0.4 0.00 1.63 C16:0 22.56 14.6 39.14 NA C18:0 4.28 1.2 6.72 NA C18:1 3.00 1.7 7.05 NA C18:2n-6 21.32 10.6 23.35 15.76 C18:3n-3 46.21 68.4 15.93 26.68 C20:4n-6 0.00 NA5 0.00 0.35 C20:5n-3 0.00 NA 0.00 0.36 C22:6n-3 0.00 NA 0.00 0.25 1 Presented as g fatty acid/100 g fat. 2 From the present study. 3 From Elgersma et al., 2003. 4 From O’Connor et al., 2004. 5 NA = information not available. Elongation of and Competition Between n-6 and n-3 Families As stated earlier, both LA and ALA can be elongated and desaturated to form their longer chain derivatives (Fi gure 2-1). This conversion happens in the endoplasmic reticulum (Benatti et al., 2004). The first st ep of the mechanism converting LA to AA is catalyzed by 6-desaturase, the rate-limiting step of the pathway. This enzyme acts on LA to insert a double bond between carbons 6 and 7. This product is then elongated by the addition of two carbon units to form dihomo-linoleic acid (C20:3). Further desaturation by 5-desaturase inserts a double bond between carbons 5 and 6, thereby creating AA. Arachidonic acid can then be el ongated to form adreni c acid (C22:4). The enzyme 6-desaturase inserts a double bond between carbons 4 and 5 of adrenic acid to form 6-docosapentaenoic acid (C22:5) (Innis, 1991).

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14 Diet (Vegetable fats and oils) C18:2n-6 C20:4n-6 C22:6n-3 C20:5n-3 C18:3n-3 C20:3n-6 C22:4n-6 C22:5n-6 C20:4n-3 C22:5n-3 6-desaturation elongation 5-desaturation elongation 6-desaturation elongation Diet (fish fat) Diet (animal fat) Figure 2-1. Essential fatty acid metabo lism. Adapted from Innis, 1992a. The conversion of ALA to its longer chain derivatives us es the same pathway and enzymes as LA. The enzyme 6-desaturase acts first on ALA to form stearidonic acid (C18:4). This acid is then elongated and desaturated by 5-desaturase to form EPA. To form DHA, EPA is elongated to form 3-docosapentaenoic acid (DPA; C22:5), which is then desaturated by 6-desaturase to form DHA (Innis, 1991). However, there is a marked inefficiency of conversion of ALA to EPA, with only about 0.2% of plasma ALA fated for synthesis of EPA in human blood (P awlosky et al., 2001). There is 10-fold greater rate of transfer, how ever, of EPA to DHA than there is from ALA to EPA, showing that the initial desa turation/elongation to EPA is th e most restrictive (Pawlosky et al., 2001). The difficulty of conversion of ALA to DHA has been shown in rats, where maternal rats were fed a diet high made in ALA by the addition of flaxseed oil (Bowen and Clandinin, 2000). Maternal rats were started on the experimental diet on the day of

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15 parturition and their pups were sacrificed at two weeks of age. Bowen and Clandinin (2000) showed that supplementing maternal ra ts with a high ALA diet did not increase the DHA content of the whole body, skin, epidid ymal fat pads or muscles in rat pups, therefore suggesting that the conversion of ALA to DHA is inefficient in the rat. However, the efficiency at which the hor se converts ALA to EPA and DHA is unknown. Therefore, providing animals w ith a dietary source of EPA a nd DHA (such as fish or fish oil) may be a better way to ensure incorpora tion of these FA into the body than feeding a source of ALA. Because the n-6 and n-3 families use the same enzymes in the process of desaturation to their longer chain derivativ es, there is competition between them. The major site of competition occurs at the site of 6-desaturase action, the rate limiting reaction for PUFA desaturation. There is a strong preferential substrate affinity of the 6desaturase for n-3 PUFA, especially AL A over LA (Innis, 1991; Drevon, 1992). Therefore, feeding animals a source of n-3 PUFA will often decrea se the amount of n-6 PUFA processed in the body, as more of the 6-desaturase will act on the n-3 PUFA and less on the n-6. Studies have shown, in both animals and humans, that providing a dietary source of n-3 PUFA reduces the amount of AA found in the blood (Fritsche et al., 1993; Sauerwald et al., 1996). This compe tition between n-3 and n-6 PUFA has been established in sows assigned to diets cont aining 7% added fat wher e menhaden fish oil was substituted for lard at 0, 3.5 and 7% of th e total dietary fat (Fr itsche et al., 1993). Sows were fed from 107 days of gestation to 28 days of lactation. The substitution of fish oil for lard at both 3.5 and 7% decr eased serum levels of AA by approximately 50% in sow serum (Fritsche et al., 1993). However, the opposite phenomenon has been

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16 documented as well. Extensive research has sh own that providing a diet rich in LA but poor in ALA will result in the accumu lation of AA and very little EPA and DHA (Wiseman, 1997). Eicosanoid Production and Function Eicosanoids are a large family of oxyge nated 20-carbon FA (Smith, 1989) that act as local hormones to modulate the intensity and duration of inflammatory and immune responses (Yaqoob, 2004). The family is ma de up of three groups: the prostanoids (prostaglandins and th romboxanes) which are synthesi zed by cyclooxygenase (COX), the leukotrienes which are synthesized by lipoxyge nase (LOX) and the epoxides synthesized by epoxygenase. Eicosanoids are produced fr om 20-carbon PUFA containing three to five cis methylene-interrupted double bonds. Thes e PUFA include AA, a member of the n-6 family, and EPA, a member of the n3 family. Linoleic acid (18 carbons) and DHA (22 carbons) can be converte d to eicosanoid homologues, but these are not actual eicosanoids and are thought to have limited bi ological function. Because AA is the most abundant C20 polyunsaturate in mammalian system s, it is the major precursor of eicosanoids (Smith, 1989). Macrophages a nd monocytes are important sources of eicosanoids, as their membranes typically contain large amounts of AA (Yaqoob, 2004). Arachidonic acid and EPA each produce eicosanoids of a different series. Arachidonic acid is a substrate for the 2-series prostaglandins (PG), namely prostaglandin E2 (PGE2) and prostaglandin F2 (PGF2) and the 4-series leukotrienes (LT), namely leukotriene B4 (LTB4). Prostaglandin E2 and LTB4 have powerful proinflammatory actions (James et al., 2000). Prostaglandin E2 induces fever and increases vascular permeability, vasodilation, pain and edema. However, PGE2 also suppresses the production of inflammatory cytokines TNF, IL-1 and IL-6 by macrophages and T cells.

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17 Leukotriene B4 increases vascular permeability and blood flow, is a chemotactic agent for leukocytes, induces the release of neutrophi l lysosomal enzymes, and enhances the generation of reactive oxyge n species. Leukotriene B4 also increases production of TNF, IL-1 and IL-6 by macrophages (Calder, 2001; Yaqoob, 2004). In contrast to AA, EPA is a substrate for the 3-series PG, namely PGE3, and the 5-series LT, namely LTB5. These eicosanoids have the same types of in flammatory effects as those generated from AA, but they are far less biologically poten t (Calder, 2001). Therefore, production of eicosanoids from EPA could m odulate the immune response. The Immune System Acquired Immunity The acquired immune system is capable of recognizing and se lectively inhibiting specific foreign antigens (Gol dsby et al., 2003). T cells, B ce lls, antigen-presenting cells, the major histocompatibility complex (MHC), and immunoglobulins all play important roles in the acquired immune system. This sy stem of immunity is classified as acquired because the immune cells must be exposed to an antigen once to develop, or acquire, memory for that antigen. A second exposure to the same antigen will trigger an enhanced state of immune reactivity (Goldsby et al., 2003). Immunoglobulins Along with playing an important role in acquired immunity, immunoglobulins are also an important part of humoral immunity, or the type of immunity pertaining to extracellular fluids including the plasma and lymph (Goldsby et al., 2003). Humoral immunity is driven by B cells, which orig inate and mature in the bone marrow (Kuby, 1992). Immunoglobulins are a group of larg e glycoproteins found on B-cell membranes or secreted by plasma cells. They are found most prevalently in blood serum but are also

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18 present in mucosal tissues a nd external secretions such as milk. An antibody is an immunoglobulin (Ig) that exhibi ts antigen-binding ability. Therefore, all antibodies are Ig, but not all Ig are necessa rily antibodies. The two term s, however, are often used interchangeably. Antibodies have a wide range of functions, including targeting infectious organisms, neutraliz ation of toxins and removal of foreign antigens from body circulation (Peakman and Vergani, 1997). An tibodies can serve as diagnostic tools for clinical evaluations of immune diseases or disorders. For example, immunoglobulin G (IgG) is measured in the serum of foals to determine if there has been a successful transfer of maternal antibodies. In horses, the major imm unoglobulins are IgG, IgM, IgA and IgE (Nezlin, 1998). Average concentrations of immunoglobulins in the serum of mature horses are presented in Table 2-1. Table 2-1. Immunoglobulin c oncentrations of serum and milk in mature horses1 Sample IgG IgM IgA Adult horse serum 1000-1500 100-200 60-350 Mare colostrum 1500-5000 100-350 500-1500 Mare milk 20-50 5-10 50-100 1 From Tizard, 1996; presented as mg/dL. IgG is synthesized and secreted from pl asma cells found in the spleen, lymph nodes and bone marrow (Tizard, 1996). IgG molecule s have a long half-life (23-25 days) and there is a continuous high-level stimulat ion for IgG production. As a result, the concentration of IgG in blood and colostru m is higher than any other immunoglobulin (Tizard, 1996). IgG is the smallest of the imm unoglobulin classes, so it is therefore more able to move through the body to travel to needed areas (Widmann and Itatani, 1998). Four immunoglobulin subclasses have been de scribed in horses: IgGa, IgGb, IgGc and

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19 IgG(T) (Sheoran et al. 2000). IG(T) has al so been divided into the subclasses IgG(Ta) and IgG(Tb) (Tizard, 1996). These subclasse s are distinguished from one another by molecular structural differences and slight variations in biologi cal function (Kuby, 1992). Like IgG, IgM is also made and secreted from plasma cells in the spleen, lymph nodes and bone marrow. It is found in the second highest concentration in serum, following IgG (Tizard, 1996). IgM is the first immunoglobulin class produced by the maturing B cell, and the first class synthesized by the neonate (Kuby, 1992). It is also the first antibody produced in a primary response to an antigen (Widmann and Itatani, 1998; Kuby, 1992). IgM is more efficient than other immunoglobulins in binding antigens because of its larger molecular size (largest of the immunoglobulin classes) and its larger number of binding sites. Because of its high er efficiency, IgM is also more able to neutralize viral infectivity, cause agglu tination and activate compliment than IgG (Goldsby et al., 2003). The immunoglobulin IgA is produced ma inly by plasma cells in muscosaassociated lymphoid tissues beneath surface epithelium (Widmann and Itatani, 1998). While it is manufactured more than any ot her immunoglobulin class, serum concentration of IgA is relatively low. This low concentra tion is due to the secre tion of IgA in fluids present on the epithelial surfaces of the alim entary, respiratory and reproductive tracts and in such fluids as urine, saliva, tears and milk (Widmann and Itatani, 1998). Because IgA is the major immunoglobulin in the external secretions of horses, it plays a vital role in protecting the intestinal tract, respirator y tract, urogenital tract, mammary gland and eyes against microbial invasion (Tizard, 1996).

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20 Like IgM, IgE is produced predominantly by plasma cells located beneath body surfaces. It is found in very low concentrations in the serum of healthy animals, partially because the molecule is fairly unstable and has the shortest half-life of all the classes of immunoglobulins (Tizard, 1996). IgE anti bodies mediate immediate (type I) hypersensitivity reactions that cause the sy mptoms of hay fever, asthma, hives and anaphylactic shock (Kuby, 1992). IgE is also thought to be largely responsible for immunity against parasitic worms (Tizard, 1996). Passive Immunity in the Foal Due to the mare’s diffuse epitheliochorial placenta, there is no significant transfer of immunoglobulins to the fetal circulat ion during pregnancy (Jeffcott, 1972, 1974a; Erhard et al., 2001). Therefore, foals ar e born with a near absence of circulating immunoglobulins and an easily compromised imm une system. Although they are able to produce their own antibodies soon after birth, foals will not produce levels approaching those of the adult horse until 3-4 months of age (Jeffcott, 1974a). Foals receive the needed antibodies via passive transfer from co lostrum, or the mare’s first milk. Prior to birth, the mare’s mammary gland is capable of selecting and concentrating a wide range of serum Ig into the colostrum (Jeffcott, 1974a, 1975). Wh en foals suckle this colostrum after birth, they take the antibody -rich fluid into their digestiv e tracts where the Ig can be absorbed into the circulating blood. For the transfer of passive immunity to be successful, the mare’s colostrum must contain adequate amounts of the appropria te immunoglobulins, es pecially IgG (Rooke and Bland, 2002). In addition, the immunoglobulin s must be delivered intact to the site of absorption and absorbed intact (Rooke and Bland, 2002). Because of the very low level of proteolytic activity in the digestive tract of young foals, most immunoglobulins

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21 are kept intact as they pass with the co lostrum through the foal’s stomach and small intestine. Trypsin inhibitors found in co lostrum further reduce the degradation of immunoglobulins in the foals digestive tract (Kruse, 1983; Tizard, 1996). The immunoglobulins in colostrum ar e rapidly absorbed by non-specific pinocytosis into the small intestine enterocy tes. Maximum absorption occurs soon after birth and declines thereafter, completely ceasing by 24 hours after bi rth (Raidal et al., 2000). The foal’s intestine shows selective pe rmeability, with a greater affinity for IgG and IgM (Tizard, 1996). Once inside the en terocyte, individual immunoglobulins merge together to form one or more larger gl obules. These larger globules pass from the enterocyte into the local lymphatics and late r reach the systemic circulation (Jeffcott, 1974a). The critical event in the tran sfer of intact immunoglobulin to the foal’s circulation is cessation of transfer across the enterocyte basolateral membrane. For this reason, “gut closure” is the term used to define the cessation of transfer of IgG to the foal’s circulation. Gut closure, usually reac hed around 24 hours of age (Rooke and Bland, 2002), is characterized by a repl acement of the immature ep ithelial cells with more mature cells that no longer enga ge in pinocytosis (Kruse, 1983). IgG displays a unique behavior in foal seru m. At birth, before the foal has suckled, foal serum IgG may be as low as 30 mg/dL (Erh ard et al., 2001). Howe ver, foal IgG rises rapidly after colostrum is ingested. Peak Ig G values in foal serum occur between 18 and 24 hours after birth (Jeffcott, 1974a) and have been reported to be as high as 2,160 mg/dL (McGuire and Crawford, 1973). The IgG values in foal plasma appear to stay at near peak levels for at least the first two days after foaling (J effcott, 1974b; Duvaux-Ponter et

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22 al., 2004). After this peak, passively derive d IgG molecules will gradually decline until they are completely absent by around 5 months of age (Jeffcott, 1974a). Foals may begin to process their own IgG molecules as early as 2 weeks of age, but levels reaching those of the adult horse are not seen until around 4 mo nths of age (Jeffcott, 1974a). Erhard et al. (2001) reported that 7 day old foals had a mean IgG value of 1000 ml/dL. This value then decreased, indicating the elimination of maternal IgG, and reached the lowest level of 790 mg/dL at 35 days of age. Howeve r, foal serum IgG increased to around 1100 mg/dL at 42 days after birth, indicating th at endogenous IgG production was increasing in the foal (Erhard et al., 2001). Therefore, behavior of IgG in the foal seems to begin with a very low presuckle value, experience a dramatic rise after co lostrum ingestion, undergo a steady decline as maternal IgG is elim inated and shows an increase as the foal begins to produce its own IgG. Failure of Passive Transfer Failure of passive transfer (FPT) is define d as the failure of ab sorption of maternal immunoglobulins by the neonatal foal, a conditio n that predisposes the foal to lifethreatening infections (Kohn et al., 1989). Failure of passive tr ansfer is the most commonly recognized immune defici ency in horses and may predispose affected foals to septicemia, infective arthritis and pneumoni a (Raidal, 1996; Raidal et al., 2000). There are conflicting views in the literature as to what antibody levels actually constitute failure of passive transfer. Liu (1980) and McGuir e et al. (1977) define d failure of passive transfer as less than 200 mg IgG/dL seru m and partial failure as between 200 and 400 mg/dL. LeBlanc et al. (1986) suggested failu re of passive transfer as levels below 400 mg/dL, while Raidal (1996) and Tyler-McG owan et al. (1997) noticed an increased susceptibility of foals to disease when IgG levels dropped below 800 mg/dL. Today, it is

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23 common to define failure of passive tran sfer as IgG levels below 400 mg/dL serum (Tizard, 1996; Erhard et al ., 2001) and partial failure as levels between 400 and 800 mg/dL. IgG levels above 800 mg/dL are considered necessary to provide optimal immune function (Erhard et al., 2001). In orde r to prevent failure of passive transfer, the minimal concentration of colostral immunogl obulin required has been estimated to be between 1,000 and 3,000 mg IgG/dL colostrum (L eBlanc et al., 1986). The possibility of failure of passive transfer cannot be evaluate d until the foal is about 18 hours of age, as antibody absorption is essentially complete at this time (T izard, 1996). Therefore, the standard industry practice of testing foal Ig G levels at 12 hours af ter foaling may give misleading results, as complete antibody abso rption has not happened yet. This practice may still be needed, however, in order to be able to administer plasma or colostrum to the foal before the foal’s ability of absorption is completed. Possible causes of failure of passive tran sfer fall into three categories: production failure, ingestion failure and absorption failure (Tizard, 1996). A failure of the mammary gland to concentrate immunoglobulins from the blood into colostrum can occur in maiden mares foaling for the first time. Premat ure lactation, however, is the most common production failure cause of failure of passive transfer. In th is case, initial colostrum may be of adequate amount with adequate IgG concentration, but the mare will commence lactation prior to parturition. This steady l eak of colostrum may occur for several hours or several days before birth and significantl y reduces the amount of IgG available to the foal (Jeffcott, 1974a). While less common, inabilities of ingestion and absorption are additional failure of passive transfer causes. Ingest ion failures can arise from a mare not allowing her foal to

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24 nurse, weak or deformed foal s that take longer than norma l to stand, or a delayed or defective suckling reflex (Je ffcott, 1974a; Tizard, 1996). Fo als usually overcome these factors, but it may take longe r than the 24-hour period of inte stinal permeability to IgG. Absorption failures can be linked to stress at the time of parturition. The adrenal hormones play important roles in the onset of parturition and can influence changes in the permeability of small intestine cells after birth (Jeffcott, 1972). In conditions of stress at parturition, the mare or foal could produ ce abnormal amounts of co rticosteroids which would therefore have a detrimental affect on the foal’s antibody absorption (Jeffcott, 1974a). Innate Immunity Innate immunity is the first line of defense in fighting an invading organism (Goldsby et al., 2003). The skin, mucosal su rfaces, macrophages and neutrophils all play important roles in the innate immune syst em. The skin and mucosal surfaces act as barriers against infection, a nd the macrophage and neutrophils act to phagocytize and kill invading foreign cells. Infla mmation is also an important part of innate immunity and functions to draw immune cells to areas of injury or antige n attack. Because the innate immune system is less specific than the acqui red immune system, the innate system can act quickly to begin an immune response (Goldsby et al., 2003). Inflammation By definition, inflammation is the response of tissue to the presence of microorganisms or injury (Tizard, 1996). In flammation is a vital protective mechanism and the means by which defensive molecules an d phagocytic cells gain access to the sites of tissue microbial invasion or damage. In flammation is classified according to its severity and duration, with acute inflammation developing in less than an hour after

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25 tissue damage and chronic inflammation occurr ing a much slower rate and being more constant. There are five symptoms of acute inflammation: heat, redness, swelling, pain and loss of function. These symptoms are a result of changes in the small blood vessels in the damaged tissue (Tizard, 1996; Goldsby et al., 2003). Immediately following microbial invasion or injury, blood flow to the effected area greatly increases. This increase is due to a transient constriction of local arterioles and dilation of all the small blood vessels in the area. The bl ood vessel permeability is also increased, allowing fluid to move from the bl ood into the tissues where it causes edema and swelling (Tizard, 1996). The changes in blood vessels allow an influx of lymphocytes, neutrophils, monocyt es and other immune cells in to the area to participate in clearance of the antigen (Kuby, 1992). Neutro phils are the first immune cells to arrive in the inflamed tissues, followed by the slow er moving monocytes. Once within the inflamed tissues, these cells are attracted to sites of bacterial growth and tissue damage and phagocytize and destroy any foreign materi al present. Monocytes will also remove dead and dying tissue (Tizard, 1996). Cytokines play an important role in the acute-phase inflammatory response. These low-molecular-weight proteins secreted by macrophages exert a variety of effects on lymphocytes and other immune cells to regulate the intensity and duration of an immune response. The three cytokines that play the largest role in acute inflammation are tumor necrosis factor(TNF), interleukin 1 (IL-1) and inte rleukin 6 (IL-6). All three cytokines act locally on endothe lial cells to induce coagulat ion and increase vascular permeability (Kuby, 1992). TNF, IL-1 and IL-6 also act on the brain to induce fever and suppress appetite and on skeletal muscle to drive protein catabolism and mobilize

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26 available amino acids. In addition, these cy tokines operate on liver cells to increase protein synthesis and secretion of clotting fa ctors, complement components and protease inhibitors, all of which ai d in the host defense (Tizar d, 1996). All three cytokines activate B and T cells, while IL-6 can also increase immunoglobulin synthesis (Goldsby et al, 2003). Effects of Dietary PUFA Supplementation on Inflammation and Immune Function Blood and Tissue Responses to Exp erimental Feeding of n-3 PUFA Numerous studies have inves tigated the levels of diffe rent n-3 PUFA resulting in the blood when feeding ALA and DHA, either alone or in combination. In humans, many studies have looked at providing adults with dietary fish oil, a good source of EPA and DHA. Helland et al. (1998) supplemented pregnant women with cod liver oil for 14 days, between three and eight weeks post part um. The women were divided into four groups: Group 1 served as the contro l and received no supplementation, Group 2 received 2.5 mL of cod liver oil/day, Group 3 received 5 mL of cod liver oil/day, and Group 4 received 10 mL of cod liver oil/da y. Helland et al. (1998) found that the pregnant women in Groups 3 and 4 (recei ving 5 and 10 mL of cod liver oil/day, respectively) showed a decreased plasma LA content and an increased ALA and DHA plasma content. When EPA and DHA intake were computed on a bodyweight basis, the women receiving 5 mL of cod liver oil were consuming the equivalent of 14 mg EPA and DHA/kg of bodyweight and the women receiving 10 mL of cod liver oil were consuming the equivalent of 28 mg of EPA and DHA/kg bodyweight. Henderson et al. (1992) also supplemente d pregnant women with EPA and DHA, but not in the form of fish oil. Henders on and coworkers supplemented pregnant women with six capsules of Bio-EFA for a tota l supplement weight of six grams of

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27 supplementation. This supplement provi ded women with 1080 mg EPA and 720 mg DHA per day. Assuming an average bodywei ght of 70 kg, this dosage provided 15.43 mg EPA/kg BW and 10.29 mg DHA/kg BW. Si milar to Helland et al. (1998), however, Henderson et al. (1992) also started their supplementati on period after lactation had already commenced, supplementing women between two and five weeks post partum for a total of 21 days. The results of He nderson et al. (1992) showed that daily supplementation of lactating women with 6 g of an EPA and DHA source increased the women’s red blood cell content of EPA, DP A and total n-3 PUFA. Although it was not significant, there was also a trend toward re d blood cell DHA increase. Infant red blood cells were also affected by supplemen tation of the mother, as EPA and DPA concentrations of infant red blood cells signi ficantly increased af ter the supplementation period. However, similar to maternal result s, there was no significant change in infant red blood cell DHA. Unfortunately, this study only used five women and their infants, so it may have been hampered by a small sample size. Further evidence suggests that infants br east fed from omnivorous mothers have a higher DHA concentration in their red blood cells than do infants of vegan mothers (Sanders and Reddy, 1992). In fact, the di fference in infant red blood cell DHA was quite large in this study, with infants feed ing from vegan mothers having 1.9% of the total FA found in their red blood cells as DHA and infants feeding from omnivorous mothers having 6.2% of their total red blood cell FA as DHA. The content of DHA in breast milk reported by Sanders and Reddy (1992) was also significantly lower in vegan women when compared to omnivorous women ( 0.14 and 0.37% of fat, respectively). In addition, infants fed conventional formula (low in DHA) have consistently lower plasma

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28 and red blood cell levels of DHA than infa nts fed breast milk, which is higher in DHA (Innis, 1991; Innis, 1992b). The ability to increase blood concentrati ons of n-3 PUFA by feeding sources of these FA has also been documented in animals. Bauer et al. (1998) fed adult dogs either ground flax or sunflower seeds for 84 days and showed that plasma ALA, EPA and DPA were elevated when dogs were fed flaxseed, compared to when dogs were fed sunflower seeds. Plasma DHA, however, remained unchanged in the flax fed dogs, showing the difficulty in converting ALA to DHA. The flax fed dogs also showed a plasma reduction in AA and 22:5 n-6, providing evidence of co mpetition between n-3 and n-6 PUFA for the 6-desaturase in dogs (Bauer et al., 1998). However, the exact amount of supplement Bauer and coworkers added to the diets of th e dogs was not state d, so it is therefore difficult to compare levels of suppl ementation to other studies. In horses, Hansen et al. (2002) examin ed the effects of ALA supplementation on equine fatty acid status by f eeding adult horses a diet consis ting of 8% flaxseed oil for 18 weeks. Hansen and coworkers found that th e flaxseed oil supplemented horses showed an increased plasma ALA and EPA compared to horses that did not receive any fat supplementation. On the other hand, there were no increases in DHA noticed. A weakness of this study, however, is the low sa mple size of only 12 horses (6 horses in the control group, 6 horses in the supplemented group). Duvaux-Ponter et al. (2004) also tested the effects of ALA on horses, but used pregnant mares and young foals as subjects. In this study, 26 pregnant mares were divide d into two groups. The first group acted as the control and was fed extruded rapeseed (h igh in n-6 FA), while the second group was fed extruded linseed (high in n-3 FA). The mares were supplemented 1.5 months prior to

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29 foaling until one month after foaling. While mare blood was not tested, supplementation with extruded linseed caused an increase in the ALA content of foal plasma from foaling until 4 weeks post parturition, and this increase wa s greater than the increase seen in foals nursing the mares given rapeseed (Duvaux-Pont er et al., 2004). However, the exact amount of linseed provided to the mares is uncle ar, as it was not stated in the paper. The effects of feeding sources of EPA and DHA have also been documented in horses. Hall et al. (2004a) fed ten adult mare s either menhaden fish oil or corn oil for a period of 14 weeks. Mares fed the menhaden fish oil consumed 22.93 g EPA per day and 19.58 g DHA per day. These amounts equate d to a daily intake of 4.6 g EPA/100 kg bodyweight and 3.9 g DHA/100 kg bodyweight. As a result of this supplementation, Hall et al. (2004a) noticed higher plasma ALA, EPA and DHA and lower plasma LA in the mares fed fish oil compared to the mares fed co rn oil. Brinsko et al (2005) examined the effects of feeding a DHA source to stalli ons to determine the effects of FA supplementation on semen. In this study, eight stallions were used in a 2 x 2 crossover design. Stallions were fed a grain mix t op-dressed daily with either 250 g of a commercial nutriceutical containi ng 30% n-3 FA (resulting in 75 g of n-3 FA) or a grain mix with no supplementation. Stallions were fed their respective diets for 14 weeks, separated by a 14 week wash out period, befo re treatments were switched for another 14 weeks of supplementation. The authors found that when stallions were supplemented with n-3 FA, their semen had almost th ree times the levels of DHA/billion sperm compared to when stallions were not supplem ented. Even though the relative percentage of DHA in semen fatty acids was not signi ficantly different between the two groups, treated stallions showed a 1.5fold increase in their semen DHA:DPA ratio when they

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30 received n-3 supplementation (Brinsko et al., 2005). Therefore, it seems that supplementation of DHA in horses may have the ability to af fect the fatty acid composition of body constituents other than just the plasma. Effects of PUFA supplementation on the acqui sition of passive immunity in the foal In order for IgG to be maximally absorbed into the foal’s intestinal cells, the cell membranes must be fluid enough to allow the molecules to navigate through the membrane. Membrane bilayers tend to exist at the transition point between a fluid and solid-like (gel) state. The phospholipid fatty acyl chains present in membranes are one of the key chemical determinants of this balance. PUFA of the cis configuration tend to increase the fluidity of the membrane (Mur phy, 1990; Mills et al., 2005). The fatty acid composition of membrane phospholipids is also easily changed by manipulation of dietary fat (Murphy, 1990), which, in turn, can influence membrane fluidity. Brasitus et al. (1985) showed that adjusting the fatty acid composition of the diet in rats changed the composition of their enterocyte membranes. To do so, rats were fed either unsaturated or saturated triglycerid es provided by corn oil or butter fat, respectively, for 6 weeks. The supplementation of corn oil, which is rich in LA, caused an enhanced fluidity of the membranes of seve ral intestinal cells (B rasitus et al., 1985). When humans were supplemented with di etary n-3 PUFA, the fluidity of their erythrocyte membranes was substantially in creased (Lund et al., 1999). In this study, 17 adults were supplemented with three 1 g capsules of fish oil per day for 42 days. Fluidity of the red blood cell membrane was determ ined by measuring the lateral diffusion coefficient of the fluorophore ODAF by fluores cence recovery after photobleaching. The results of Lund et al. (1999) suggest that supplementation with fish oil increased the lateral diffusion coefficient of ODAF, therefor e increasing the membra ne fluidity. This

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31 increase in fluidity was seen at 21 days after supplementation and continued to rise until the termination of the study at 42 days (Lund et al., 1999). A correlation between membrane fluidity and permeability was shown in young rats by Meddings and Theisen (1989). Thes e researchers examined the changes that naturally occur in the membrane of jejunal mi crovilli in rats as they aged from 9 to 25 days. Study results showed a decreasing lipi d fluidity as the rats aged, assessed by a steady-state fluorescence polarizat ion technique. This decrease in membrane fluidity correlated to a decrease in membrane permeability (Meddings and Theisen, 1989). This correlation may suggest that if it is possible to enhance membrane fluidity by feeding n-3 FA, it may therefore be possible to augment th e amount of IgG that travels both into the mare’s mammary gland and across the foal’s intestine. To determine the effects of feeding PUFA on the IgG content of mare colostrum, Kruglik et al. (2005) fed mares either corn oi l (rich in LA) or encapsulated fish oil (rich in EPA and DHA) from 60 days before foali ng to 21 days after foaling. The mares fed encapsulated fish oil consumed 8.6 g of EP A and 10.4 g of DHA per day. The results of Kruglik et al. (2005) showed a higher presuckl e colostrum IgG content in the fish oil fed mares, suggesting that supplementation with fi sh oil may have improved the fluidity and permeability of mammary epithelial cells. Howe ver, Kruglik et al. (2005) did not specify the amount of colostrum collected, and it has been reported that IgG amounts can vary between the first 250 and 500 mL of colostrum (Lavoie et al., 1989). Therefore, if the volume of colostrum gathered was different be tween mares, the differences seen in IgG may have been attributed to colostrum volume and not to treatment. Studies have also been performed that suggest that n-6 PUFA may increase mare colostrum IgG. Hoffman

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32 et al. (1998) fed mares a high fat diet (10 % fa t) through gestation a nd lactation. The fat in this diet was provided primarily by corn oil, which is high in LA. Colostrum IgG levels were higher in the mare s fed the high fat diet, even though the dietary fat was rich in n-6 and not n-3 FA (Hoffman et al., 2004). However, the volumes of harvested colostrum were not stated in this study. In addition, colostrum wa s collected between 6 and 12 hours after foaling. Because the IgG of colostrum can vary dramatically in the first 12 hours after foaling (Pearson et al., 1984), colostrum IgG values obtained from mares in this study may have shown differences that were due to time and not treatment. Studies have also been executed to determine the effect of feeding PUFA on foal IgG. Kruglik et al. (2005) showed that mares suppl emented with fish oil produced foals that showed no differences in IgG levels when co mpared to foals born to corn oil fed dams, even though the same study showed a higher colostrum IgG in the mares fed fish oil. Kruglik et al. (2005) sampled foal plasma at 24 hours, so peak IgG content should have been reached. Therefore, it is unclear as to why the higher IgG levels in fish oil fed mare colostrum did not cause an increase in the plas ma of foals born to these mares. DuvauxPonter et al. (2004) also faile d to show a difference in foal serum IgG when mares were supplemented with a source of n-3 FA. In th is study, mares fed extruded linseed did not produce foals with a higher serum IgG than mares fed extruded rapeseed (Duvaux-Ponter et al., 2004). Foal blood was again sampled at 24 hours after foaling in this study, so peak foal IgG should have been recorded. However, mare colostrum IgG was not tested, so it is unclear if ALA could increase colostru m IgG. More research needs to be done to determine the capability of dietary PUFA on modifying mare mammary and foal

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33 enterocyte membrane composition and fluidity on the enhancement of passive transfer of IgG. Effects of PUFA supplementation on the inflammatory response Numerous studies have shown anti-inflamma tory effects of n-3 PUFA. Sadeghi et al. (1999) fed groups of mice either a low fat di et (2.5% fat provided by corn oil) or diets high fat diets providing 20% fat by coconut (ric h in medium chain FA ), olive (rich in C18:1n-6), safflower (rich in LA) or fish oils After 5 weeks on diet, mice were injected with 1.0 mL of phosphate-buffered saline containing endotoxin from E. coli In the mice receiving the fish oil diet, lower plasma con centrations of the proinflammatory cytokines TNF, IL-1 and IL-6 were seen after the inje ction of endotoxin when compared to mice fed olive or safflower oils. However, coconut oil fed rats also showed decreased amounts of these cytokines (Sadeghi et al., 1999). Therefore, it is unclear if fish oil was specifically responsible for the decreased proi nflammatory cytokine production, or if this difference was caused by a lack of n-6 PUFA Unfortunately, the amount of feed offered to the mice was not provided by the authors, so the amount of consumed FA could not be calculated. Billiar et al. ( 1988) fed fish oil to rats for 6 weeks and observed a lower in vitro production of IL-1 and TNFby macrophages. Unfortunately, the fish oil fed rats in this study were compared to rats fed either corn or safflower oil, which are both high in n-6 FA. Therefore, it is again unclear if fish oil reduces proinflammatory cytokine production or if the feeding of n-6 FA increases cytokine production. To test the inflammatory effects of PUFA in horses, Hall et al. (2004a) fed 10 adult mares 3.0% of their total diet (as-fed ba sis) with either corn oil or menhaden fish oil. After 14 weeks of supplementation, the fish oil supplemented mares had neutrophils

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34 with a 78-fold greater concentra tion of the lesser inflammatory LTB5 when compared to the neutrophils of mares fed corn oil (Hall et al., 2004a). In the same group of mares during the same supplementation period, production of TNFby bronchoalveolar lavage fluid (BALF) cells was increased in both gr oups, but only the corn oil fed mares had an increased production of inflammatory PGE2 their BALF cells (Hall et al., 2004b). When mare BALF cells were stimulated with li popolysaccharide, mares fed corn oil also showed a higher production of inflammatory PGE2 (Hall et al., 2004b). Similar to the studies discussed previously, however, Hall et al. (2004a, 2004b) compared horses fed fish oil to horses fed corn oil and did not in clude a control group fed a diet without n-6 or n-3 FA supplementation. Because the diets of both groups of horses were altered through fat supplementation, it is unclear if the reported decreases in pro-inflammatory eicosanoids seen in horses fed fish oil woul d have resulted if these horses had been compared to a control group. The delayed-type hypersensitivity (DTH) re sponse has also been used to test the anti-inflammatory effects of n-3 PUFA. Meydani et al. (1993) supplemental adult humans with a low-fat, high-fish diet (26% calories from fat, 1.23 g EPA and DHA combined per day) or a low-fat, low-fish diet (25% calories from fat, 0.27 g EPA and DHA combined per day) for 24 weeks. This treatment period was compared to a previous 6 week period where subjects had been eating a current Am erican diet of 35% of calories from fat and 0.8% of calories from n-3 FA. A delayed-type hypersensitivity (DTH) test was administered before and af ter the supplementation period using several different antigens, including tetanus toxoid and Streptococcus (group C). Results of Meydani et al. (1993) showed that the DTH response of adults consuming the low-fat,

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35 high-fish diet was significantly less than the response of those consuming the low-fat, low-fish diet, with diameter measurements of the DTH reactions of the low-fat, high-fish diet participants bei ng reduced by half. Changing the n-6:n-3 ratio in dogs was al so shown to effect the inflammatory response (Wander et al., 1997). In this st udy, dogs were fed diet s containing n-6:n-3 ratios of 31:1, 5.4:1 or 1.4:1 for 16 weeks, where the n-6 FA was provided by corn oil and the n-3 FA was provided by fish oil. Dietary ratios were changed mostly by a reduction in LA simultaneous to an increase in EPA and DHA. When the diameter of a DTH response to keyhole limpet hemocyanin (KLH) was measured, dogs fed a n-6:n-3 ratio of 1.4 showed a much smaller reaction co mpared to the dogs fed ratios of 34:1 and 5.4:1 (Wander et al., 1997). Because the amount of n-6 FA in these diets decreased as the n:6-n:3 ratios decreased (as opposed to holding the amount of n-6 FA stable and increasing the amount of n-3), it is again unc lear if differences seen in DTH response were strictly caused by the increase in n-3 FA. It is quite plausible that these differences may have been influenced by the decreasing n-6 FA. In contrast to dogs, the DTH response of horses sensitized with KLH show ed no differences between horses fed 3% of the total diet (as-fed basis) either fi sh oil or corn oil (Hall et al., 2004b). Effects of PUFA supplementation on disease resistance and survival The majority of studies on inflammation and PUFA supplementation have shown positive results with n-3 PUFA, particularly when n-3 supplementation reduces n-6 FA in the diet. However, studies on the effect of PUFA on disease resist ance show conflicting results. When guinea pigs were fed diet s high in either n-3 FA (1.4% and 0.9% fat calories from EPA and DHA, re spectively) or n-6 FA (15.4% fat calories from LA) for 13 weeks and infected with M. tuberculosis the guinea pigs fed a diet high in n-3 FA

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36 showed a higher number of mycobacteria recovered from the spleen, the most pronounced progression of the disease and a high er mean size of th e tuberculin reaction (Paul et al., 1997). The authors suggested that possible explanations for these results may include the lower production of inflammatory me diators and the impairment in release of lysosomal enzymes that kill mycobacteria (P aul et al., 1997). The study performed by Paul et al. (1997) is possibly one of the be st studies done to examine n-3 FA effects on disease resistance, as animals consuming both fat supplemented diets were compared to a no fat added control diet. In addition, the study utilized animals consuming the experimental diets but that were not infected. These animals therefore acted as uninfected controls within each diet. The benef its of a study design such as this is that a direct comparison can be made between th e n-3 FA supplemented group and the control group, which in turn helps to determine disease effects are due strictly to the addition of dietary n-3 FA. Another well designed study compared di sease responses of mice infected with influenza (Byleveld et al., 1999). Challengi ng fish oil fed mice with influenza virus produced a higher lung viral load, lower body weights and impaired production of IgG and lung IgA when compared to mice fed beef tallow. Mice were fed fish oil or beef tallow at 20% of dietary fat for 14 days, afte r which half of the mice from each treatment were infected with influenza while the othe r half served as noninfected controls. D’ambola et al. (1991) supplemented newborn rabbits with high (5 g/kg) or low (0.22 g/kg) doses of fish oil, safflower oil or saline for 7 days after birth. When the young rabbits were supplemented with the higher leve ls of fat, both the fish and sunflower oil supplemented rabbits had an impaired ability to clear Staphylococcus aureus when

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37 compared to the saline control group (D’ambol a et al., 1991). However, the low doses of fish and safflower oil did not produce the same impaired ability to cl ear the bacteria. In light of these results, the authors of this study concluded that high does of both n-3 and n6 FA can reduce the host’s ability to kill S. aureus (D’ambola et al., 1991). Positive results of supplementing with n3 PUFA were shown when neonatal rat pups were infected with group B streptococcus (Rayon et al., 1997). In this study, researchers fed gestating rats a control diet (no fat added) or diets supplemented with either corn or menhaden fish oil. Supple mentation was begun on day 2 of gestation and continued through lactation, but the amounts of diets and supplements fed were not provided by the authors. Rat pups were then infected with the streptococcus bacteria at 7 days of age. The results of Rayon et al. ( 1997) showed that pups from mothers who had been fed fish oil during gesta tion showed a significantly high er rate of survival (79%) than those born to corn oil fed dams (49%), though this difference was not significant. In this study, the lowered production of inflamma tory mediators by fish fed rats when compared to corn oil fed rats may have been responsible for the highe r survival rates, as group B streptococcal infections induce elevated levels of pr oinflammatory cytokines that lead to septic shock (Rayon et al., 1997). Feeding fish oil to weanling mice has b een shown to prolong mice survival to a murine retrovirus-induced immunodeficiency syndrome (MAIDS) that mimics human AIDS (Fernandes, et al., 1992). Mice in this study were fed diets consisting of 5% corn oil fed at an energy restriction of 40%, or di ets fed ad libitum consisting of 5% corn oil, 20% corn oil or 20% menhaden fish oil. Mice were fed for 8 weeks before being injected with the MAIDS plaque-forming units (Ferna ndes et al., 1992). Mice fed both the 5%

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38 corn oil energy restricted and 20% fish oil di ets showed significantly longer survival rates than mice consuming the other diets. The aut hors explained the increase in survival rates of these two groups as a result of a sl owed the progression of the MAIDS disease (Fernandes et al., 1992). Thors et al. (2004) also showed positive immune effects on mice when feeding fish oil. In this study, 120 female mice were fe d a standardized, control diet for 6 weeks before being divided into four groups and fed two different diets. The first two groups were fed a diet enriched with fish oil at 10% of total diet weight, and the remaining two groups were fed a diet enriched with corn oil at 10% of the total diet weight (Thors et al., 2004). However, the amount of time these di ets were fed was not clear. Mice were intranasally inoculated with either Kleb siella or Streptococcus pneumoniae and the inoculum was aspirated into the lungs. Survival rates of th e mice fed a fish oil diet and infected with Klebsiella pneumoniae were signi ficantly higher than the rates seen in corn oil fed mice infected with the same disease. However, survival rates of mice infected with Streptococcus pneumoniae did not differ between the fish or corn oil fed mice (Thors et al., 2004). In general, the conflicting results of studi es examining the eff ects of dietary PUFA supplementation on disease resistance may be caused in part by study differences in the type of animal used, type and amount of pa thogen utilized, route of pathogen infection and amount and duration of dietary PUFA s upplementation. Because many of the above studies did not clearly state th is information, it is difficult to establish which differences in disease response between studies could be attributed to PUFA treatment and which could be attributed to differences in e xperimental design. However, Anderson and

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39 Fritsche (2002) suggest that c onflicting results may be rooted in the host’s ability to find a proper balance between the necessary and excessive production of various proinflammatory mediators. Characteristics of Mare Milk Mare Colostrum Colostrum is the mare’s first milk and is vital in transferring immunity to the newborn foal. It has a much th icker, stickier consistency than milk and is often a pale to deep yellow in color. Colostrum, produ ced in the mammary gland during the last trimester of pregnancy, is only secreted for a very short time (Lavoie et al., 1989). By 24-96 hours after foaling, mammary secreti ons have completely transitioned from colostrum to milk (Ullrey et al., 1966). Com positionally, colostrum is higher than milk in fat content (Csap et al., 1995). The most important colostrum constituent, however, is the immunoglobulins. Colostrum has high c oncentrations IgG but lower IgM and IgA (Lavoie et al., 1989). Colostral IgG declines within the first 24 hours after birth. This decline often corresponds to th e change of a thick, pale yellow fluid to one of a thinner consistency with a gray-wh ite color (Pearson et al., 1984) Average colostral Ig concentrations are shown in Table 2-1. Factors Affecting Mare Colostrum IgG Content Premature lactation, or “prela ctation,” is considered th e most important cause of failure of passive transfer in foals, as it is one of the main determin ants of colostral IgG levels (Jeffcott, 1974). Causes of premature lactation include placentitis and/or placental separation, but the condition can occur without obvious pla cental pathology (Jeffcott, 1974b, 1975). Mares that experience prelactati on for longer than 24 hours before foaling tend to have lower colostral IgG concentrations than those who lactate normally (Koterba

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40 et al., 1990). Morris et al. (1985) found th at as the proportion of mares on a breeding farm experiencing prelactation increased, so did the proportion of mares with low colostral IgG concentrations. In addition, the proportion of foals with low serum IgG concentration also increased. Breed of mare may also affect colostral IgG concentration. Pearson et al. (1984) found a significantly higher IgG concentration of more than 5,000 mg IgG/dL colostrum in Arabian mares when compared to Thoroughbr ed mares. Average time from birth until colostrum IgG concentration declined to 1,000 mg/dL (the IgG concen tration that cannot prevent failure of passive transfer) was 19.1 hours for the Arabians and only 8.9 hours for the Thoroughbreds. LeBlanc et al. (1992) f ounder higher IgG colostra l concentrations in Thoroughbreds and Arabians when compared to Standardbreds. However, in another study, LeBlanc et al. (1986) reported no differe nces between IgG colostral concentrations in Thoroughbred, Quarter Horse, Arabian a nd Standardbred mares. The conflicting results seen between these two studies shoul d not have been due to different sampling times or colostrum amounts taken, as both stud ies tested 10 mL of pr esuckle colostrum. Therefore, the conflicting results may be explained by differences in body size and weight between breeds. Larger breeds can sometimes produce larger volumes of colostrum, and this large volume may lead to a dilution effect. However, the age of the mare, number of lactations and herd mana gement are factors that probably influence colostral IgG concentration. A dditionally, there is large indi vidual variation in colostral IgG content, making it difficult to attribute di fferences in colostral IgG as purely breed oriented (Pearson et al., 1984). Further studies are needed to examine what, if any, influence breed has on colostral IgG content.

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41 Conflicting results exist in regard to the connection between a mare’s age and her colostrum quality. In a study involving Standardbred, Thor oughbred and Arabian mares, mares between the ages of 3 and 10 years had the highest colostral IgG concentration and FPT was most prevalent in foals born to dams of over 15 years (LeBlanc et al., 1992). However, Morris et al. (1985) and Erhard et al. (2001) saw no signi ficant effects of age on IgG in mares of varying breeds. Both LeBl anc et al. (1992) and Erhard et al. (2001) sampled colostrum before the foal had been allowed to suckle. However, Morris et al. (1985) sampled colostrum during the first 2 hours after foaling. Since Morris et al. (1985) sampled colostrum at a later time than the other two studies, any difference seen in the colostrum of this study could have been attributed to time. However, time should not have affected the values of LeBlanc et al. (1992) and Erhard et al. (2001). Therefore, discrepancies in data reflecting the effect of mare age of colostrum IgG could be explained by outside factor s such as individual mare variation and management differences. Composition of Mare Milk In mares kept without human influence, lactation lasts about one year, and drying of the udder occurs several weeks to several days before the next foaling. There have been, however, extreme cases noted of 2or 3-year-old suckling foals (Feist and McCullough, 1976). Today, the drying process is initiated by weaning foals at 4-6 months of age. Actual daily lactation yields of nursing mares are not well known, but are estimated to be between 10 and 30 kg for li ght breed nursing mares (Doreau and Boulot, 1989). Peak lactation seems to occur at about two months postpartum (Bouwman and van der Shee, 1978).

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42 Compositionally, the fat content of mare milk is very low (Doreau and Boulot, 1989) but can be influenced by diet. Milk fat is also influenced by mare body condition at foaling, with fat mares producing milk with a higher fat content than thin mares. The increased lipid mobilization of fat mares ma y be explained this phenomenon (Doreau et al., 1993). Crude protein in milk exists at between 1.7 and 3.0% (Doreau and Boulot, 1989) and decreases throughout lact ation (Oftedal et al., 1983). Mare milk is different from the milk of other species as it cont ains higher amounts of the amino acids cystine and glycine (Doreau and Boulot, 1989). Milk carbohydrates are almost entirely made of lactose, with very low levels of free glucose. Mare milk is also extremely low in ash, with 0.7% as extreme (Doreau and Boulot, 1989) Milk is also different than colostrum in the amounts of immunoglobulins present. Le vels of IgG, IgA and IgM all decrease as colostrum transitions into milk and IgA beco mes the predominant Ig present (Norcross, 1982). Average immunoglobulin concentrations in mare milk are shown in Table 2-1. Peak colostrum IgG content is observed at foaling and rapidly declines during the first 24 hours after foaling (Lavoie et al., 1989). In colostrum sampled within 2 hours after foaling, mean IgG values were show n to be 16,583 mg/dL (Lavoie et al., 1989). At 4 hours post foaling, another study showed mean Ig G values that were at lower levels of 5,450 mg/mL, and these values fell even further to 1,010 mg/dL by 9-12 hours after foaling (Erhard et al., 2001). Colostru m IgG fell below 1,000 mg/dL by 13-16 hours post foaling and continued to decrease until day 14 (Erhard et al., 2001). Duvaux-Ponter et al. (2004) showed that these low milk IgG levels did not show any changes by 21 days after foaling, suggesting that mare milk IgG levels stay at this low leve l for the duration of lactation.

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43 Effect of Diet on Fat and Fatty Acid Composition of Milk Milk fatty acids are either synthesized de novo by acetyl-CoA carboxylase and fatty acid synthase or are supplied exogenously. The mammary epithelial cells of lactating animals are highly active in trig lyceride biosynthesis (Clegg et al., 2001). If the FA are not synthesized in the mammary epithelial ce lls, they can enter the cells either from albumin in the plasma or from hydrolysis of chylomicron triglycerides by lipoprotein lipase. Once inside the cell, FA are bound to fatty acid bind ing protein in the cytoplasm or activated with ace tyl-coenzyme A (CoA) and used for triglyceride synthesis. The endoplasmic reticulum synthesizes microlipid droplets that fuse to form cytoplasmic droplets which move to the apical membrane where they are enveloped to form the milk fat globule. This globule is then secreted in a membrane-bound form into the milk (Neville and Picciano, 1997). Mare milk contains relatively little fat, with triglycerides as the predominate lipid class (Dils, 1986). Mare milk naturally contai ns very small quantities of stearic (C18:0) and palmitoleic (C16:0) acids and high quant ities of linolenic (C18:3n-3) and linoleic (C18:2n-6) acids (Csap et al., 1995). The higher amounts of unsaturated FA are explained by the fact that horses consume la rge amounts of forages rich in unsaturated FA (Csap et al., 1995). Milk compositi on, however, may be changed by manipulating the diet, with the largest effects seen in th e fat content (Sutton and Morant, 1989). Mare milk long-chain FA composition is strongly rela ted to the FA composition of the diet, as no microbial FA hydrogenation occurs before in testinal absorption in horses (Doreau et al., 1992; Hoffman et al., 1998). The ratio of forage to grain in the mare ’s diet can effect her milk composition. Generally, fat content decreases as the pe rcentage of grain in creases (Doureau and

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44 Boulot, 1989). Doreau et al (1992) fed nursing mares diet s containing either 95% hay and 5% grain or 50% hay and 50% concentrate. Milk fat concentrations were higher for the mares fed the 95:5 forage:grain diet comp ared to the 50:50 forage:grain diet. The mares eating mostly forage also had highe r linolenic and lower linoleic acid milk contents than those eating mostly grain (Doreau et al., 1992). This effect is understandable considering the fact that fo rage is high in lino lenic acid. However, because exact amounts of hay and grain fed and the fat composition of the diet ingredients was not given, it is difficult to de termine accurate values for percent fat of each diet. Studies in humans have also examined the effect of dietary fat on milk fat composition. Henderson et al. (1992) found th at supplementing pregnant women with 6 g of an EPA and DHA supplement for 21 days significantly increased EPA, DPA and DHA and decreased total n-6 PUFA levels in breast milk when compared to presupplementation levels. Helland et al. (1998) observed an increase in EPA and DHA in breast milk when women were supplemented with 5 and 10 mL cod liver oil daily for 14 days compared to women receiving 5 mL of cod liver oil/day and those receiving no supplementation. The changes in breast m ilk FA composition reported by Henderson et al. (1992) and Helland et al. (1998) were noted as early as day two of supplementation. Interestingly, daily supplementation of wome n with 20 g of flaxseed oil (approximately 10.7 g ALA/d) for 4 weeks increased the EPA a nd DPA breast milk content but failed to produce an increase in DHA (Francois et al ., 2003). The authors speculated that the excess ALA supplied from flax oil may have competitively inhibited 6-desaturase from converting DPA to DHA (F rancois et al., 2003).

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45 In dogs, feeding fat supplements with va rying ratios between ALA and the sum of EPA and DHA produced milk fat compositions hi ghly correlated to the diet fed (Bauer et al., 2004). Dogs were fed one of four diets containing 15% total fat as beef tallow and varying amounts of linseed and menhaden fish oil to provide specific levels of ALA, EPA and DHA. The diets were formulated as follows: the Lo/Lo diet contained 0.14% ALA and 0.04% EPA and DHA, the Lo/Mod diet contained 0.29% ALA and 0.24% EPA and DHA, the Lo/Hi diet contained 0.20% ALA and 0.66% EPA and DHA and the Hi/Lo diet contained 6.82% ALA and 0.04% EPA a nd DHA (fatty acids are expressed as a percentage of dry matter). B itches fed the Hi/Lo diet had th e highest milk ALA content, while bitches fed the Lo/Hi diet had the hi ghest EPA and DHA milk content. Milk responses of EPA, DPA and DHA content were seen as a function of increasing dietary n-3 PUFA content. There was no enrichme nt of DHA when the Hi/Lo diet was fed, showing that ALA is inefficiently convert ed to DHA in the dog (Bauer et al., 2004). Davidson et al. (1991) showed that mares fed a diet with 5% added fat produced milk with a higher fat content than mares who were not supplemented with fat (2-3% dietary fat). However, no diffe rences in milk fat production were noted when mares were fed a sugar and starch diet with 2.4% fat compar ed to a fat (corn oil) and fiber diet with 10.4% fat (Hoffman et al., 1998). Nonetheless, the FA composition of the milk mirrored the FA supplied by the diet. The mares eat ing the high fat diet showed higher milk concentrations of LA and lower concentrations of ALA, which can be explained, in part, by the n-6 PUFA content of the corn oil (Hof fman et al., 1998). Spearman et al. (2005) found that feeding gestating mares a mix of co rn oil and linseed oil increased milk ALA content when compared to mares fed corn oil. Duvaux-Ponter et al. (2004) observed

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46 higher levels of ALA in mare milk when ma res were supplemented with linseed oil. Feeding mares 454 g of encapsulated fish oil per day increased EPA and DHA in the milk but did not affect the ALA content when compar ed to mares fed corn oil (Kruglik et al., 2005). Together, these studies show that the fat content and FA composition of the mare’s diet can influence milk composition. Fatty Acid Transfer across the Placenta The placenta is a pivotal organ in provi ding the developing fetus with essential fatty acids. During the last trimester of pregnancy, fetal requirements for AA and DHA are especially high due to rapid synthesis of brain tissue. To obtain these FA, the fetus depends upon placental transfer, and thus on the FA status of the mother (Al et al., 2000). Much of the research of placental FA tran sfer has been performed in humans, who possess a discoid hemochorial placenta. In these studies, there has been considerable evidence of transfer of ALA, EPA and DHA across the placenta (Innis, 2005). This transfer is a multi-step process of FA uptake by fatty acid binding proteins and intracellular translocatio n of the FA from the maternal to fetal environment. The fatty acid binding proteins that facilitate this pr ocess favor the uptake of n-6 and n-3 PUFA over non-essential FA (Innis, 2005). Human placental preference for transfer of FA has been reported by one author to be DHA>ALA>LA>AA (Haggarty et al., 1997), while others have speculated that DHA and AA are preferred over all other FA (Campbell, 1996; Crawford, 2000). Fetal plasma concentrations of AA and DHA ar e reported to be 300to 400-fold higher than maternal plasma levels while their LA and ALA levels are lower (Elias and Innis, 2001). However, human placenta does contain 6and 5-desaturases (Innis, 2005), so

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47 the higher concentration of AA and DHA in fe tal circulation may be partially produced by placental conversion of these FA from their 18 carbon precursors. Human studies have shown that the matern al dietary intake of n-6 and n-3 PUFA influences placental transfer of AA and DHA. Connor et al. (1996) supplemented pregnant women with sardines and fish oil from the 26th to the 35th week of pregnancy in amounts to provide 2.6 g of n-3 FA per day. When DHA blood levels of newborn infants born to supplemented women were compared to those of newborn infants born to unsupplemented women, newborn babies born to supplemented mothers had 35.2% more DHA in red blood cells. Infants from supplem ented women also showed a plasma DHA content 45.5% higher than infants from unsupplemented mothers, concluding that placental transfer of DHA in women is in creased by maternal supplementation with DHA (Connor et al., 1996). However, de Groot et al. (2004) reported that supplementing pregnant women with ALA did not increase umbilical cord blood DHA, suggesting that the placenta could not efficiently convert ALA to DHA. In this study, pregnant women were supplemented daily with either 9.02 g LA and 2.82 g ALA (experimental group) or 10.94 g LA and 0.03 g ALA (control group) in th e form of margarine. Supplementation was provided from week 14 of pregnancy unt il delivery (de Groot et al., 2004). While the umbilical venous plasma obtained from the subjects at delivery showed no differences in DHA content between groups, the experiment al group did show an EPA concentration twice that of the control gr oup, suggesting that conversion of ALA to EPA in the human placenta may be possible (de Groot et al., 2004). In spite of its complex six-layered placenta the transfer fatty acids from mare to fetus is possible. Equine studies, while few in number, have shown a positive correlation

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48 between maternal and umbilical vein plasma free FA levels (Stammers et al., 1991). However, the same study also showed a difference in FA composition between maternal and umbilical vein plasma. The phospholip ids portion of the umbilical venous plasma contained more longer chain derivatives of LA and ALA than was found in maternal plasma, suggesting that these longer chain FA were of placenta origin, because maternal plasma phospholipids in the horse contain very little longer chain PUFA (Stammers et al., 1991). The presence of 6 or 5-desaturase, to the author ’s knowledge, has not been established in the equine placenta. However, many studies have produced results that would imply these enzymes ar e present. In natural si tuations, long-chain PUFA (particularly DHA) are virtually absent from maternal ci rculation and in very low concentrations in other matern al lipid compartments. In sp ite of this occurrence, foal plasma phospholipids are rich in long-chain PUFA which must ther efore be provided to the foal by placental formation and transfer (Stammers et al., 1987). Stammers et al. (1988) showed that foals had higher plasma concentrations of AA, EPA and DHA than did their dams. A 30 hour fast of the pregna nt mares resulted in an even greater fetal concentration of these fatty acids, resulting from the increased lipid mobilization in the mares (Stammers et al., 1988). When Stammers et al. (1994) incuba ted equine placenta in media enriched with LA, the lipid fracti ons released from the placenta consisted of long-chain PUFA derivatives of LA such as C20:3n-6, C20:4n-6 and C22:6n-6. This finding suggests that these PUFA would be seen in the umbilical plasma lipids rather than the maternal plasma lipids. No studies exist in mares to test the abil ity of manipulation of

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49 dietary fat to influence placental FA transfer, so much research needs to be done in this area. Conclusions Because many of the studies investigating th e effects of feeding n-3 FA to the horse have not utilized a true cont rol group that received no fat supplementation, research is needed to compare the effects of n-3 suppl ementation with no n-3 supplementation (i.e., unaltered diet). This is especially important considering the fact that high forage diets contain significant quantities of n-3 FA, but the addition of grain to the diet shift the proportion of FA in favor of n-6. Studies co mparing n-3 FA supplementation to baseline diets are needed to validate that the biological effects obser ved when feeding n-3 FA are truly due to the increase in these FA, and not to a decrease in n-6 FA. In addition, little research has addressed responses yi elded by different n-3 FA (e.g., ALA, EPA, DHA) to determine if diffe rences in dietary FA source can influence biological responses in the horse. In particular, little data ex ists that compares the effects of different n-3 FA sources fed to the mare and the subsequent response of her nursing foal. It is unclear if supple menting the mare during gestati on with n-3 FA can affect the IgG composition of her colostrum and milk a nd subsequently the IgG concentration in her foal. Furthermore, it is unknown if increa sing the gestating mare’s n-3 FA intake can result in greater placental transfer of n-3 FA therefore allowing the foal to be born with an already elevated le vel of these FA. Lastly, clear effects of supplementation with ALA or an EPA/DHA combination on the inflammatory response in horses have yet to be elucidated. Ther efore, in an attempt to answer some of these questions, the objectives of this study were:

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50 1. Examine the effect of dietary n-3 supple mentation of mares on the FA composition of mare milk and mare and fo al plasma and red blood cells; 2. Examine the difference of efficiencies of ground flaxseed (ALA) and encapsulated fish oil (EPA and DHA) in augmenting EPA and DHA in the mare and foal; 3. Determine if n-3 FA supplementation of th e mare can increase the IgG content of colostrum, milk and foal plasma. 4. Determine in supplementation with flaxseed or fish oil can alter the inflammatory response in mares and foals.

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51 CHAPTER 3 MATERIALS AND METHODS Animals This trial used 36 pregnant Thoroughbred (n=24) and Quarter Horse (n=8) mares and their subsequent foals. Mare age range d from 4 to 20 years with a mean of 10.5 4.1 years (mean SE). Mares were paired acco rding to breed and st ratified according to expected foaling date before being assigne d to three treatment groups. The order of treatment assignment was determined by numbering three pennies, each penny corresponding to a separate treatment, and plac ing them into a hat. Pennies were then drawn at random to determine the order of treatment assignment. Treatment groups were then balanced for mare age and parity. For the duration of this trial, mares and foals were housed at the University of Florida’s Horse Research Center in Ocala, Florida. Pregnant mares were housed on pasture until signs of foaling were evident. At this time, mares were moved into small paddocks until foaling. All mares, with the exception of one, foaled outside. After foaling, mares and foals were kept in a box stall for 24 hours and then turned out in a small paddock for one week before being returned to pasture. A routine vaccination and anthelmintic schedule was followed for all animals. This experiment was performed in accordance with the regulations and approval of the Institutional Animal Care and Use Committee of the University of Florida.

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52 Diets and Treatments The basal diet for all treatment groups consisted of a comm ercial grain-based concentrate (Gest-O-Lac; Ocala Breeders Sales, Ocala, Florid a) and pasture or hay. The grain-based concentrate was offered at 1.0% BW in late gestation and 1.0-2.0% BW during lactation in order to maintain bodyw eight and a minimum body condition score of 5. The concentrate was formulated to meet or slightly exceed nutrient requirements for late gestation and lactation based on N RC recommendations (NRC, 1989). From December to March, mares were fed Coastal bermudagrass hay ad-libitum and had access to dormant bahiagrass pasture. From April to June, mares only had access to bahiagrass pasture. Trace mineralized salt blocks were available at all times Foals were provided with access to the same grain-based concentrat e that was fed to mares via creep feeders that were placed in the pasture. Mares received one of three treatments : 1) basal diet with no supplementation (CON, n = 12); 2) basal diet supplemented with milled flaxseed (Pizzey’s Milling, Manitoba, Canada; FLAX, n=12); or 3) basal diet supplemented with encapsulated fish oil (United Feeds, Inc., Indiana; FISH, n = 12). Both FLAX and FISH were fed to mares in amounts to provide 6 g total n-3 FA /100 kg BW per day. This level of supplementation was chosen based on the stud ies of O’Connor et al (2004) and Siciliano et al. (2003) which demonstrated changes in plasma fatty acid composition when horses were supplemented with similar levels of fish oil. Mares and foals were brought in from pasture at 0700 and 1500 h each day, placed into box stalls and individually fed the grain mix concentrate. Half of the daily allotment of flaxseed or fish oil supplement was hand mixed into the grain provided in the morn ing feeding and the remaining half of the supplements were mixed into the grain provide d in the afternoon f eeding. Foals had the

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53 opportunity to share the mares’ feed, but th is depended upon the individual temperament of each mare. Supplementation began 28 days before the expected foaling date and continued until 84 days post-partum. The nutrient composition of the grainbased concentrate and the flaxseed and encapsulated fish oil supplements is presente d in Table 3-1. The nutrient content of the Coastal bermudagrass hay and bahiagrass pasture is presented in Table 3-2. Table 3-1. Nutrient composition of the grain mix concentrate and the milled flaxseed and encapsulated fish oil supplements Nutrient1 Concentrate Flaxseed Fish Oil DM, %2 92.7 91.5 91.2 DE, Mcal/kg3 3.41 3.0 3.7 CP, % 15.5 22.9 11.8 ADF, % 11.9 19.0 5.9 NDF, % 26.3 40.0 9.9 Fat, % 4.2 37.7 21.5 Ca, % 1.06 0.24 0.33 P, % 0.70 0.74 0.15 Zn, mg/kg 248 41 33 Cu, mg/kg 64 11 4 1 Values are presented on a 100% DM basis (except DM). 2 DM, dry matter; DE, digestible energy; CP, crude protein; ADF, ac id detergent fiber; NDF, neutral detergent fiber. 3 Calculated using the equation: DE (Mcal/kg) = 4.07 – 0.055(%ADF) (NRC, 1989).

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54 Table 3-2. Nutrient composition of the bahi agrass pasture (by month) and Coastal bermudagrass hay Pasture Nutrient1 Dec. Jan. Feb. March April May June Hay DM, %2 45.2 64.1 65.0 44.1 30.5 23.0 17.5 90.8 DE,Mcal/kg3 1.9 1.9 2.0 1.9 2.2 2.4 2.3 1.9 CP, % 11.2 10.7 11.7 11.8 16.0 19.2 19.4 8.9 ADF, % 42.6 41.4 40.2 43.5 35.4 34.4 36.6 38.1 NDF, % 69.3 68.5 64.5 67.7 54.7 59.4 63.0 71.4 Fat, % 1.9 2.1 2.5 2.4 3.1 3.1 3.0 1.5 Ca, % 0.53 0.61 0.68 0.64 0.72 .50 0.40 0.35 P, % 0.29 0.24 0.25 0.25 0.36 0.39 0.40 0.21 Zn,mg/kg 27 38 36 40 32 33 30 46 Cu,mg/kg 6 6 6 8 8 8 9 5 1 Presented on a 100% DM basis (except DM). 2 DM, dry matter; DE, digestible energy; CP, crude protein; ADF, aci d detergent fiber; NDF, neutral detergent fiber. 3 Calculated using the equation: DE (Mcal/kg) = 4.22 – 0.11(%ADF) + 0.0332(%CP) + 0.00112(%ADF)2 (NRC, 1989). Bodyweights Mares were weighed at 28 and 14 d prior to expected foaling date (d-28, d-14), at foaling (d0) and every 14 days thereafter. Foals were wei ghed at birth (d0) and every 14 days thereafter. A digital liv estock scale with an accuracy of 0.5 kg was used to obtain body weights. Blood Sample Collection and Processing Blood samples were collected from mares by jugular venipunctu re at 28 and 14 d prior to expected foaling, at foaling ( d0), and at 28, 56 and 84 d after foaling for acquisition of plasma, serum and/or red bl ood cells. Blood samples were collected from

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55 foals via jugular venipuncture at birth before the foal was allowed to nurse (d0), 36 h post-parturition, and 7, 28, 56 and 84 d postfoaling for acquisition of plasma, serum and/or red blood cells. A square patch of hair was shaved over the foal’s jugular vein to allow for easier blood sampling. Precisi on Glide Vacutainer brand blood collection needles (20G, 1 in. for mares; 20G, 1 in. fo r foals) were used to collect blood into Beckton Dickinson Vacutainers containing sodi um heparin, to facilitate harvesting of plasma and red blood cells, or tubes containi ng no anticoagulant for harvesting of serum. With the exception of samples obtained at birth or 36 h post-parturition, all blood samples were collected between 0700 and 0900 h and prior to the mare’s morning grain feeding. After collection, blood samples were immediately placed on ice and transported to the Animal Nutrition Laboratory for further processing. In the laboratory, blood samples for obtain ing serum were allowed to clot for 30 min to 1 h and then centrifuged at 5590 x g fo r 7 min to allow for separation of serum. Serum was collected with plastic disposable pipets and aliquoted into polypropylene cryogenic vials (2-3 vials, 0.5-1.0 mL each). Samples were frozen at -80C until further analysis for IgG using a commercially avai lable single radial imm unodiffusion kit (SRID Kit, VMRD, Inc., Pullman, WA). See Appendix B for a description of the IgG analysis. Blood samples for obtaining plasma and red blood cells were first used to determine the hematocrit (packed cell volume). Hematocrit values were determined in duplicate using whole blood drawn into a micro capillary tube, centrif uged and read on a microcapillary reader. After determination of hematocrit, each vacutainer was gently rotated and 5.0 mL of whole bl ood was pipetted into a separa te glass tube, labeled, and centrifuged at 5590 x g for 15 minutes to sepa rate the plasma and red blood cells. A

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56 pipet was used to transfer 1.0 mL of plas ma to each of four polypropylene cryogenic vials. Samples were frozen on a slant at 20C to increase the surface area and ensure more efficient freeze drying before being stored at -80C until further analysis of fatty acids. Once plasma had been removed, an aspirator was used to remove any additional plasma and the thin layer of while blood cells lining the top of the red blood cells in each tube. Two mL of cold saline was then adde d to each tube and the tubes were gently mixed and centrifuged at 5590 x g for 7 min. After centrifuging, th e supernatant was aspirated off and an additional 2.0 mL of cold saline was added. The tubes were again mixed and centrifuged at 5590 x g for 7 min. This procedure was repeated once more for a total of three saline washes. After the supe rnatant of the final wash had been aspirated off, exactly 2.0 mL of cold saline was adde d to the remaining re d blood cells in each tube. The tubes were mixed well before 2.0 mL of the red blood cell suspension was transferred into labeled polypr opylene cryogenic vials. These tubes were frozen at an angle at -20C before being placed into st orage at -80C until analyzed for fatty acid content. Colostrum and Milk Collection and Processing Colostrum was obtained from the mare within 1 h of birth and before the foal had suckled (d0). Approximately 120 mL of colo strum was recovered in to a pre-labeled, preweighed plastic cup. The cup was covered with a lid and stored at 4C until transfer to the Animal Nutrition Labor atory for processing. Milk samples were obtained 36 h post-partum and between 0700 and 0900 h on 7, 14, 28, 56 and 84 d post-foaling for determination of fatty acid and IgG content. To facilitate milk collection, foals were muzzled for approximately 30 min to allow the

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57 mare’s udder to fill. The entire udder was then milked out into a pre-labeled, preweighed plastic cup. If the udder contained mo re milk than one cup could hold, the udder was milked out into multiple cups whose content was then mixed in a larger container and approximately 120 mL was transferred to the pre-labeled, pre-weighed sample cup. The excess milk was discarded. After collectio n, milk samples were immediately placed on ice and transported to the Animal Nutr ition Laboratory for further processing. In the laboratory, colostrum and milk sa mples were gently swirled to mix and strained through four layers of cheesecloth to remove any dirt and debris in the sample. The samples were then returned back to the original pre-weighed sample cups. After straining, the sample was mixed again and a pproximately 1.0 mL was aliquoted into each of three pre-labeled polypropylen e cryogenic vials. These vials were then stored at -80C until further analysis for IgG content. The remaining colostrum or milk sample was weighed to determine a wet sample weight and then freeze dried. Freeze dried milk samples were stored at -20C until used for the determination of fatty acid composition. Fatty Acid Analysis Fatty acids in plasma and red blood cells were extracted and methylated using the procedure of Folch et al. (1957). Fatty acids were analyzed by gas chromatography (CP3800 Gas Chromatograph, Varian, Inc., Palo Alto, CA) using a WCOT fused silica column (CP-SIL 88, length100 m, internal diameter 0.25 mm, flow rate 5.0 mL/min, Varian, Inc., Palo Alto, CA). The carrier ga s was helium with a pressure of 29.5 psi (1 min), 35.4 psi (0.42 psi/min, total of 45 min) and 37.9 psi (0.17 psi/min, held for 50 min, total of 110 min). The temperature program was 120C for 1 min, increased to 190C at 5C/min and held at 190C for 30 min (total of 45 min), increased to 220C at 2C/min and held at 220C for 50 min, giving a to tal run time of 110 min. Fatty acids were

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58 identified by comparison of peak retenti on times for samples and reference standards (Nu-Chek Prep, Inc., Elysian, MN). The FA identified included C8:0, C10:0, C12:0, C14:0, C14:1, C16:0, C16:1, C17:0, C17:1, C18:0, C18:1n-9, C18:2n-6 (LA), C18:3n-3 (ALA), C20:0, C20:1, C20:2, C20:3, C20:4n6 (AA), C20:5n-3 (EPA), C22:0, C22:5n-3, C22:6n-3 (DHA) and C24:1. Nonadecanoic aci d (C19:0) was added to the samples and used as an internal standard to assess FA r ecovery. Total n-6 FA were defined as the sum of C18:2 n-6 and C20:4n-6 while total n-3 FA were defined as the sum of C18:3n-3, C20:5n-3, C22:5n-3 and C22:6n-3. Intradermal Skin Test To examine the effect of n-3 FA suppl ementation on the inflammatory response, mares and foals were sensitized with phytohemagglutinin (PHA; Lectin from Phaseolus vulgaris Sigma-Aldrich, Inc., St. Louis, Missour i) at 84 d post-partum. Twenty-five milligrams of PHA was reconstituted in 16.7 mL of phosphate buffered saline (PBS) to give a final concentration of 150 g/100 L. A 4 x 4 cm patch of hair was surgically clipped on the midsection of both sides of the neck on mares and foals and injected intradermally with 100 L of the PHA suspen sion. Precision Glide brand intradermal injection needles (26 G, 3/8 in.) were used to deliver the PHA. Needles were changed between each injection site on the right and left side of the neck. Skin thickness measurements were obtained by pinching the skin between the thumb and forefinger and measuring the skin fold thickness in mm with an electronic digital micrometer (Marathon Watch Company, Ltd., Ontario, Ca nada). Measurements of each injection site were obtained after clipping but before injecting (h 0) and at 2, 4, 6, 8, 12, 24 and 48 h after injection. Skin thickness measurements from the right and left sides of the neck were averaged to give a single thickness m easurement for each time point.

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59 Supplement and Feed Sample Analysis The same batch of milled flaxseed, encapsulated fish oil and Coastal bermudagrass hay were available for the duration of the tria l. However, the source of commercial grain mix was replenished approximately every 2 wk due to storage limitations and the volume of feed needed. Samples of the flaxseed, encapsulated fish oil and grain mix were obtained at 4 wk intervals. These samples we re then dried at 60C and stored at 20C for later analysis. Samples of bahiagrass pastur e were obtained at 4 wk intervals from four, 16 ha pastures. Pasture grass clippings were only obtained from ar eas where grazing was evident. At each 4-wk collection, clippings from the four pastures were composited, dried at 60C and stored at 20C for later an alysis. Throughout the trial, each round bale of Coastal bermudagrass hay that was offered to the mares was core sampled (5 cores per bale), dried at 60C and stored at 20C. After the completion of the trial, all samples of Coastal bermudagrass hay were composited into one sample for anal ysis. All feeds and supplements were analyzed for fatty acid co ntent using the method described above. In addition, feeds were analyzed for DM, DE, CP NDF, ADF, total fat, Ca, P, Mg, Zn and Cu by wet chemistry (Dairy One Forage Analysis Lab, Ithaca, NY). Statistical Analysis Four mares either delivered dead foals or their foals died shortly after birth. Only pre-foaling data was used from these mare s. One mare experienced a red bag during foaling and her foal was subse quently given plasma, so IgG data from this mare and foal were not included in the statisti cal analysis. One foal was euthanized at 30 d of age, so only data taken up to that time point were use d. The final number of mare and foal pairs successfully completing this study was 11 CON, 11 FLAX and 9 FISH.

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60 The MIXED procedure of SAS (V. 9.1, SAS Inst., Inc., Cary, NC) was used to analyze fatty acid composition of colostrum, m ilk, plasma and all feeds, IgG content of colostrum, milk, mare serum and foal se rum, and mare and foal bodyweights. The sources of variation included treatment, ti me and treatment x time interaction. Breed effects were also tested for mare and foal bodyweights, mare serum IgG, mare colostrum and milk IgG and foal serum IgG. Sex eff ects were tested for foal serum IgG. In addition, principle forage source (hay or pasture) was examined as a main effect for mare plasma and red blood cell fatty acids. Fa tty acids analyzed included linoleic (LA), linolenic (ALA), arachidonic (AA), eicosa pentaenoic (EPA) and docosahexaenoic (DHA) acids as well as total n-3 and total n-6 fatty aci ds and the ratio of n-6:n-3 fatty acids. For IgG and fatty acid analysis, horse nested w ithin treatment was considered as a random variable and used as an error te rm to test the effects of all sources of variation. Dunnett’s test was used to separate means. The hom ogeneity of regression for skin thickness values was evaluated using the GLM and MIXED pro cedures in SAS. Horse nested within treatment was used as an error term. Due to missing values and unbalanced trea tment groups after foaling, all data are expressed as least square mean s SE unless otherwise state d. Values were considered significant at p 0.05 and trends were considered at p 0.10.

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61 CHAPTER 4 RESULTS Feed and Supplement Analysis The fatty acid composition of the grain mix concentrate and the flaxseed and encapsulated fish oil supplements is presen ted in Table 4-1. The fatty acid composition of pasture forage was similar from Decem ber through March (Appendix A). Therefore, the fatty acid composition of pasture samples collected in December, January, February and March was averaged and presented as “win ter” pasture (Table 4-2). Similarly, the fatty acid composition of pasture forage was not different between the months of April, May and June (Appendix A). Thus, the fatty acid composition of pasture samples from these months was also averaged and pres ented as “spring” pa sture (Table 4-2). Spring pasture contained lower quantities of C18:0 (P = 0.01) and C18:1 (P = 0.004) and higher quantities of ALA (P = 0.03) and total n-3 FA (P = 0.03) than winter pasture (Table 4-2). Hay c ontained higher concentrations of C16:0 (P = 0.0001), C18:0 (P = 0.003) and C18:1 (P = 0.0001) compared to winter and spring pasture forage (Table 4-2). In addition, hay contained lower concen trations of ALA (P = 0.0001) resulting in a lower total n-3 FA content (P = 0.0001) and a higher n-6:n-3 FA ratio (P = 0.0001) in hay compared to winter and spring pasture (Table 4-2). No differences were observed in LA, AA, EPA, DHA or total n-6 FA content between hay and pasture forage. When principle forage source (hay or pasture) was included in the model as a main effect, forage source did not influence FA levels in any of the milk or blood samples examined in this study (P = 0.11).

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62 Mare Fatty Acid Intake Horses were housed on bahiagrass pastures th roughout the trial. Because of winter dormancy and reduced quantity of pasture fo rage, mares were offered unlimited access to Coastal bermudagrass hay during the months of December, January, February and March. During this four month period, hay was assumed to be the primary forage source. Limited evidence of grazing in pastures and reasonable consumption of hay (based on the number of round bales fed and expected DM intake) during this period support this assumption. All hay was removed from pastures in the first week of April. Therefore, pasture served as the primary forage source fr om April until the conclusion of the trial in late June. Average daily intake of long chain FA by mares on each treatment from December to March (when Coastal bermudagrass hay wa s the primary forage source) and from April to June (when bahiagrass pasture was th e primary forage source) is shown in Tables 4-3 and Table 4-4, respectively. From December to March (when hay was th e primary forage source), FLAX mares consumed 255% more n-3 FA and FISH mare s consumed 257% more n-3 FA than CON mares. From April to June (when pastur e was the primary forage source), FLAX and FISH mares consumed 138% and 137% more n-3 FA than CON mares, respectively. This change in percentages reflects the higher n-3 FA content of spring bahiagrass pasture compared to Coastal bermudagrass ha y. From December to March, the total diet provided a total n-3 FA intake of 4.3 g n-3 FA/100 kg BW in CON mares, 11.3 g n-3 FA/100 kg BW in FLAX mares and 11.3 g n-3 FA/100 kg BW in FISH mares. From April to June, the total diet provided a tota l n-3 FA intake of 17.4 g n-3 FA/100 kg BW in CON mares, 24.8 g n-3 FA/100 kg BW in FL AX mares and 24.3 g n-3 FA/100 kg BW in

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63 FISH mares. Within the supplemented groups, the milled flaxseed and encapsulated fish oil supplied 6.5 to 7.0 g total n-3 FA/100 kg BW or approximately 65% of the total n-3 FA intake in the winter and 30% of the total n-3 FA intake in the spring. For the duration of the trial, FLAX mares consumed higher ALA (P = 0.0001) than FISH and CON mares while FISH mares consumed higher EPA (P = 0.0001) and DHA (P = 0.0001) than FLAX and CON mares. There were no differences between the consumption of total n-3 FA between FISH and FLAX mares (P = 0.94), but both treatments consumed more total n-3 FA than CON mares (P = 0.0001). No treatment effect was observed for tota l n-6 FA intake (P = 0.12). Mare and Foal Bodyweight Treatment had no effect on mare BW at any time during the trial (Table 4-5). CON mares foaled 3 colts and 9 fillies, FLAX mares foaled 7 colts and 5 fillies and FISH mares foaled 4 colts and 8 fillies. There were no differences in foal BW due to sex (P = 0.58), breed (P = 0.62) or treatment (P = 0.75) At birth, CON foals weighed 51.0 4.1 kg and gained 107.3 4.1 kg over the trial peri od. FLAX foals weighed 54.4 3.5 kg at birth and gained 103.9 3.5 kg, and FISH foals weighed 56.3 3.8 kg at birth and gained 107.6 3.9 kg over the trial period (Table 4-6). There was a significant effect of time (P = 0.0001) on foal BW, which reflected an increase in BW as foals grew from birth to 84 d of age. Mare Plasma Fatty Acid Composition Omega-6 Fatty Acids The FA found in the highest concentrati on in mare plasma was LA, which made up almost half of the total FA f ound in plasma (Table 4-7). An overall treatment effect was noted for mare plasma LA, AA and total n-6 FA (Table 4-7). Before supplementation

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64 began (d-28), plasma n-6 FA concentrations we re similar between trea tments (Table 4-8). In response to supplementation, mares fed FISH had lower plasma LA (P = 0.05), greater plasma AA (P = 0.03) and tended to have lo wer plasma total n-6 FA (P = 0.10) than FLAX or CON mares (Tables 4-7 and 4-8). An overall effect of time was detected for plasma LA (P = 0.07), AA (P = 0.01) and total n-6 FA (P = 0.08) and may have reflected the effects of both parturition and dietary treatment (Table 4-8). Plasma LA declined fr om baseline (d-28) to foaling (d0) in CON (P = 0.05) and FISH mares (P = 0.02). Af ter foaling, plasma LA returned to pretreatment levels in CON mares but remained lower in FISH mares. Plasma AA increased (P = 0.01) from baseline to foaling in FISH mares but did not change in CON mares. Total plasma n-6 FA decreased from d-28 to d0 in CON (P = 0.05) and FISH mares (P = 0.04, Figure 4-1). In contrast to the responses seen in FISH and CON mares, plasma LA, AA and total n-6 FA did not change over th e course of the trial in FLAX mares. Omega-3 Fatty Acids The n-3 FA found in the highest concentr ation in mare plasma was ALA, with concentrations ranging from 2.99 to 3.65 g ALA/1 00 g fat (Table 4-7). Overall treatment effects were detected for plas ma ALA, EPA, DHA and total n-3 FA (Table 4-9). Before supplementation, no differences in plasma n3 concentrations were observed between treatment (Table 4-9). In response to diet ary treatment, FISH mares had higher plasma EPA (P = 0.0001), higher plasma DHA (P = 0.0001) and higher plasma total n-3 FA (P = 0.01) than CON mares (Table 4-7). When ma res were fed FLAX, plasma ALA tended to be higher (P = 0.09) than that observed in th e plasma of CON or FISH and total n-3 FA plasma content was similar to both FI SH and CON mares (Table 4-7).

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65 Overall effects of time were detected in plasma ALA (P = 0.02), EPA (P = 0.0001), DHA (P = 0.001) and total n-3 FA (P = 0.0005; Table 4-9). From d-28 to d0, plasma ALA increased in FLAX mares (P = 0.05) but d ecreased in FISH mare s (P = 0.02). After foaling, the plasma ALA of FISH mares retu rned to baseline leve ls while the plasma ALA of FLAX mares remained at an elevated level. Plasma ALA did not change over time in CON mares. Plasma EPA increased (P = 0.002) through d+28 in mares fed FISH, after which this FA stabilized at levels a bove CON and FLAX mares. Plasma DHA and total n-3 increased (P = 0.001) in response to FISH, but remained unchanged in the plasma of CON or FLAX mares for the duration of the trial (Table 4-9; Figure 4-2). In contrast to the effects obser ved in FISH mares, plasma EPA, DHA and total n-3 FA did not change in response to diet ary treatment in FLAX or CON mares (Table 4-9; Figure 42). Treatment did not affect the ratio of n-6:n-3 FA in mare plasma (P = 0.24; Table 410). However, an overall effect of time was detected, as the ratio of plasma n-6:n-3 FA decreased over the course of the trial in all treatments (P = 0.02; Table 4-10). Mare Colostrum and Milk Fatty Acid Composition Treatment had no effect on the total fat c ontent of mare colostrum (P = 0.95) or milk (P = 0.12, Table 4-11). As colostrum transitioned into milk, the total fat content increased (P = 0.0003) for all treatments (Tab le 4-11). The FA found in the highest concentrations in mare colostrum and milk were C16:0, C18:1 and LA (Table 4-12). An overall effect of time was detected for all FA examined in mare milk (Tables 413 and 4-14). All treatments experienced a de crease in total milk n-6 FA (P = 0.0001) and an increase in total milk n-3 FA (P = 0.0001) as lactation progressed (Tables 4-13 and 4-14). As a result, the ratio of n-6:n3 FA decreased in mare milk from foaling

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66 through 84 d post-foaling (P = 0.0001; Table 4-10). From 36h to through 14 d postfoaling, milk LA and total n-6 FA decreased in FLAX (P = 0.0005) and FISH mares (P = 0.0003), and then remained constant for the dura tion of the trial (Table 4-13). Milk from mares fed FISH showed an increase in EPA (P = 0.0001) and DHA (P = 0.0001) content from 36h to through 14 d post-foaling, and these levels remained steady until 84 d postfoaling (Table 4-14). Overall effects of treatment were not not ed for any of the n-6 FA examined in mare milk (Table 4-12, Figure 4-3). However, overall effects of treatment were observed for milk ALA (P = 0.0001), EPA (P = 0.0001), DHA (P = 0.0001) and n-6:n-3 FA ratio (P = 0.01; Tables 4-10 and 4-12). At foali ng, the colostrum of FLAX mares contained higher levels of ALA (P = 0.05) than CON and FISH mares (Table 414, Figure 4-4). As lactation progressed, FLAX mares continued to have a higher ALA content in their milk compared to FISH or CON mares (P = 0.01) FISH mares had a higher colostrum DHA content than CON and FLAX mares (P = 0.03) and had higher EPA (P = 0.0001) and DHA (P = 0.0001) concentrations in milk than CON or FLAX mares as lactation progressed (Table 4-14, Figure 4-4). The colostrum of FL AX mares contained greater total n-3 FA than the colostrum of CON mares (P = 0.05), but total n-3 FA was not different than FISH mares. Over the course of lactation, the n-6:n-3 FA ratio tended to be lower in the milk of FLAX mares (P = 0.09) when compared to the milk of CON and FISH mares (Table 4-10). Foal Plasma Fatty Acid Composition Omega-6 Fatty Acids Similar to the mare, the FA found in the hi ghest concentration in foal plasma was LA, making up roughly one third of the total FA found in plasma (Table 4-15). An

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67 overall treatment effect was not observed for an y of the n-6 FA examined in foal plasma (Table 4-16, Figure 4-5). However, at foa ling (d0), plasma AA concentrations were highest in foals born to FLAX mares (P = 0.04, Table 4-16). At 14 d post-foaling, foals suckling FISH mares showed a higher plasma AA concentration than foals suckling CON mares (P = 0.04), but were similar to foals suckling FLAX mares (P = 0.30). No other effects of treatment on n-6 FA were detected at any time point over the course of the trial. An overall effect of time was detected in plasma LA (P = 0.0001), AA (P = 0.0001) and total n-6 FA (P = 0.0001; Table 4-16, Figur e 4-4). Plasma LA and total n-6 FA increased (P = 0.0001) and plasma AA decreased (P = 0.0001) from foaling to 14 d postfoaling in all treatments (Table 4-16). Plas ma LA and total n-6 FA increased from 14 to 84 d of age in foals suckling CON (P = 0.005) and FISH mares (P = 0.008), but remained stable in foals nursing FLAX ma res. Plasma AA increased from 14 to 84 d of age in Omega-3 Fatty Acids The n-3 FA found in the highest concentration in foal plas ma was ALA, with levels ranging from 2.48 to 3.33 g ALA/100 g fat (Table 4-15). An overall effect of treatment was observed in foal plasma ALA, EPA, DHA and total n-3 FA (Table 4-15, Figure 4-6). At foaling, foals born to FISH mares tended to have a higher total n-3 FA plasma content than foals born to CON or FLAX mares (P = 0.09; Table 4-17, Figure 4-6). Foals suckling FLAX mares had higher plasma ALA (P = 0.04) than foals suckling CON mares and foals nursing FISH mares had higher plasma EPA (P = 0.0001), DHA (P = 0.0001) and total n-3 FA (P = 0.002) than foals nur sing both CON and FLAX mares (Table 4-15 and 4-17). An overall effect of time was detected in all n-3 FA in foal plasma (P = 0.0001; Table 4-17, Figure 4-6). From foaling to 84 d of age, the plasma ALA and total n-3 FA

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68 content increased in foals, regardless of mare treatment (P = 0.0001). Plasma EPA increased in FLAX foals from foaling to 28 d of age (P = 0.0001), but returned to foaling levels by 56 d of age (Table 4-17). Plasma EP A increased from birth to 14 d of age in FISH foals (P = 0.0001), but decreased from 28 to 56 d of age. However, the plasma EPA concentration in FISH foals was still highe r at 84 d of age than the concentrations at foaling (P = 0.0005). From birth to 14 d of age, plasma DHA decreased in CON (P = 0.0001) and FLAX (P = 0.0001) foals and then rema ined steady until the end of the trial. However, the DHA concentration in the plasma of FISH foals remained elevated through 56 d of age, declining slightly by 84 d (Table 4-17). Omega-6:Omega-3 Fatty Acid Ratios An overall effect of treatment on the n-6: n-3 ratio was observed in foal plasma (Table 4-10). At birth, no difference in n-6: n-3 FA ratio was detected between treatments. After suckling treated mares, FI SH foals had a lower n6:n-3 FA ratio (P = 0.002) than FLAX or CON foals (Table 4-10). An overall effect of time on the n-6:n-3 FA ratio was also detected in foal plasma (P = 0.001, Table 4-10). From birth to 14 d of age, the plasma n-6:n-3 ratio increased in CON (P = 0.001) and FLAX (P = 0.01) foals. The plasma n-6:n-3 FA ratio returned to le vels seen at foaling by 28 d of age in FLAX foals, while the plasma n-6:n-3 FA ratio of CON foals did not return to baseline levels until 56 d of age. The plasma n-6:n-3 ratio in FISH foals remained steady over the course of the trial (Table 4-10). Fatty Acid Correlations Positive correlations (P = 0.0001) between mare plasma and milk FA were found for ALA, EPA, DHA and total n-3 FA, while a negative, but weak correlation between mare plasma and mare milk was found for total n-6 FA (P = 0.003; Table 4-18). No

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69 correlation was found between mare plasma LA and mare milk LA, while mare plasma AA and mare milk AA tended to be negatively correlated (P = 0.10). Mare milk ALA, EPA, DHA and total n3 FA were positivel y correlated (P = 0.0001) with foal plasma ALA, EPA, DHA and total n-3 FA (Table 4-18). Mare milk AA and total n-6 FA were negatively correlate d to foal plasma AA (P = 0.0001) and total n-6 FA (P = 0.03). No correlation between m ilk LA and foals plasma LA was detected. Fatty Acid Composition of Red Blood Cells Mare Red Blood Cell Fatty Acids Fatty acids with chain lengths longer than 18 carbons were not detected in mare red blood cells, and LA was the only n-6 FA observe d (Table 4-19). An overall effect of treatment was noted for LA (Table 4-19, Fi gure 4-7). While no differences in LA concentration were found in mare red blood cells before supplementation, there was a tendency (P = 0.10) for FISH mares to have a higher red blood cell LA content than both CON and FLAX mares (P = 0.10, Table 4-19). An overall effect of time was not detected for mare red blood cell n-6 FA content (Table 4-20, Figure 4-7). However, the red blood cell LA content of FISH mares increased fr om pre-supplementation to foaling (P = 0.02; Table 4-20). The LA content of CON and FLAX red blood cells did not fluctuate during the study (Table 4-20). Foal Red Blood Cell Fatty Acids Linoleic acid was the only n-6 FA and AL A was the only n-3 FA found in foal red blood cells; fatty acids with chain lengths longer than 18 carbons were not detected (Table 4-21). An overall effect of treatme nt was detected for red blood cell LA, but not ALA (Table 4-21). At foaling, no differences were observed in red blood cell LA content (Table 4-22, Figure 4-8). In response to su ckling supplemented mares, FISH foals had a

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70 higher red blood cell LA content than both CON and FLAX foals (P = 0.04, Table 4-21, Figure 4-8). Foals belonging to FLAX ma res had higher (P = 0.03) ALA in red blood cells at birth than foals be longing to CON mares, but had similar red blood cell ALA as foals born to FISH mares. Treatment of the mare did not affect ALA content of foal red blood cells at any other time point during the study (Table 4-22, Figure 4-9). An overall effect of time was found in foal red blood cell LA (P = 0.03) but not ALA (Table 4-22). The LA content of red blood cells increased in FISH foals from foaling to 14 d of age (P = 0.01) and stayed elevated for the duration of the study. In contrast, the LA in red blood cells of C ON and FLAX foals did not change during the trial (Table 4-22). Mare Serum, Colostrum and Milk IgG An overall effect of treatment was not de tected in mare serum or colostrum IgG concentrations (Table 4-23). Mare breed (P = 0.78) or age (P = 0.56) did not affect serum IgG content. Similarly, colostrum IgG was not affected by mare breed (P = 0.67) or age (P = 0.58). Milk IgG was not affected by treatment (P = 0.65) or breed (P = 0.67, Table 4-24). However, an overall effect of time on milk IgG was detected (P = 0.0001, Table 4-24). Milk from all mares showed a decline in IgG from 36 h through 84 d post-foaling (Table 4-24). The overall decline in milk IgG con centration from 36 h to 84 d post-partum was 139.4 630.7 mg/dL for CON mares, 157.0 677.5 mg/dL for FLAX mares and 132.5 659.2 mg/dL for FISH mares. Mare serum IgG at foaling was not corre lated with mare age (Table 4-25). Similarly, colostrum IgG was not correlated with mare age, although FLAX mares tended to show an inverse relations hip (r = -0.58, P = 0.06) between mare age and colostrum IgG

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71 (Table 4-25). Mare serum IgG at foaling was not correlated to colostrum IgG, and colostrum IgG was not correlated to foal se rum IgG at 36 h post-foaling. However, a weak correlation between mare serum IgG at foaling and foal serum IgG at 36 h postfoaling was detected across treatments (r = 0.42, P = 0.02; Figure 4-10). Within treatments, d0 serum IgG from CON and FLAX mares showed no correlation with foal 36h serum IgG content, but serum IgG from FISH mares at d0 was correlated to FISH foals serum IgG at 36 h post-fo aling (r = 0.63, P = 0.05, Table 4-25). Foal Serum IgG All foals had serum IgG concentrations that were very low at bi rth and reflected the pre-suckle status of the foal (Figure 4-11). The IgG content of foal serum increased to, and peaked at, 36 h post-foaling, indicating that passive transfer of IgG had taken place. An overall effect of time was noted for fo al serum IgG (P = 0.0001), as the IgG of all foals steadily declined from 36 h to 84 d post-foaling (Table 4-25, Figure 4-12). No overall effect of treatment was observ ed for foal serum IgG (Table 4-25). However, foals suckling FISH mares tended to have lower serum IgG than foals nursing FLAX mares at 36h (P = 0.09) and 7 d post-foal ing (P = 0.10). In addition, FISH foals tended to have lower IgG than CON foal s at 28 d post-foaling (P = 0.10). Mare and Foal Responses to the Intradermal Skin Test Mare Response to PHA An overall effect of treatment was not dete cted in the skin thickness of mares in response to a paired intradermal skin test using PHA as the stimulant (P = 0.89; Table 426). However, an overall effect of time was observed (P = 0.0001; Table 4-26). Before injection, no differences were observed in ma re skin thickness (P = 0.56; Figure 4-13). All mares experienced a signifi cant increase in skin thickness from 0 to 2 h (P = 0.0001)

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72 and from 2 to 4 h post-injection (P = 0.0001; Table 4-26, Figure 4-13). Skin thickness was greatest between 4 and 8 h post-injection an d then decreased. At 48 h, skin thickness was still elevated above that measured before PHA injection at 0 h (P = 0.0001). Foal Response to PHA An overall effect of time (P = 0.0001) on skin thickness in foals in response to PHA injection was detected, reflec ting an inflammatory response (Figure 4-14). Foal skin thickness increased (P = 0.0001) from 0 to 4 h, remained elevated through 8 h postinjection and then declined through 48 h pos t-injection (P = 0.0001, Figure 4-14). At 48 h post-injection, skin thickness had not yet declined to baseline thickness measured before PHA injection (P = 0.0001). An overall effect of treatment on foal sk in thickness was not detected (P = 0.58; Table 4-27). However, CON foals peaked at 4 h (P = 0.0001), whereas skin thickness remained elevated in FLAX and FISH foal s through 6 h (P = 0.0001; Figure 4-14, Table 4-27). At 6 h post-injection, FLAX foals had greater skin thickness than CON foals (P = 0.02), while the skin thickness of FISH foal s was intermediate between FLAX and CON foals. Comparing Mare and Foal Responses to PHA Across treatments, skin thickness in response to PHA injection was different between mares and foals (P = 0.0001; Table 428, Figure 4-15). Although thickness was not different before injection of PHA ( 0h), mares exhibited a greater (P = 0.0001) inflammatory response to intradermal PHA comp ared to foals (Table 4-28, Figure 4-15). The skin thickness of neither the mares or the foals returned to preinjection values by 48 h post-injection (P = 0.0001).

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73 Table 4-1. Fatty acid composition of the grain mix concentrate and the milled flaxseed and encapsulated fish oil supplements1 Fatty acid Grain mix Flaxseed Fish Oil C8:0 ND ND ND C10:0 ND ND ND C12:0 ND ND ND C14:0 ND ND 8.62 C16:0 17.18 5.60 21.14 C16:1 0.21 ND 13.77 C17:0 ND ND ND C17:1 ND ND ND C18:0 2.20 2.77 3.79 C18:1 26.28 13.90 7.87 C18:2n-6 (LA) 49.63 16.31 7.23 C18:3n-3 (ALA) 3.72 61.20 2.35 C20:4n-6 (AA) ND ND 0.69 C20:5n-3 (EPA) ND ND 15.03 C22:5 n-3 (DPA) ND ND 2.11 C22:6n-3 (DHA) ND ND 12.54 Total n-62 49.63 16.31 7.92 Total n-33 3.72 61.20 32.03 n-6:n-3 13.34 0.27 0.25 1 Presented as g fatty acid per 100 g fat; ND = not detected in the feedstuff. 2 Calculated as C18:2 + C20:4. 3 Calculated as C18:3 + C20:5 + C22:5 + C22:6.

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74 Table 4-2. Fatty acid composition of winter and spring bahiagrass pasture and Coastal bermudagrass hay1 Pasture Fatty acid Winter2 Spring3 Hay C8:0 ND ND ND C10:0 ND ND ND C12:0 ND ND ND C14:0 ND ND ND C16:0 22.07 0.69a 23.22 0.67a 39.30b C16:1 ND ND ND C17:0 0.93 0.05a 0.53 0.28a 0.00b C17:1 ND ND ND C18:0 4.97 0.38a 3.36 0.22b 6.65c C18:1 4.21 0.60a 1.39 0.02b 7.08c C18:2n-6 (LA) 23.71 1.96 18.13 1.55 23.48 C18:3n-3 (ALA) 41.52 3.28a 52.47 1.76b 15.90c C20:4n-6 (AA) ND ND ND C20:5n-3 (EPA) ND ND ND C22:5 n-3 (DPA) ND ND ND C22:6n-3 (DHA) ND ND ND Total n-64 23.71 1.90 18.13 1.55 23.48 Total n-35 41.52 3.28a 52.47 1.76b 15.90c n-6:n-3 0.59 0.08a 0.35 0.04a 1.45b 1 Presented as g fatty acid per 100 g fa t; ND = not detected in the forage. 2 Winter = Mean of December, January, February and March. 3 Spring = Mean of April, May and June. 4 Calculated as C18:2 + C20:4. 5 Calculated as C18:3 + C20:5 + C22:5 + C22:6. a,b,c Values in the same row having diffe rent superscripts differ at P < 0.05.

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75 Table 4-3. Mare average daily fatty acid intake from December-March1 Mare diet Fatty acid Treatment2 Grain Hay3 Supplement Total diet C18:2n-6 (LA) CON 135.49 21.37 ND 156.86 FLAX 129.24 20.66 10.45 160.35 FISH 137.57 21.37 8.7 167.64 C18:3n-3 (ALA) CON 10.16 14.58 ND 24.73 FLAX 9.69 14.10 39.22 63.01 FISH 10.31 14.58 2.83 27.72 C20:4n-6 (AA) CON ND ND ND ND FLAX ND ND ND ND FISH ND ND 0.83 0.83 C20:5n-3 (EPA) CON ND ND ND ND FLAX ND ND ND ND FISH ND ND 18.10 18.10 C22:6n-3 (DHA) CON ND ND ND ND FLAX ND ND ND ND FISH ND ND 15.10 15.10 Total n-64 CON 135.49 21.37 ND 156.86 FLAX 129.24 20.66 10.45 160.35 FISH 137.57 21.37 9.54 168.48 Total n-35 CON 10.16 14.58 ND 24.73 FLAX 9.69 14.10 39.22 63.01 FISH 10.31 14.58 38.56 63.45 n-6:n-3 CON 13.34:1 1.47:1 ND 6.34:1 FLAX 13.34:1 1.47:1 0.27:1 2.54:1 FISH 13.34:1 1.47:1 0.25:1 2.66:1 1 Presented as g fatty acid/d; ND = not detected in any of the feedstuffs. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 3 Hay intake estimated at 1.0% BW (DM basis). 4 Calculated as C18:2 + C20:4. 5 Calculated as C18:3 + C20:5 + C22:5 + C22:6.

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76 Table 4-4. Mare average daily fa tty acid intake from April-June1 Mare diet Fatty acid Treatment2 Grain Spring pasture3 Supplement Total diet C18:2n-6 (LA) CON 135.49 30.91 ND 166.40 FLAX 129.24 31.47 9.84 170.55 FISH 137.57 30.91 8.24 176.72 C18:3n-3 (ALA) CON 10.16 89.46 ND 99.62 FLAX 9.69 91.09 36.91 137.69 FISH 10.31 89.46 2.68 102.45 C20:4n-6 (AA) CON ND ND ND ND FLAX ND ND ND ND FISH ND ND 0.82 0.82 C20:5n-3 (EPA) CON ND ND ND ND FLAX ND ND ND ND FISH ND ND 17.06 17.16 C22:6n-3 (DHA) CON ND ND ND ND FLAX ND ND ND ND FISH ND ND 14.34 14.34 Total n-64 CON 135.49 30.91 ND 166.40 FLAX 129.24 31.47 9.84 170.55 FISH 137.57 30.91 9.03 177.51 Total n-35 CON 10.16 89.46 ND 99.62 FLAX 9.69 91.09 36.91 137.69 FISH 10.31 89.46 36.50 136.27 n-6:n-3 CON 13.34:1 0.35:1 ND 1.67:1 FLAX 13.34:1 0.35:1 0.27:1 1.24:1 FISH 13.34:1 0.35:1 0.25:1 1.30:1 1 Presented as g fatty acid/d; ND = not detected in any of the feedstuffs. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 3 Pasture intake estimated at 1.0% BW (DM basis). 4 Calculated as C18:2 + C20:4. 5 Calculated as C18:3 + C20:5 + C22:5 + C22:6.

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77 Table 4-5. Mare bodyweights1 Treatment2 Time3 CON FLAX FISH SEM d-28 629.2 619.0 635.9 13.66 d-14 631.3 626.3 639.7 13.51 d0 554.9 544.2 559.2 8.83 d+14 553.0 551.7 559.3 8.81 d+28 556.0 550.7 562.5 8.81 d+42 560.9 552.9 567.5 8.87 d+56 561.7 548.2 567.4 8.84 d+70 556.6 542.8 557.7 9.00 d+84 556.6 552.4 565.0 8.90 1 Presented in kg. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 3 d-28 to d-14 = d before expected foaling; d0 = foaling; d+14 to d+84 = d post-foaling. Table 4-6. Foal bodyweights1,2 Treatment3 Time4 CON FLAX FISH SEM d0 51.0a 54.4a 56.3a 2.21 d+14 74.1b 75.5b 75.4b 2.20 d+28 91.9c 95.4c 95.0c 2.20 d+42 109.4d 116.0d 115.0d 2.25 d+56 125.1e 127.6e 131.5e 2.23 d+70 144.8f 142.4f 144.4f 2.34 d+84 158.3g 158.5g 163.9g 2.25 1 Presented in kg. 2 Effect of time (P = 0.0001), e ffect of treatment (P = 0.75), effect of treatment x time (P = 0.31). 3 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 4 d0 = foaling; d+14 to d+84 = d post-foaling. a,b,c,d,e,f,g Values in the same column having differe nt subscripts are different at P < 0.05.

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78 Table 4-7. Overall effect of treatment on the fatty acid composition of mare plasma1 Treatment2 Fatty Acid CON FLAX FISH SEM P-value C8:0 ND ND ND NA NA C10:0 ND ND ND NA NA C12:0 ND ND ND NA NA C14:0 ND ND ND NA NA C16:0 16.15 16.01 16.48 0.25 0.42 C16:1 0.88 0.88 1.10 0.09 0.17 C17:0 0.70 0.73 0.73 0.04 0.78 C17:1 ND ND ND NA NA C18:0 20.08 20.18 20.45 0.32 0.72 C18:1 10.28 9.78 9.70 0.28 0.29 C18:2n-6 (LA) 46.43 46.87 44.37 0.71 0.05 C18:3n-3 (ALA) 2.99 3.65 3.06 0.23 0.09 C20:4n-6 (AA) 1.50 1.33 1.82 0.13 0.03 C20:5n-3 (EPA) 0.02 0.02 0.56 0.06 0.0001 C22:6n-3 (DHA) 0.05 0.03 0.61 0.05 0.0001 Total n-63 48.64 48.92 47.04 0.64 0.10 Total n-34 3.03 3.69 4.22 0.26 0.01 n-6:n-3 16.33 16.21 13.32 1.35 0.24 1 Presented as g fatty acid per 100 g fat, ND = not detected in plasma, NA = not applicable. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 3 Calculated as C18:2 + C20:4. 4 Calculated as C18:3 + C20:5 + C22:5 + C22:6.

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79Table 4-8. Omega-6 fatty acid content of mare plasma1 Time2 P-values Fatty acid d-28 d0 d+28 d+56 d+84 SEM Treatment Time Treatment x Time C18:2 (LA) 0.05 0.07 0.79 CON 47.0y 43.1z 47.5y 46.9y 47.6a,y 0.70 FLAX 45.8 45.5 47.2 47.7 48.1a 0.73 FISH 46.7y 42.3z 44.6z 44.9z 43.4b,z 0.73 C20:4 (AA) 0.03 0.01 0.60 CON 1.7y,z 2.2a,b,y 1.3z 1.2z 1.2z 0.12 FLAX 1.8 1.5a 1.2 1.1 1.1 0.13 FISH 1.7y 2.7b,z 1.4y 1.7y 1.6y 0.13 Total n-63 0.10 0.08 0.79 CON 49.2y 45.8z 49.5y 48.9y 49.7y 0.63 FLAX 48.4 47.6 49.1 49.5 50.0 0.65 FISH 49.2y 45.7z 46.8y,z 47.6y,z 45.9z 0.65 1 Presented as g fatty acid per 100 g fat. 2 d-28 = d before expected foaling; d0 = foaling; d+28 to d+84 = d post-foaling. 3 Calculated as C18:2 + C20:4. a,b Values in the same column for each fatty acid not sharing a common superscrip t are different at P < 0.05. y,z Values in the same row not sharing a co mmon superscript are different at P < 0.05.

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80Table 4-9. Omega-3 fatty acid content of mare plasma1 Time2 P-values Fatty acid d-28 d0 d+28 d+56 d+84 SEM Treatment Time Treatment x Time C18:3 (ALA) 0.09 0.02 0.12 CON 3.0 2.3a 2.8 3.4 3.4 0.23 FLAX 2.5x 3.3b,y 3.6y 4.2y 4.5y 0.23 FISH 3.2x 2.2a,y 3.3x 2.9x 3.8x 0.24 C20:5 (EPA) <0.0001 <0.0001 <0.0001 CON 0.0 0.01 0.0a 0.02a 0.03a 0.06 FLAX 0.0 0.0 0.1a 0.0a 0.0a 0.06 FISH 0.0x 0.3y 1.1b,z 1.0b,z 0.5b,y 0.06 C22:6 (DHA) <0.0001 0.001 0.0004 CON 0.0 0.17a 0.0a 0.04a 0.04a 0.05 FLAX 0.0 0.0a 0.1a 0.0a 0.03a 0.05 FISH 0.0x 0.64b,y 0.95b,y 0.89b,y 0.71b,y 0.05 Sum n-33 0.01 0.0005 0.01 CON 2.9 2.5 2.9a 3.4a 3.5a 0.25 FLAX 2.6 3.3 3.8a 4.2a,b 4.5a,b 0.26 FISH 2.9x 3.0x 5.3b,y 4.8b,y 5.1b,y 0.26 1 Presented as g fatty acid per 100 g fat. 2 d-28 = d before expected foaling; d0 = foaling; d+28 to d+84 = d post-foaling. 3 Calculated as C18:3 + C20:5 + C22:5 + C22:6. a,b Values in the same column for each fatty acid not sharing a common superscrip t are different at P < 0.05. y,z Values in the same row not sharing a co mmon superscript are different at P < 0.05.

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81Table 4-10. Omega-6:omega-3 fatty acid ratios in mare and foal plasma and mare milk1 Time2 P-values Sample d-28 d0 36h d+14 d+28 d+56 d+84 SEM Treatment Time Treatment x Time Mare plasma 0.24 0.02 0.79 CON 19.0y,z 22.7y ----15.0z 12.2z 12.8z 1.35 FLAX 21.6y,z 17.2y,z ----14.5y,z15.0y,z12.8z 1.40 FISH 17.5y 17.2y ----9.1z 11.8y 10.9y,z 1.40 Mare milk 0.01 0.0001 0.66 CON --3.4a,y 3.2a,y 1.6z 1.2z 1.2z 1.0z 0.12 FLAX --2.4b,y 2.4b,y 1.4z 1.0z 0.7z 0.7z 0.12 FISH --3.6a,y 3.0a,b,y 1.5z 0.9z 1.0z 1.0z 0.12 Foal plasma 0.002 0.001 0.03 CON --11.1y --19.7a,z17.2a,z10.4y 11.5y 1.08 FLAX --11.4y --17.1a,z9.9b,y 9.7y 9.1y 0.94 FISH --11.0 --8.3b 6.5b 6.5 7.8 1.00 1 Calculated as total n-6 / total n-3. 2 d-28 = d before expected foaling; d0 = foaling; 36h = h post-foaling; d+14 to d+84 = d post-foaling. a,b Values in the same column for each fatty acid ha ving different superscripts are different at P < 0.05. y,z Values in the same row having different superscripts are different at P < 0.05.

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82 Table 4-11. Overall effect of treatment on th e total fat content of mare colostrum and milk1 Treatment2 Sample CON FLAX FISH SEM P Value Colostrum 0.90a 0.99a 0.96a 0.20 0.95 Milk 1.54b 1.42b 1.33b 0.07 0.12 1 Presented as g fat/100 g milk (wet basis). 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. a,b Values in the same column having differe nt superscripts are different at P < 0.05. Table 4-12. Overall effect of treatment on the fatty acid composition of mare colostrum and milk1 Treatment2 Fatty acid CON FLAX FISH SEM P-value C8:0 5.69 6.20 6.23 0.18 0.08 C10:0 10.00 10.78 10.78 0.41 0.32 C12:0 8.53 9.26 9.23 0.38 0.34 C14:0 5.74 5.92 6.01 0.21 0.67 C16:0 17.73 16.99 17.69 0.22 0.04 C16:1 5.74 5.02 5.37 0.18 0.03 C17:0 0.05 0.05 0.08 0.01 0.33 C17:1 0.31 0.29 0.26 0.02 0.31 C18:0 1.42 1.49 1.53 0.05 0.33 C18:1 16.16 14.69 14.58 0.50 0.06 C18:2n-6 (LA) 15.82 14.52 15.03 0.58 0.31 C18:3n-3 (ALA) 11.71 13.06 10.87 0.48 0.01 C20:4n-6 (AA) 0.19 0.20 0.20 0.03 0.96 C20:5n-3 (EPA) 0.01 0.02 0.43 0.03 0.0001 C22:6n-3 (DHA) 0.03 0.03 0.62 0.04 0.0001 Total n-63 16.46 15.22 15.59 0.60 0.34 Total n-34 11.74 13.11 12.02 0.48 0.12 n-6:n-3 1.95 1.40 1.83 0.12 0.09 1 Presented as g fatty acid per 100 g fat. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 3 Calculated as C18:2 + C20:4. 4 Calculated as C18:3 + C20:5 + C22:5 + C22:6.

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83Table 4-13. Omega-6 fatty acid content of mare colostrum and milk1 Time2 P-values Fatty acid d0 36h d+14 d+28 d+56 d+84 SEM Treatment Time Treatment x Time C18:2 (LA) 0.31 0.0001 0.50 CON 20.71x 16.52y 15.24a,y 14.05y 15.05y 13.32y 0.59 FLAX 19.86x 17.25y 11.58b,z 12.43z 13.61z 12.38z 0.59 FISH 21.85x 17.34y 11.98b,z 12.37z 12.49z 14.16z 0.59 C20:4 (AA) 0.96 0.0001 0.72 CON 0.02x 0.01x 0.35y 0.12z 0.39y 0.26y 0.03 FLAX 0.02x 0.07x 0.35y 0.15x 0.38y 0.24z 0.03 FISH 0.02x 0.10x 0.30y 0.03x 0.48z 0.28y 0.03 Total n-63 0.34 0.0001 0.46 CON 21.38x 16.84y 16.15a,y 14.71y 15.80y 13.87y 0.59 FLAX 20.73x 17.80y 12.47b,z 13.06z 14.34z 12.93z 0.59 FISH 22.57x 17.72y 12.65b,z 12.92z 13.13z 14.57z 0.60 1 Presented as g fatty acid per 100 g fat. 2 d0 = colostrum collected at foaling; 36h = h post-foaling; d+14 to d+84 = d post-foaling. 3 Calculated as C18:2 + C20:4. a,b Values in the same column for each fatty acid ha ving different superscripts are different at P < 0.05. x,y,z Values in the same row having different superscripts are different at P < 0.05.

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84Table 4-14. Omega-3 fatty acid content of mare colostrum and milk1 Time2 P-values Fatty acid d0 36h d+14 d+28 d+56 d+84 SEM Treatment Time Treatment x Time C18:3 (ALA) 0.01 0.0001 0.17 CON 6.73a,w 4.70a,w 10.25x 13.33y 15.81a,y 19.44z 0.48 FLAX 9.49b,w 8.01b,w 10.54x 13.02y 19.53b,z 17.74z 0.48 FISH 6.89a,w 6.30a,b,w 8.44w 12.92x 14.34a,x 16.34x 0.49 C20:5 (EPA) 0.0001 0.002 0.005 CON 0.00 0.00a 0.05a 0.00a 0.00a 0.00a 0.03 FLAX 0.00 0.00a 0.00a 0.09a 0.00a 0.00a 0.03 FISH 0.23x 0.28b,x,z 0.63b,y 0.69b,y 0.43b,y 0.27b,z 0.03 C22:6 (DHA) 0.0001 0.0004 0.003 CON 0.00a 0.00a 0.05a 0.03a 0.08a 0.00a 0.04 FLAX 0.00a 0.00a 0.00a 0.12a 0.06a 0.00a 0.04 FISH 0.29b,x 0.37b,x,z 0.94b,y 0.95b,y 0.66b,y 0.47b,z 0.04 Total n-33 0.12 0.0001 0.20 CON 6.70a,w 4.66a,w 10.32x 13.40y 15.87a,y 19.48z 0.48 FLAX 9.47b,w 7.99b,w 10.57x 13.22y 19.63b,z 17.80z 0.47 FISH 7.38a,b,w 6.94a,b,w 10.18x 14.58y 15.69a,y 17.37y 0.48 1 Presented as g fatty acid per 100 g fat. 2 d0 = colostrum collected at foaling; 36h = h post-foaling; d+14 to d+84 = d post-foaling.. 3 Calculated as C18:3 + C20:5 + C22:5 + C22:6. a,b Values in the same column for each fatty acid ha ving different superscripts are different at P < 0.05. w,x,y,z Values in the same row having different superscripts are di fferent at P < 0.05.

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85 Table 4-15. Overall effect of treatment on the fatty acid composition of foal plasma1 Treatment2 Fatty acid CON FLAX FISH SEM P-value C8:0 ND ND ND NA NA C10:0 0.17 0.23 0.36 0.11 0.50 C12:0 0.68 0.75 0.69 0.07 0.70 C14:0 0.63 0.64 0.60 0.06 0.88 C16:0 17.96 17.54 18.11 0.21 0.16 C16:1 2.27 2.13 2.12 0.08 0.28 C17:0 0.35 0.36 0.43 0.03 0.19 C17:1 0.15 0.19 0.15 0.03 0.48 C18:0 20.83 21.18 20.51 0.25 0.20 C18:1 10.90 10.67 10.03 0.20 0.01 C18:2n-6 (LA) 36.99 36.45 33.67 0.85 0.56 C18:3n-3 (ALA) 2.48 3.33 2.72 0.23 0.04 C20:4n-6 (AA) 2.79 3.01 2.97 0.20 0.74 C20:5n-3 (EPA) 0.05 0.09 0.89 0.06 0.0001 C22:6n-3 (DHA) 0.48 0.53 1.74 0.11 0.0001 Total n-63 40.76 39.95 39.12 0.75 0.34 Total n-34 3.10 4.12 5.80 0.30 0.0001 n-6:n-3 13.97 11.43 8.03 0.96 0.002 1 Presented as g fatty acid per 100 g fat, ND = not detected in plasma, NA = not applicable. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 3 Calculated as C18:2 + C20:4. 4 Calculated as C18:3 + C20:5 + C22:5 + C22:6

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86.Table 4-16. Omega-6 fatty acid content of foal plasma1 Time2 Fatty acid d0 d+14 d+28 d+56 d+84 SEM Treatment Time Treatment x Time C18:2 (LA) 0.56 0.0001 0.60 CON 18.79w 39.32x 39.92x 42.31x,y 44.62y 0.90 FLAX 16.92w 39.98x 40.07x 41.97x 43.32x 0.76 FISH 19.89w 37.73x 37.27x 40.41x,y 43.06y 0.84 C20:4 (AA) 0.74 0.0001 0.003 CON 6.00a,w 1.40a,x 2.34y 2.32y 1.89x,y 0.22 FLAX 6.92b,w 1.88a,b,x 2.13x 2.17x 1.95x 0.18 FISH 5.30a,w 2.35b,x 2.73x 2.31x 2.14x 0.20 Total n-63 0.34 0.0001 0.81 CON 24.98w 42.11x 43.85x,y 45.47y,z 47.41z 0.80 FLAX 23.78w 42.72x 42.81x 44.75x 45.68x 0.69 FISH 25.20w 40.66x 40.61x 43.40x,y 45.76y 0.74 1 Presented as g fatty acid per 100 g fat. 2 d0 = foaling; d+14 to d+84 = d post-foaling. 3 Calculated as C18:2 + C20:4. a,b Values in the same column for each fatty acid ha ving different superscripts are different at P < 0.05. w,x,y,z Values in the same row having different superscripts are di fferent at P < 0.05.

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87Table 4-17. Omega-3 fatty acid content of foal plasma1 Time2 P-values Fatty acid d0 d+14 d+28 d+56 d+84 SEM Treatment Time Treatment x Time C18:3 (ALA) 0.04 0.0001 0.42 CON 0.18x 2.16y 2.72a,y 3.78a,z 3.55a,z 0.25 FLAX 0.1x 2.2y 4.2b,z 5.0b,z 5.1b,z 0.21 FISH 0.28x 1.62y 3.24a,z 4.19a,z 4.5a,z 0.24 C20:5 (EPA) 0.0001 0.0001 0.0001 CON 0.01 0.13a 0.02a 0.06a 0.02a 0.07 FLAX 0.03x 0.11a,x,y 0.25a,y 0.01a,x 0.02a,x 0.06 FISH 0.21x 1.26b,y 1.41b,y 0.91b,z 0.65b,z 0.06 C22:6 (DHA) 0.0001 0.0001 0.0001 CON 1.52x 0.36a,y 0.20a,y 0.23a,y 0.08a,y 0.12 FLAX 1.57x 0.37a,y 0.48a,y 0.14a,y 0.06a,y 0.10 FISH 1.82x 1.91b,x 2.09b,x 1.55b,xy 1.34b,y 0.11 Total n-32 0.0001 0.0001 0.01 CON 1.89d,x 2.78a,x,y 2.97a,y 4.19a,z 3.67a,y,z 030 FLAX 1.75d,x 2.94a,y 5.13b,z 5.31a,z 5.48b,z 0.26 FISH 2.85e,x 5.28b,y 7.25c,z 7.15b,z 6.49b,z 0.28 1 Presented as g fatty acid per 100 g fat. 2 d0 = foaling, d+14 = 14 d post-foaling, d+28 = 28 d post-foaling, d+56 = 56 d post-foaling, d+84 = 84 d post-foaling. 3 Calculated as C18:3 + C20:5 + C22:5 + C22:6. a,b,c Values in the same column for each fatty acid having different superscripts are different at P < 0.05. d,e Values in the same column for each fatty acid ha ving different superscripts are different at P < 0.10. x,y,z Values in the same row having different superscripts are different at P < 0.05.

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88 Table 4-18. Correlations between mare milk a nd mare plasma fatty acid concentrations and mare milk and foal plasma fatty acid concentrations Correlation r-value P-value Mare milk and plasma C18:2 (LA) -0.01 0.90 C18:3 (ALA) 0.63 <0.0001 C20:4 (AA) -0.18 0.10 C20:5 (EPA) 0.92 <0.0001 C22:6 (DHA) 0.69 <0.0001 Total n-6 -0.32 0.003 Total n-3 0.55 <0.0001 Mare milk and foal plasma C18:2 (LA) -0.04 0.69 C18:3 (ALA) 0.70 <0.0001 C20:4 (AA) -0.43 <0.0001 C20:5 (EPA) 0.78 <0.0001 C22:6 (DHA) 0.58 <0.0001 Total n-6 -0.20 0.03 Total n-3 0.50 <0.0001

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89 Table 4-19. Overall effect of treatment on th e fatty acid content of mare red blood cells1 Treatment2 Fatty acid CON FLAX FISH SEM P-value C8:0 ND ND ND NA NA C10:0 ND ND ND NA NA C12:0 ND ND ND NA NA C14:0 ND ND ND NA NA C16:0 41.48 41.20 39.57 0.87 0.28 C16:1 0.44 0.25 0.29 0.11 0.42 C17:0 0.37 0.26 0.28 0.06 0.39 C17:1 ND ND ND NA NA C18:0 28.43 28.47 27.18 0.52 0.17 C18:1 24.33 24.32 24.97 0.52 0.62 C18:2n-6 (LA) 4.85 5.41 7.57 0.89 0.10 1 Presented as g fatty acid per 100 g fat, ND = not detected in re d blood cells, NA = not analyzed. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil.

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90Table 4-20. Linoleic acid cont ent of mare red blood cells1 Time2 P-values Fatty acid d-28 d0 d+28 d+56 d+84 SEM Treatment Time Treatment x Time C18:2 (LA) 0.10 0.31 0.43 CON 4.92 4.84a 4.41 3.90a 6.20 0.88 FLAX 5.94 5.81a 4.51 4.33a 6.50 0.88 FISH 5.89y 9.85b,z 6.85y,z 8.34b,y,z 6.92y,z 0.92 1 Presented as g fatty acid per 100 g fat. 2 d-28 = d before expected foaling date; d0 = foaling; d+28 to d+84 = d post-foaling. a,b Values in the same column for each fatty acid ha ving different superscripts are different at P < 0.05. y,z Values in the same row having different superscripts are different at P < 0.05.

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91Table 4-22. Linoleic and alpha-linolenic ac id contents of foal red blood cells1 Time2 P-values Fatty acid d0 d+14 d+28 d+56 d+84 SEM Treatment Time Treatment x Time C18:2 (LA) 0.04 0.03 0.31 CON 5.82 7.61ab 9.63 7.69 7.96a 1.39 FLAX 4.03 4.73b 7.56 7.50 6.25a 1.38 FISH 6.53x 11.50a,y 10.92y 12.62y 15.49b,y 1.47 C18:3 (ALA) 0.16 0.12 0.68 CON 0.08a 0.01 0.00 0.00 0.00 0.08 FLAX 0.60b,y 0.39y,z 0.00z 0.25y,z 0.00z 0.08 FISH 0.24a,b 0.00 0.00 0.33 0.00 0.09 1 Presented as g fatty acid per 100 g fat. 2 d0 = foaling; d+14 to d+84 = d post-foaling. a,b Values in the same column for each fatty acid ha ving different superscripts are different at P < 0.05. x,y,z Values in the same row having different superscripts are different at P < 0.05.

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92 Table 4-21. Overall treatment effect on the fatty acid composition of foal red blood cells1 Treatment2 Fatty acid CON FLAX FISH SEM P-value C8:0 ND ND ND NA NA C10:0 ND ND ND NA NA C12:0 ND ND ND NA NA C14:0 ND ND ND NA NA C16:0 36.80 37.18 33.95 1.0 0.07 C16:1 2.97 2.87 2.90 0.33 0.97 C17:0 0.15 0.18 0.08 0.08 0.66 C17:1 0.18 0.50 0.24 0.21 0.51 C18:0 21.85 21.60 19.78 0.57 0.03 C18:1 28.65 27.90 28.54 0.92 0.82 C18:2n-6 (LA) 7.74 6.01 11.41 1.41 0.04 C18:3n-3 (ALA) 0.02 0.25 0.11 0.09 0.16 1 Presented as g fatty acid per 100 g fat, ND = not detected in re d blood cells, NA = not analyzed. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil.

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93 Table 4-23. Overall effect of treatment on mare serum and colostrum IgG content at foaling1 Treatment2 Sample type CON FLAX FISH SEM P-value Serum 2015.5 2406.7 2295.7 590.9 0.48 Colostrum 15570.0 15703.0 13560.0 1544.3 0.55 1 Presented as mg/dL. 2 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. Table 4-24. IgG content of mare milk1,2 Treatment3 Time postfoaling4 CON FLAX FISH SEM 36h 211.8a 236.8a 212.7a 381.0 d+14 143.2b 149.8b 139.7b 381.0 d+28 108.2b 117.4b 105.4b 388.1 d+56 95.0b 95.0b 101.1b 414.5 d+84 72.4b 79.8b 80.2b 387.0 1 Presented as mg/dL. 2 Overall effect of treatment (P = 0.65), overall effect of tim e (P = 0.0001), overall effect of treatment x time (P = 0.82). 3 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 4 36h = h post-foaling; d+14 to d+84 = d post-foaling. a,b Values in the same column having differe nt superscripts are different at P < 0.05.

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94 Table 4-25. Correlations between IgG content of mare and foal serum, colostrum, and mare age Correlation r P-value Mare age and d0 serum Across treatments 0.13 0.50 CON -0.13 0.74 FLAX 0.31 0.38 FISH 0.15 0.68 Mare age and colostrum Across treatments -0.10 0.58 CON -0.10 0.78 FLAX -0.58 0.06 FISH 0.27 0.46 Mare d0 serum and colostrum Across treatments 0.24 0.21 CON -0.06 0.87 FLAX 0.24 0.50 FISH 0.54 0.11 Mare d0 serum and foal 36h serum All treatments 0.42 0.02 CON 0.32 0.40 FLAX 0.32 0.37 FISH 0.63 0.05

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95 Table 4-26. IgG content of foal serum1,2 Treatment3 Time4 CON FLAX FISH SEM d0 31.3a 88.5a 72.6a 103.1 36h 2603.1b 2608.4b 2198.8b 102.9 d+7 2160.8c 2355.1b 1933.3b 102.9 d+28 1603.5d 1430.1c 1184.1c 102.1 d+56 933.0e 1101.6d 705.0d 104.9 d+84 734.0e 761.6d 708.4d 104.2 1 Presented as mg/dL. 2 Overall effect of treatment (P = 0.32), overall effect of tim e (P = 0.0001), overall effect of treatment x time (P = 0.48). 3 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. 4 d0 = foaling; 36h = h post-foaling; d+7 to d+84 = d post-foaling. a,b,c,d,e Values in the same column having differe nt superscripts are different at P < 0.05. Table 4-27. Skin thickness of mares in re sponse to an intradermal injection of phytohemagglutinin1,2 Treatment3 Hour CON FLAX FISH SEM 0 4.7a 4.5a 4.2a 0.34 2 12.0b 11.4b 12.3b 0.34 4 15.6c 14.6c 16.1c 0.34 6 15.9c 14.9c 15.8c 0.34 8 15.1c 15.3c 15.6c 0.34 12 12.5b 13.0b 12.8b 0.34 24 12.6b 12.6b 12.2b 0.34 48 9.0d 8.8d 8.7d 0.34 1 Presented in mm. 2 Overall effect of treatment (P = 0.89), overall effect of tim e (P = 0.0001), overall effect of treatment x time (P = 0.95). 3 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. a,b,c,d Values in the same column having differe nt subscripts are different at P < 0.05.

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96 Table 4-28. Skin thickness of foals in re sponse to an intradermal injection of phytohemagglutinin1,2 Treatment3 Hour CON FLAX FISH SEM 0 4.3u 3.9u 4.1u 0.20 2 10.3v 10.3vw 9.9v 0.20 4 13.2w 14.0x 13.2w 0.20 6 12.4a,x 13.9b,x 12.9a,b,w 0.20 8 12.1x 13.0y 11.8x 0.20 12 10.0v 10.8v 10.6v 0.20 24 9.6v 9.7w 10.2v 0.20 48 6.4y 6.7z 7.0y 0.20 SEM 0.46 0.44 0.49 0.20 1 Presented in mm. 2 Overall effect of treatment (P = 0.58), overall effect of tim e (P = 0.0001), overall effect of treatment x time (P = 0.15). 3 CON = no supplement, FLAX = supplemented with milled flaxseed, FISH = supplemented with encapsulated fish oil. a,b Values in the same row having differe nt subscripts are different at P < 0.05. u,v,w,x,y,z Values in the same column having different supe rscripts are different at P < 0.05.

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97 Table 4-29. Skin response of mares and foals pooled across treatments to an intradermal skin test using phytohemagglutinin as the stimulant1,2 Hour Mare Foal SEM 0 4.5a,v 4.1a,v 0.36 2 11.9a,w 10.2b,w 0.36 4 15.4a,x 13.5b,x 0.36 6 15.5a,x 13.1b,x 0.36 8 15.3a,x 12.3b,y 0.36 12 12.7a,y 10.4b,w 0.36 24 12.5a,w,y 9.8b,w 0.36 48 8.9a,z 6.7b,z 0.36 1 Presented in mm. 2 Overall effect of age (P = 0.0001), overall effect of time (P = 0.0001). a,b Values in the same row having different subscripts are si gnificant at P < 0.05. v,w,x,y,z Values in the same column having differe nt superscripts are different at P < 0.05. 40 45 50 55 d-28d0d+28d+56d+84 Days preor post-foalingg n-6 FA/100 g fat CON FLAX FISH Figure 4-1. Total omega-6 fatty acid content in mare plasma from 28 d pre-partum to 84 d post-foaling.

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98 0 1 2 3 4 5 6 d-28d0d+28d+56d+84 Days preor post-foalingg n-3 FA/100 g fat CON FLAX FISH Figure 4-2. Total omega-3 fatty acid content in mare plasma from 28 d pre-partum to 84 d post foalingOmega-6:Omega-3 Fatty Acid Ratios 0 5 10 15 20 25 d036hd+14d+28d+56d+84 Hours or days post-foalingg n-6 FA/100 g fat CON FLAX FISH Figure 4-3. Total omega-6 fatty acid content of mare milk from foaling (d0) through 84 d post-foaling.

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99 0 5 10 15 20 25 d036hd+14d+28d+56d+84 Hours or days post-foalingg n-3 FA/100 g fat CON FLAX FISH Figure 4-4. Total omega-3 FA content of mare s milk from foaling (d0) through 84 d postfoaling. 0 10 20 30 40 50 60 d0d+14d+28d+56d+84 Days post-foalingg n-6 FA/100 g fat CON FLAX FISH Figure 4-5. Total omega-6 fatty acid content of foal plasma from birth (d0) through 84 d of age.

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100 0 2 4 6 8 d0d+14d+28d+56d+84 Days post-foalingg n-3 FA/100 g fat CON FLAX FISH Figure 4-6. Total omega-3 fatty acid content of foal plasma from birth (d0) through 84 d of age. 0 2 4 6 8 10 12 d-28d0d+28d+56d+84 Days preor post-foalingg LA/100 g fat CON FLAX FISH Figure 4-7. Linoleic acid content of mare re d blood cells from 28 d pre-partum to 84 d post-foaling.

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101 0 2 4 6 8 10 12 14 16 18 d0d+14d+28d+56d+84 Days post-foalingg LA/100 g fat CON FLAX FISH Figure 4-8. Linoleic acid content of foal red blood cells from birth (d0) to 84 d of age. -0.2 -0.1 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 d0d+14d+28d+56d+84 Days post-foalingg ALA/100 g fat CON FLAX FISH Figure 4-9. Alpha-linolenic acid content of foal red blood cells from birth (d0) to 84 d of age

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102 0 500 1000 1500 2000 2500 3000 3500 4000 4500 5000 500100015002000250030003500 Mare d0 Serum IgG (mg/dL)Foal 36h Serum IgG (mg/dL) Figure 4-10. Correlation between mare serum Ig G concentration at foaling (d0) and foal serum IgG concentration 36 h post-foaling. The equation of th e line is y = 0.6543x + 1042.1, r = 0.42, P = 0.02. 0 40 80 120 160 200 240 280 d0IgG (mg/dl) CON FLAX FISH Figure 4-11. Foal serum IgG concentr ation at birth and before nursing.

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103 0 500 1000 1500 2000 2500 3000 36hd+14d+28d+56d+84 Hours or days post-foalingIgG (mg/dl) CON FLAX FISH Figure 4-12. Foal serum IgG content after colostrum ingestion from 36 h to 84 d postfoaling. 0 2 4 6 8 10 12 14 16 18 02468122448 Hours post-injectionSkin thickness (mm) CON FLAX FISH Figure 4-13. Skin thickness of mares in response to an intrad ermal injection of phytohemagglutinin.

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104 0 2 4 6 8 10 12 14 16 02468122448 Hours post-injectionSkin thickness (mm) CON FLAX FISH Figure 4-14. Skin thickness of foals in response to an intradermal injection of phytohemagglutinin. 0 2 4 6 8 10 12 14 16 18 02468122448 Hours post-injectionSkin thickness (mm) Mares Foals Figure 4-15. Skin thickness of mares and foals in response to an intr adermal injection of phytohemagglutinin.

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105 CHAPTER 5 DISCUSSION Fatty Acid Composition of Feeds and Supplements Almost half of the total FA in the basal grain mix concentrate was made up of LA. In contrast, ALA made up a very small propor tion of the total FA in the grain mix. Commercial feeds formulated for horses typical ly contain cereal grains such as oats, corn and barley, as well as soybean meal. Despite being relatively low in total fat (~2-3% of total DM), these ingredients contain a greater proportion of n-6 to n-3 FA (Ellis and Hill, 2005; Chen et al., 2006). The addition of fat to the diet is a comm on trend in the horse industry. Fat is typically provide d in the form of soybean oil or corn oil, which increases the total amount of FA provided, but does not necessarily alter the FA composition of the grain mix. For example, O’Connor et al. ( 2004) offered horses a commercial grain mix concentrate in which soybean oil had been added (6.5% crude fat), but the relative proportions of n-6 and n-3 FA were similar to that found in the grain mix of the present study, even though oil was not included in th e basal mix (3% crude fat). Ultimately, grain mixes can be a significant source of n6 FA, particularly if horses consume a high grain, low forage diet. In contrast to the grain mix, flaxseed is an excellent source of ALA. The milled flaxseed used in the present study containe d 61.20 g ALA/100 g fat, which was slightly higher but within range of prev ious reported values (Bauer et al., 1998; Francois et al., 2003). The milled flax fed to horses in the current study was a human food-grade

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106 product. Flax of higher quality can be expected to have greater levels of ALA, as well as increased resistance to lipid peroxidation. Although low in ALA, fish oil is also a significant source of n-3 FA, predominantly EPA, DPA and DHA. The EPA concentration of the encapsulated fish oil supplement used in the current study was 1.4 to 1.6 times values reported for menhaden fish oil (Hall et al., 2004a, 2004b; O’Connor et al., 2004) and cod liver oil (Helland et al., 1998), whereas the DHA concentration of the encap sulated fish was 1.5 times that found in menhaden fish oil (Hall et al., 2004a, 2004b; O’Connor et al, 2004), but similar to that found in cod liver oil (Helland et al., 1998). Th e encapsulated fish oil used in the present study was derived from menhaden fish oil; however it is likely that sl ight variations in FA content between different sources of fish oil accounted for the differences in EPA and DHA between this study and others. The ALA content of bahiagrass pasture incr eased from winter to spring months in the current trial. In an evaluation of several species of temperate grasses, Dewhurst et al. (2001) reported a decline in ALA from Apr il to June/July, with a slight rebound in ALA concentration from September through Novemb er. However, in a later study, Dewhurst et al. (2002) observed a steady increase in ALA of perenni al ryegrass pasture samples from May through November. The authors ex plained this differe nce in ALA response was likely due to the interruption of flow ering and inflorescence emergence, because pasture samples were obtained with great er frequency in the later trial (20-30 d regrowth), compared to their previous study (40 d regrowth). In the current study, bahiagrass pasture sa mples were obtained at approximately 30 d intervals. More importantly, samples were obtained from areas where there was

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107 evidence of grazing. Horses ar e selective grazers, preferring short, vegetative growth and avoiding tall, more mature gras ses. Therefore, pasture sa mples were primarily made up of pre-florescent plant material, which could explain the increase in ALA noted between winter and spring months. In addition, th e growth of bahiagrass slows or ceases completely in the winter months in north centr al Florida. Changes in the FA content of pasture forages are more pronounced when the plant is actively grow ing (Dewhurst et al., 2001 and 2002). Although bahiagrass is a warm-season forage, the ALA content of bahiagrass pasture was within the range of values reported by Dewhurst et al. (2001) for temperate pasture grasses, including orchardgrass, ta ll fescue, meadow fescue, timothy, annual ryegrass and perennial ryegrass. However, the LA content of bahiagrass pasture was almost double of that observed by Dewhurst et al. (2001) for temperate grasses. These differences in LA may be due to differenc es in FA accumulation between cool-season (temperate) and warm-season grasses. O’Kelly and Reich (1976) reported the fatty acid composition of several tropical grasses and legume s harvested from pastures in Australia. The LA content of these tropi cal pasture forages was similar to the LA found in the bahiagrass in the current study; however, the ALA content of the Australian tropical forage was substantially lower than bahiagra ss. To the author’s knowledge, the current study is the first to report the FA co mposition of freshly cut bahiagrass. The FA profile of the Coastal bermudagra ss hay fed in the current study contained 25% more LA and 45% less ALA than the ti mothy hay fed to horses by O’Connor et al. (2004). When compared to meadow bromeg rass hay, Coastal bermudagrass had a similar ALA concentration, but about 40% more LA (P .D. Siciliano, unpublished data). Both the

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108 timothy and meadow brome hays had more total n-3 FA than total n-6 FA (n-6:n-3 ratio of 0.6 to 0.8:1), whereas the Coastal bermudagr ass hay had more total n-6 FA (n-6:n-3 ration of 1.45:1). The difference in the FA composition of these hays may not only be due to species, but also to morphological differences between cool-season and warmseason grasses. Unfortunately, the availabl e literature on the FA composition of warmseason hays is lacking. Nonetheless, tropical forage grasses collected from Australian pastures in the winter months (July-September) also contained more n-6 FA than n-3 FA, yielding an n-6:n-3 FA rati on of 1.2 to 2.1:1 (O’Kelly and Reich, 1976). Although these tropical grasses were obtained from pasture cl ippings, the authors not ed the grasses were “dormant and dried,” which may provide a similar comparison to dried hay. Additional study is necessary to better characterize the FA profiles of warm season grasses commonly fed to horses in the southern United States. Mare and Foal Bodyweight After foaling, all mares were able to maintain BW, indicating that DE intake was likely sufficient to meet the needs of lacta tion in all treatments. The amounts of DE provided by the milled flaxseed and encapsulated fish oil fed in this study were relatively small. The milled flaxseed contributed approximately 0.5 Mcal/d and the encapsulated fish oil contributed approximately 2.0 Mcal/d ay, equating to between 1.0 and 5.0% of the total DE requirement for lactating br oodmares (NRC, 1989). Because CON mares showed no difference in bodywei ght when compared to FLAX and FISH mares and there was no difference in grain intake between treatm ents, it is reasonable to assume that CON mares were able to adjust their hay and gr azing intake to meet their DE needs. Foal bodyweight was also not affected by trea tment of the mare. In part, this can be explained by the fact that gestation length did not differ between CON (351 1.89

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109 days), FLAX (354 1.82 days) or FISH mares (350 2.35 days) in the present experiment (P = 0.84). The lack of effect on le ngth of gestation is c ontrary to the positive correlation noted between dietary fish oil inta ke for the entire durat ion of pregnancy and a longer gestation length in rats (Olsen et al ., 1990). In sheep, the continual infusion of fish oil for 24 hours prior to induction of pr emature delivery also delayed the onset of labor and time of delivery (Ba guma-Nibasheka et al., 1999). Eicosanoids, particularly t hose derived from AA, regulat e gestation length and the onset of parturition (Allen and Harris, 2001). Because n-3 FA compete with n-6 FA for desaturation enzymes, a high dietary intake of n-3 FA can lead to an increased production of the 3-series prostaglandins from EPA and a decreased production of the 2-series prostaglandins from AA, ultimately inhibiti ng the onset of parturition (Mattos et al., 2000). Omega-3 FA also promote vasodila tation and reduce blood viscosity, both of which facilitate placental blood flow and im prove fetal growth, thus allowing for an increased birth weight (Baguma-Nibashek a et al., 1999). However, the lack of differences for length of gestation and fo al bodyweights seen in the present study are supported by studies performed on sows and ma res that also showed no differences in gestation length or newborn bodyweights when dams were fed n-3 FA from 7 to 45 days prior to parturition (Fr itsche et al., 1993; Duvaux-Ponter et al., 2004). Mare Plasma Fatty Acid Content This study showed that mare plasma n-3 FA profiles were altered after 28 days of FA supplementation. Sicilia no et al. (2003) found significan t changes in plasma FA levels within 14 d of supplementing with flax or fish oil. The fatty acid profiles of mare plasma in the present study mirrored the PUFA content of the supplements fed. FISH mare s had higher plasma concentrations of EPA

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110 and DHA, reflecting the content of the encapsu lated fish oil supplement. Similarly, the FLAX mares, who consumed a supplement rich in ALA, tended to have higher ALA. FLAX and FISH mares had similar plasma to tal n-3 FA concentrations, reflecting the nearly equal quantities of total n-3 FA c onsumed by the two groups. The transition in principle forage source from hay to spring pa sture resulted in a pr oportional increase in total n-3 FA intake for all mares. Nonethele ss, mares supplemented with flax or fish oil continued to receive approximately 30% more total n-3 FA than unsupplemented mares. In addition, the differences in plasma FA be tween treatments were maintained over the course of the trial and were unaffected when forage source was included as a variable in the statistical analyses. Therefore, the e ffects of FA supplementation observed in this study can be primarily attributed to the flax or fish oil consumed by the mares. All mares consumed similar levels of LA, while only FISH mares consumed AA. In the blood, LA increased over time in C ON and FLAX mares but st ayed level in FISH mares. Plasma AA was elevated only at foaling in CON and FISH mares. An explanation of the elevated AA concentration at foaling could be that the onset of foaling caused an increase in the synthe sis of prostaglandins. Pros taglandins, particularly PGF2 and PGE2, are present at high concen trations immediately befo re and during parturition (Mattos et al., 2000) and are synthesized from AA Therefore, more LA would need to be converted to AA to fuel the prostaglandin synthesis. However, prostaglandins were not determined in the present experiment. Differences in LA and AA at foaling between treatments could also be related to differen ces in ALA in the diet. FLAX mares had the highest ALA intake and the highest ALA pl asma levels, and this ALA could have competed with LA for conversion enzymes, particularly 6-desaturase. Therefore, the

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111 increased ALA in FLAX mares could explai n why these mares did not have elevated plasma AA at foaling. Mare Milk Fatty Acid Content Data in the current study confirmed that ma re milk is rich in short and medium chain FA, making up approximately 30% of all FA detected, which agrees with reports in other studies (Doreau et al., 1993; Csapo et al., 1995; Duva ux-Ponter et al., 2004). The present study also confirmed the low proporti on (1-2%) of stearic acid (C18:0) in mare milk and the relatively high proportion (5-6 %) of palmitoleic acid (C16:1) when compared to cow’s milk (Doreau and Boulot, 1989). The presence of odd chain length FA (C17:0 and C17:1; present at less than 1 %) in mare could reflect the comparatively high pH in the horse stomach, which woul d allow for bacterial hydrogenation and the formation of odd chain FA (Doreau et al., 1993; Hoffman et al., 1998; Duvaux-Ponter et al., 2004). The LCFA detected in the greatest quanti ty in mare milk was LA, which agrees with data from other studies (Doreau a nd Boulot, 1989; Csap et al., 1995). After supplementation, mares fed flaxseed had hi gher milk ALA than FISH mares and CON mares. In response to dietary treatment, FISH mares had a greater milk EPA and DHA content than FLAX mares. Th is occurrence supports that diet influences milk FA composition. The low levels of EPA and DHA in FLAX mares also supports the idea that the conversion of ALA to EPA and DHA is difficult in the mare udder and occurs at a low rate. Studies in women have supporte d this idea by showing that supplementation with flaxseed oil during lactation did not increase the women’s breast milk DHA content (Francois et al., 2003). When using dogs as subjects, supplementation during gestation and lactation with menhaden fish oil promot ed an increase in DHA milk content, while

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112 supplementation with linseed oi l did not (Bauer et al., 2004). This same occurrence was observed in mares, where supplementation w ith linseed oil during gestation or and lactation did not increase mare milk DHA (D uvaux-Ponter et al., 2004; Spearman et al., 2005). Consequently, it seems that supplementi ng the mare with ALA is not an effective method of increasing EPA and DHA in milk. The only way of increasing EPA and DHA in milk appears to be to suppl y it in the diet of the mare. Strong correlations were obs erved between mare plasma and milk for ALA, EPA and DHA, but not for AA. In women, plasma EPA and DHA have been correlated to breast milk EPA and DHA (Helland et al., 199 8). The strong correlation between mare plasma and milk ALA, EPA and DHA seen in the present study may suggest that EPA and DHA are entering the mammary gland from the plasma. In contrast, the lack of correlation between mare plasma and milk AA suggests that the mammary gland may be capable of synthesizing AA from LA. Foal Plasma Fatty Acid Content At birth, a complete absence of short and medium-chain FA in the plasma of foals suggests that these FA are pref erentially used as energy sources by the suckling foal. A similar finding was reported in newborn cal ves (Hocquette and Bauchart, 1999). Fatty acids with chain lengths of less than 16 carbons are transported direc tly to the liver via the portal vein where they ar e catabolized (Duvaux-Ponter et al., 2004). While plasma concentrations of these shortand medium-cha in FA increased slightly as the foals aged, overall plasma levels were still quite low. This phenomenon, coupled with the fact that mare milk contained relatively high amounts of short and medium chain FA, shows that foals may use these FA for energy production through 84 days of age.

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113 Supplementation of the mare also appeared to affect circulating concentrations of longer chain PUFA in the newborn foal. Prior to suckling, foals born to mares supplemented with flaxseed had an elevated level of AA in plasma. One explanation for this occurrence may be that FLAX foals conve rted more LA to AA while in utero. Blood in the umbilical vein, which drains the placenta, passes through the foal’s liver. Hence, the fetal horse liver could use the enzyme 6-desaturase to covert LA to AA (DuvauxPonter et al., 2004). Direct assessment of placental transfer of FA was not undertaken in this study; however, it is also possible th at FLAX mares transferred more AA across the placenta than did mares of other treatments. Mares exhibited lower plasma AA at foaling when supplemented with flaxseed, which coul d have resulted from sending more of the mare’s plasma AA across the placenta to the fo al. However, it is unclear as to why any of these events would take place in re sponse to flaxseed vs. fish oil or no supplementation. In contrast to Stammers et al. (1987) but in agreement with Kruglik et al. (2005), the present study showed the presence of EP A and DHA in the jugular blood of newborn foals. Since foals had not yet had access to mares’ milk, these FA must have resulted from a transfer across the placenta from mare to foal. Work by Stammers et al. (1987, 1991) has demonstrated that FA are capable of crossing the placenta from mare to foal. Foals born to fish oil supplemented mares s howed a tendency to have a higher plasma total n-3 FA content at foaling, primarily due to an increase in DPA. This increased plasma DPA was likely a result of the hi gh amount of DPA present in the fish oil supplement fed to the mares.

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114 The feeding of both flaxseed or encaps ulated fish oil to mares significantly modified the plasma PUFA profiles of foal s suckling those mares. Foals suckling FLAX mares had higher plasma ALA, while foals nursing FISH mares had higher plasma EPA and DHA, as well as a higher plasma total n-3 FA content. These results agree with those described for foals suckling mares fed linse ed (Duvaux-Ponter et al., 2004) and foals suckling mares fed a marine-derived protecte d n-3 FA source (Kruglik et al., 2005). The FA composition of foal plasma mirrored that of mare milk, as FLAX mares had higher milk ALA and FISH mares had higher milk EPA and DHA. However, FISH foals had the highest plasma total n-3 FA, even though mare milk did not differ in total n-3 FA content. It is possible that since foals had the opportunity to c onsume the mare’s grain, both FLAX and FISH foals were able to consume some of the mare’s supplement. Foals may not have been as capable of digesting th e flaxseed with the same efficiency as the fish oil, which could have altered plasma n-3 FA concentrations. The plasma of all foals also showed drama tic increases in FA from birth to 14 d of age. Similar observations were noted in fo als (Duvaux-Ponter et al., 2004) and piglets (Fritsche et al., 1993). The increases seen in n-3 PUFA in foal plas ma suggest that the foal is capable of digesting and ab sorbing long chain FA from milk. Mare and Foal Red Blood Cell Fatty Acid Content Although n-3 PUFA have been found in adult human (Makrides et al., 1996; Francois et al., 2003) and adult horse RBC (King et al., 2005), these FA were not detected in the RBC of mares in the presen t study. Linoleic acid was the longest chain PUFA discovered in mare RBC, and FISH mare s had a higher LA content. This higher LA content cannot easily be e xplained, as it disagrees with the results of past research

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115 examining human and horse red blood cell FA contents after dietary supplementation with DHA (Makrides et al., 1996; King et al., 2005). To the author’s knowledge, no studies exist that have examined the FA content of newborn foal RBC. However, studies on humans have shown that the n-3 FA concentrations of infant RBC increase when th e concentrations of these FA increase in the diet (Henderson et al, 1992; Innis, 1992b). Studies conducted in rats have shown that increasing maternal dietary ALA increases the ALA content of rat pup whole body and tissue (Bowen and Clandinin, 2000). The only PUFA found in foal RBC in the present study were LA and ALA. Similar to the results of mare RBC, FISH foals had a significantly higher LA red blood cell content, and no treatmen t differences were noted in ALA. It is again unclear as to why FISH foals had a higher LA content, especially considering there was no difference in foal plasma LA content. Further research is needed to determine how FA supplementati on of the mare can influence uptake and incorporation of FA into foal cell membranes. Evidence of FA transfer across the placenta was also demonstrated by the FA composition of red blood cells in newborn foal s. Foals born to FLAX mares had higher ALA in red blood cells in samples obtained be fore they first suckled. The finding of ALA, but not EPA or DHA, in newborn foal RBC suggests that the high requirement for long-chain PUFA, particularly DHA for fetal brain development in late gestation, may preferentially direct these FA into brain ti ssue rather than RBC membranes. However, supporters of this theory also hold that si nce ALA is a precursor to EPA and DHA, ALA would not be present in RBC membranes either as it would be converted into its longer chain derivatives (Duvaux-Ponter et al., 2004) The findings of ALA in newborn foal

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116 RBC of the present study may show that not all ALA is prefer entially incorporated into brain tissue and some may be retained in RBC membranes. It is also possible that the ALA supplied from the mare’s intake of flaxseed may have exceeded amounts required for fetal development and was therefore stored in all membranes. In the present study, the ability to accurate ly determine mare and foal red blood cell FA content may have been undermined because of laboratory procedures. The centrifuge used to process RBC was non-refrigerated. In order to process the large number of horses that were sampled at each time peri od, the centrifuge was frequently in use for long periods of time, which may have allowed excessive heating of the sample. In light of research done in other laboratories that has shown the occurrence of PUFA in animal RBC and of further tests performed in our labor atory, we believe the heating action of the RBC in the centrifuge could have resulted in the degradation of the small amounts of PUFA that may have been present in the sample. Effect of n-3 Supplementation on IgG The IgG content of mare colostrum was much higher than observed by others (Duvaux-Ponter et al., 2004; Kohn et al., 1989; Pearson et al., 1984), but was similar to that measured from mares in a previous st udy conducted at the same facility (Spearman, 2004). Breed and age did not appear to aff ect mare colostrum IgG. Breed effects on colostrum IgG have been noted in other st udies, which the aut hors attributed to differences in body size between breeds (LeB lanc et al., 1986, 1992). Larger breeds are capable of greater colostrum production, resulting in a dilu tion of IgG (Pearson et al., 1984). However, BW did not differ between Thoroughbred and Quarter Horse mares in this project; therefore, body size most lik ely did not contribute to colostrum IgG differences. Age has also been shown to e ffect mare colostrum IgG, with older mares

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117 having lower IgG concentrations (LeBlanc et al., 1992). However, other studies have shown age to have no effect on colostrum IgG (Morris et al., 1985; Erhard et al., 2001). The effects of breed and age on colostrum IgG content are not well defined, partly because of the high variation seen between individual mares. In addition, colostrum IgG varies dramatically according to when it is sampled. Colostrum IgG decreases markedly during the first 12 hours after bi rth, with a decrease of appr oximately 20% possible in the first 6 hours after birth (Pearson et al., 1984). Therefore, differences in sampling times may explain the differences in IgG values seen across studies. In the current study, colostrum was obtained with the first hour after birth. The fact that FISH mares had numerically lower colostrum IgG content in this study cannot easily be explained. Hoff man et al. (1998) observed higher IgG concentrations in colostrum from mares supplemented with corn oil, which is rich in LA. In contrast, Duvaux-Ponter et al. (2004) found that supplemen tation of mares with linseed oil did not affect the IgG in mare colostru m. More recently, Kruglik et al. (2005) fed mares a marine-derived protected n-3 FA source rich in EPA and DHA and compared their response to mares fed an isocaloric am ount of corn oil. Supplementation with EPA and DHA significantly increased colostrum IgG at foaling, but not at 12 or 24 hours after foaling (Kruglik et al., 2005). Low colostrum IgG has been associated with maiden mares (Jeffcott, 1972; Erhard et al., 2001) and prelac tation (Jeffcott, 1947; Morris et al., 1985; LeBlanc et al., 1992); however, the FISH treatment group did no t have a higher number of maiden mares and none of the FISH mares were observed dri pping milk prior to pa rturition. Three of the mares receiving FISH supplementation had dramatically lower colostrum IgG than

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118 any other mare on the study. When data from these mares was removed, the mean colostrum IgG of FISH mares was compar able to that observed in CON and FLAX mares. With the exception of two foals, all foals had serum IgG levels high enough to suggest passive transfer (at least 800 mg/dL) at 12 h post-foaling. The two foals that had IgG levels lower than 800 mg/dL were not gi ven any colostrum or plasma transfusions but were closely monitored for the first 48 hours after foaling. Neither foal developed any problems. The values for foal serum IgG seen in the present study were higher than those reported by others (Erhard et al., 2001; Duvaux-Ponter et al., 2004). Nonetheless, the decline in foal serum IgG before 28 d of age agrees with that commonly observed by others (Erhard et al., 2001; Duvaux-Ponter et al., 2004). No increases in serum IgG content were seen in foals at any time poi nt during the present study, suggesting that initiation of IgG production by the foals had not begun by 84 d of age. Erhard et al. (2001) reported an increase in foal serum Ig G at 47 days of age, suggesting that foals were beginning to synthesize their own IgG. However, other studies have shown that foals do not begin to produce their own IgG until four months of age (Jeffcott, 1974a, 1974b, 1975). Omega-3 supplementation of mares had no eff ect in foal serum IgG in the current study, which is likely due to th e lack of treatment effect on colostrum IgG. Although Kruglik et al. (2005) found higher colostrum IgG in mares supplemented with fish oil, the serum IgG concentration of foals was not di fferent from foals who were nursing mares supplemented with corn oil.

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119 In the present study, no relationships were found between mare serum IgG and colostrum IgG at foaling or between mare co lostrum IgG and foal serum IgG at 36 h after birth. This lack of relationshi p agrees with the work of Lavoie et al. (1989) but disagrees with Erhard et al. (2001), w ho reported a correlation between colostrum and foal serum IgG. Erhard et al. (2001) al so reported that mare serum at foaling was significantly correlated to foal serum at 36 hours, which wa s similar to that observed in the present study. The lack of correlation between mare colostrum and fo al serum, but the presence of a correlation between mare and foal seru m IgG, suggests that factors other than colostrum IgG concentration determine foal serum IgG concentrations, including the volume of colostrum produced, colostrum intake by foals and the efficiency of IgG transfer across the foal’s intestine. Mare and Foal Inflammatory Response In the current study, inflammatory response in mares and foals was evaluated in vivo using an intradermal injection of PHA. In mares, peak skin thickness responses to PHA were observed between 4 and 8 hours pos t-injection, whereas peak skin thickness responses were observed at 4 hours post-injec tion in foals. The time frame of these responses agrees with Ward et al. (1993), who observed a pe ak inflammatory response at 4 h. Mature animals have a more develope d immune system with a greater reaction capability than do young animals (Calder, 2001) ; therefore, it was not surprising that mares reacted to a greater extent than did foal s. Supplementation with flaxseed or fish oil had no detectable effects on the inflammatory re sponse to PHA in mares or foals. Hall et al. (2004b) was also unable to demonstrat e an effect of n-3 supplementation on in vivo inflammatory response as horses fed fish o il had a delayed-type hypersensitivity response similar to horses fed corn oil when cha llenged with keyhole limpet hemocyanin.

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120 Most of the work done to address the effects of fish oil supplementation on inflammatory responses in horses has focused on in vitro cellular production of eicosanoids. The intradermal skin test perf ormed in this study, while widely used, is somewhat crude. This skin test measures the cumulative effects of inflammation, but cannot directly measure immune cell respons es or eicosanoid production, so there may have been changes at the skin level that this test could not detect. It has been reported that the skin epidermis relies on the PUFA c ontent of the blood a nd that altering blood PUFA levels by dietary manipul ation can alter the synthesis of epidermal eicosanoids (Wright, 1991). When adult horses were fed Purple Viper’s Bugloss oil (contains ALA and C18:4n-3), the skin of th ese horses showed a significant increase in n-3 FA (Bergero et al., 2002). The skin of these horses also showed a selective incl usion of FA with a strong preference for n-3 FA over n-6 FA (Berge ro et al., 2002). Therefore, it may be possible that the increase in hor ses supplemented with flaxseed or fish oil in the present study could correlate to an in crease of these FA in their skin, which could potentially alter eicosanoid production in response to an antigen.

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121 CHAPTER 6 IMPLICATIONS This study demonstrated that n-3 FA supplementation of mares one month before parturition can influence FA available to the foal in utero After birth, but before suckling, foals from flax supplemente d mares had higher red blood cell ALA concentrations, and foals from fish oil supplem ented mares had elevated plasma levels of DPA and total n-3 FA. The transfer of n-3 FA across the placenta has the potential to modulate the immune response of the foal. Nonetheless, augmenting the n-3 FA content of the mare’s diet with milled flaxseed or encapsulated fish oil did not increase IgG content in mare colostrum, nor did it appear to enhance uptake of IgG by the suckling foal. Perhaps a longer period of n-3 FA s upplementation during gestation is needed to allow for greater incorporation of EPA and DHA into cell membranes. The resulting increase in membrane fluidity and permeability could permit greater entry of IgG into mammary tissue, as well as greater absorp tion of IgG by foal enterocytes, thereby facilitating passive transfer of immunity to the nave foal. Supplementing the mare with 6 g total n-3 FA/100 kg BW led to the enrichment of n-3 FA in milk, and subseque ntly, the plasma of the suck ling foal. Although flaxseed increased the quantity of ALA available to th e foal, supplementation with fish oil appears to be a more effective method of increasing EPA and DHA in plasma and milk. Despite alterations in circulation n-3 FA, supplementation of the mare with flaxseed or fish oil did not modify the inflam matory response to PHA in mares or foals as

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122 measured by skin thickness. Although crude, the method does allow cumulative assessment of innate immune response in vivo Future study should characterize the eff ects of different sources of n-3 FA on eicosanoid and cytokine production at the cellu lar level. In addition, optimal amounts of dietary n-3 FA and/or ratios of n-6:n-3 FA needed to confer immune benefits in horses deserves further investigation. Such informati on is especially relevant to the health of lactating mares and growing horses, which are typically fed large amounts of grain-based feeds that are high in n-6 FA in order to meet their high nutrient requirements. Furthermore, the popularity of fat-added feeds, most of which contain oils rich in n-6 FA, as well as reduced access to grazing, may ha ve important biological consequences as a result of reduced n-3 FA supply.

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123 APPENDIX A RAW DATA Mare Expected and Actual Foaling Dates and Dates Started on Trial Table A-1. FISH mare expected foaling dates, actual foaling dates and dates started on trial Mare Expected foaling date Actual foaling date Date on trial B46 1/21/2005 2/18/2005 12/23/2004 W69 1/24/2005 2/7/2005 12/27/2004 B33 1/30/2005 2/14/2005 1/3/2005 B14 2/8/2005 2/14/2005 1/10/2005 B01 2/20/2005 2/18/2005 1/25/2005 B31 3/2/2005 3/14/2005 2/2/2005 A59 3/6/2005 3/6/2005 2/7/2005 B47 3/10/2005 3/22/2005 2/10/2005 B35 3/20/2005 3/27/2005 2/21/2005 B24 3/24/2005 4/8/2005 2/24/2005 B23 3/25/2005 3/29/2005 2/24/2005 A66 4/11/2005 4/16/2005 3/14/2005

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124 Table A-2. FLAX mare expected foaling dates, actual foaling dates and dates started on trial Mare Expected foaling date Actual foaling date Date on trial B6 1/27/2005 2/15/2005 12/30/2004 B19 1/28/2005 2/15/2005 12/30/2004 A65 2/11/2005 2/21/2005 1/13/2005 B44 2/17/2005 2/22/2005 1/20/2005 C1 2/27/2005 3/16/2005 1/31/2005 A62 3/1/2005 3/18/2005 1/31/2005 B21 3/3/2005 3/23/2005 2/2/2005 C2 3/5/2005 3/25/2005 2/2/2005 B28 3/7/2005 3/8/2005 2/7/2005 C6 3/8/2005 3/17/2005 2/7/2005 B32 3/24/2005 4/10/2005 2/24/2005 B30 4/8/2005 4/24/2005 3/11/2005

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125 Table A-3. CON mare expected foaling dates, actual foaling dates and dates started on trial Mare Expected foaling date Actual foaling date Date on trial A61 1/16/2005 1/24/2005 12/20/2004 B26 1/20/2005 1/28/2005 12/23/2004 B41 2/9/2005 3/1/2005 1/10/2005 C4 2/13/2005 3/6/2005 1/17/2005 A54 2/27/2005 3/3/2005 1/31/2005 B13 3/3/2005 3/2/2005 2/2/2005 B43 3/5/2005 3/24/2005 2/2/2005 B18 3/8/2005 3/19/2005 2/7/2005 B29 3/9/2005 3/22/2005 2/10/2005 A64 3/18/2005 3/26/2005 2/18/2005 B45 3/24/2005 4/5/2005 2/24/2005 B36 4/9/2005 4/19/2005 3/11/2005

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126 Fatty Acid Composition of Monthly Pasture Samples Table A-4. Fatty acid composition of bahi agrass pasture (by month) and Coastal bermudagrass hay Pasture Fatty acid1 Dec. Jan. Feb. March April May June C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 22.38 23.35 20.11 22.42 22.53 22.59 24.53 C16:1 0.00 1.70 0.00 0.00 0.00 0.00 0.00 C17:0 0.99 1.02 0.84 0.86 0.70 0.00 0.90 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 3.94 5.47 5.60 4.87 3.05 3.26 3.77 C18:1 2.64 5.54 4.57 4.07 1.37 1.42 1.37 C18:2n-6 18.17 25.72 26.52 24.43 21.07 15.98 17.33 C18:3n-3 50.27 34.42 40.13 41.25 50.55 55.92 50.94 C20:4n-6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5n-3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 n-3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6n-3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 Total n-62 18.17 25.72 26.52 24.43 21.07 15.98 17.33 Total n-33 50.27 34.42 40.13 41.25 50.55 55.92 50.94 n-6:n-3 0.36 0.75 0.66 0.59 0.42 0.29 0.34 1 Presented as g fatty acid per 100 g fat. 2 Calculated as C18:2 + C20:4. 3 Calculated as C18:3 + C20:5 + C22:5 + C22:6.

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127Mare Fatty Acid Intake Table A-5. Mare daily intake of fo rage, grain and supplement by month1 Forage2 Grain Supplement Month CON FLAX FISH CON FLAX FISH FLAX FISH Dec. 6.57 0.65 5.71 0.16 6.21 0.05 6.57 0.65 5.71 0.16 6.21 0.05 0.16 0.00 0.55 0.01 Jan. 6.00 0.24 6.29 0.18 6.45 0.22 6.00 0.24 6.29 0.18 6.45 0.22 0.17 0.01 0.57 0.01 Feb. 6.14 0.16 6.05 0.13 6.09 0.13 6.55 0.28 6.09 0.26 6.52 0.13 0.18 0.01 0.57 0.01 March 5.70 0.22 5.57 0.29 5.59 0.15 6.70 0.35 6.85 0.45 7.14 0.35 0.17 0.01 0.54 0.01 April 5.47 0.14 5.64 0.09 5.53 0.10 7.83 0.26 8.17 0.28 8.08 0.19 0.16 0.01 0.53 0.01 May 5.71 0.14 5.62 0.08 5.56 0.13 8.57 0.21 8.34 0.13 8.43 0.20 0.16 0.01 0.53 0.01 June 5.25 0.30 5.60 0.12 5.50 0.11 7.87 0.43 8.41 0.18 8.23 0.16 0.16 0.01 0.53 0.01 1 Presented in kg as means SEM. 2 Estimated at 1% of mare BW.

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128 Mare Bodyweight Table A-6. FISH mare bodyweights1 Time Mare d-28 d-14 d0 d+14 d+28 d+42 d+56 d+70 d+84 B46 1401 1408 1246 1251 1259 1262 1287 NT2 1272 W69 1331 1343 1172 1222 1224 1215 1215 NT 1211 B33 1314 1326 1130 1176 1172 1174 1180 NT 1187 B14 1539 1572 1346 1389 1398 1436 1425 NT 1396 B01 1430 1428 1245 1287 1306 NT 1305 NT 1282 B31 1302 1306 1133 1089 1106 1121 1106 1072 1075 A59 1530 1551 1341 1219 1261 1290 1275 1290 1316 B47 1366 1364 1156 1203 1198 1191 1209 1136 1234 B35 1363 1378 Off trial – Dead foal (dystocia) B24 1412 1401 1280 1228 1200 Off trial –Foal euthanized B23 1395 1420 Off trial – Dead foal (dystocia) A66 1425 1412 1267 1256 1265 1287 1282 1302 1253 1 Presented in lb. 2 NT = not taken.

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129 Table A-7. FLAX mare bodyweights1 Time Mare d-28 d-14 d0 d+14 d+28 d+42 d+56 d+70 d+84 B6 1246 1250 1122 1118 1135 1133 1132 NT2 1096 B19 1266 1267 1140 1127 1158 1147 1136 NT 1111 A65 1487 1524 1393 1379 1375 1391 1377 NT 1374 B44 1343 1383 1221 1241 1244 1242 NT NT 1219 C1 1286 1329 NT 1081 1082 1142 1124 1136 1144 A62 1537 1554 1330 1376 1382 1378 1394 1405 1396 B21 1396 1387 1213 1226 1216 NT 1204 1147 1215 C2 1296 1328 1110 1175 1177 NT 1165 1138 1227 B28 1444 1445 1306 1269 1253 1266 1260 1192 1246 C6 1284 1294 1077 1082 1072 1083 1070 1105 1113 B32 1438 1447 1204 1292 1248 1217 1196 1260 1243 B30 1337 1346 Off trial – Dead foal (foal suffocated) 1 Presented in lb. 2 NT = not taken.

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130 Table A-8. CON mare bodyweights1 Time Mare d-28 d-14 d0 d+14 d+28 d+42 d+56 d+70 d+84 A61 1588 1579 1425 1419 1445 1436 1426 NT2 1438 B26 1301 1324 1124 1077 1084 1138 1103 NT 1135 B41 1338 1374 1211 1246 1255 NT 1266 1253 1250 C4 1258 1296 1103 1117 1107 1127 1115 1104 1122 A54 1135 1143 968 979 980 982 993 977 978 B13 1347 1360 1169 1152 1094 1160 1148 1126 1147 B43 1290 1267 Off trial – Dead foal (dystocia) B18 1435 1404 1214 1217 1241 1214 1231 1242 1225 B29 1485 1531 1378 1343 1378 1338 1355 1368 1370 A64 1422 1410 NT 1185 1225 NT 1275 NT 1260 B45 1449 1451 1285 1297 1289 1291 1312 1328 1278 B36 1583 1548 1376 1366 1374 NT 1386 1286 NT 1 Presented in lb. 2 NT = not taken.

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131 Foal Bodyweight Table A-9. FISH foal bodyweights1 Time Foal Sex2 d0 d+14 d+28 d+42 d+56 d+70 d+84 5W69 F 120 163 205 245 284 NT3 364 5B33 F 123 161 203 240 287 NT 364 5B14 F 123 179 200 271 316 NT 396 5B46 C 118 136 209 256 300 NT 373 5B01 F 100 133 165 NT 242 NT 305 5A59 C 141 198 238 292 337 360 386 5B31 F 109 157 200 240 236 284 322 5B47 F 130 173 214 250 287 292 342 5B24 C 123 170 204 Foal euthanized (joint ill) 5A66 F 118 156 219 246 284 312 360 5B35 Foal died at birth (dystocia) 5B23 Foal died at birth (dystocia) 1 Presented in lb. 2 C = colt, F = filly. 3 NT = not taken.

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132 Table A-10. FLAX foal bodyweights1 Time Foal Sex d0 d+14 d+28 d+42 d+56 d+70 d+84 5B06 F 108 162 207 250 291 NT 355 5B19 C 127 159 195 239 278 NT 353 5A65 C 122 177 225 272 324 NT 398 5B44 C 110 153 197 271 NT NT 312 5B28 C 112 161 208 238 276 306 327 5C1 C NT 140 169 200 236 267 298 5C6 C 116 173 203 252 252 292 323 5A62 F 130 184 239 306 330 372 413 5B21 C 119 167 209 NT 272 283 331 5C2 F 113 138 199 NT 260 297 347 5B32 F 136 187 233 265 266 316 354 5B30 Foal died at birth (suffocated) 1 Presented in lb. 2 C = colt, F = filly. 3 NT = not taken.

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133 Table A-11. CON foal bodyweights1 Time Foal Sex2 d0 d+14 d+28 d+42 d+56 d+70 d+84 5A61 F 124 198 247 287 334 NT3 444 5B26 F 110 183 195 229 262 NT 363 5B41 C 121 161 197 NT 275 314 326 5B13 F 126 177 220 262 307 335 360 5A54 C 106 149 190 237 275 322 340 5C4 F 123 160 176 212 230 264 289 5B18 F 114 150 198 244 278 303 328 5B29 F 115 167 215 249 284 323 365 5A64 F NT 145 210 NT 272 NT 354 5B45 F 120 163 202 234 264 304 334 5B36 F 123 188 222 NT 296 350 NT 5B43 Foal died at birth (dystocia) 1 Presented in lb. 2 C = colt, F = filly. 3 NT = not taken.

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134 Mare Serum IgG Table A-12. Serum IgG content of FISH mares at foaling Mare IgG1 A59 1879.0 A66 3000.4 B01 2007.2 B14 1879.0 B24 3323.7 B31 3159.4 B33 1879.0 B46 1509.5 B47 2007.2 W69 2138.3 1 Presented as mg/dL. Table A-13. Serum IgG conten t of FLAX mares at foaling Mare IgG1 A62 2410.1 A65 3159.4 B06 2007.2 B19 2846.3 B21 2696.7 B28 2272.5 B32 1390.5 B44 1509.5 C2 1753.5 C6 1753.5 1 Presented as mg/dL.

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135 Table A-14. Serum IgG conten t of CON mares at foaling Mare IgG1 A54 1630.4 A61 1753.5 B13 2551.5 B18 1273.2 B26 2551.5 B29 2846.3 B36 1753.5 B41 2846.3 C4 2551.5 1 Presented as mg/dL.

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136 Mare Colostrum and Milk IgG Table A-15. IgG content of colostrum and milk from FISH mares1 Time Mare d0 36h d+7 d+28 d+56 d+84 A59 7014.10 183.40 102.20 112.00 84.31 61.36 A66 21447.20 279.10 133.30 84.31 NT2 84.31 B01 8028.80 183.40 157.10 102.20 93.00 93.00 B14 8553.10 157.10 133.30 93.00 102.20 93.00 B24 13294.90 169.90 144.90 112.00 NT NT B31 21447.20 279.10 144.90 122.40 112.00 76.15 B33 18634.70 228.00 157.10 112.00 112.00 84.31 B46 14679.00 169.90 133.30 102.20 102.20 93.00 B47 12001.60 279.10 157.10 112.00 102.20 68.51 W69 10787.00 197.60 133.30 102.20 NT 68.51 1 Presented as mg/dL. 2 NT = not taken.

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137 Table A-16. IgG content of colost rum and milk from FLAX mares1 Time Mare d0 36h d+7 d+28 d+56 d+84 A62 16956.50 197.60 133.30 133.30 93.00 54.69 A65 16513.80 279.10 144.90 112.00 93.00 122.40 B06 14679.00 197.60 157.10 122.40 102.20 68.51 B19 14679.00 503.70 228.00 133.30 112.00 102.20 B21 15409.30 197.60 133.30 112.00 93.00 84.31 B28 25286.90 261.30 144.90 112.00 93.00 84.31 B32 15409.30 228.00 133.30 102.20 93.00 68.51 B44 16956.50 133.30 133.30 112.00 93.00 68.51 C2 10205.90 157.10 144.90 112.00 93.00 68.51 C6 10205.90 212.40 144.90 122.40 84.31 76.15 1 Presented as mg/dL.

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138 Table A-17. IgG content of colost rum and milk from CON mares1 Time Mare d0 36h d+7 d+28 d+56 d+84 A54 17778.00 197.60 133.30 102.20 84.31 84.31 A61 10205.90 197.60 157.10 112.00 102.20 76.15 A64 12001.60 279.10 169.90 NT2 84.31 61.36 B13 12001.60 228.00 122.40 112.00 93.00 84.31 B18 18634.70 169.90 133.30 102.20 84.31 48.49 B26 10787.00 157.10 144.90 93.00 102.20 84.31 B29 26505.70 244.30 157.10 112.00 93.00 48.49 B36 18634.70 183.40 122.40 102.20 NT 61.36 B41 12001.60 228.00 144.90 122.40 102.20 102.20 B45 19529.60 183.40 144.90 112.00 102.20 61.36 C4 14679.00 261.30 144.90 112.00 102.20 84.31 1 Presented as mg/dL. 2 NT = not taken.

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139 Foal Serum IgG Table A-18. IgG content of serum from FISH foals1 Time Foal d0 36h d+7 d+28 d+56 d+84 5A59 122.40 1157.20 1630.40 963.10 789.90 695.30 5A66 76.15 4658.70 3669.70 2138.30 815.20 1275.70 5B01 84.31 469.80 407.60 289.30 318.30 318.30 5B14 54.69 1630.40 1509.50 1111.10 637.90 534.60 5B24 84.31 2410.10 2007.20 1273.20 NT2 NT 5B31 61.36 3493.70 2846.30 1753.50 1273.20 939.50 5B33 54.69 2007.20 2007.20 1059.80 750.10 568.10 5B46 102.20 2410.10 1879.00 1273.20 711.60 637.90 5B47 133.30 2138.30 2007.20 1157.20 917.40 695.30 5W69 93.00 1753.50 1509.50 963.10 232.00 830.90 1 Presented as mg/dL. 2 NT = not taken.

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140 Table A-19. IgG content of serum from FLAX foals1 Time Foal d0 36h d+7 d+28 d+56 d+84 5A62 122.40 3159.40 2551.50 2138.30 1273.20 815.20 5A65 84.31 2846.30 3000.40 1630.40 1273.20 928.10 5B06 68.51 3852.30 3669.70 1879.00 NT2 928.10 5B19 68.51 2846.30 2551.50 1509.50 1273.20 789.90 5B21 61.36 2007.20 1753.50 963.10 674.20 464.10 5B28 84.31 3852.30 3323.70 1879.00 1509.50 1069.10 5B32 102.20 2846.30 2272.50 1390.50 1069.10 695.30 5B44 93.00 1390.50 1630.40 1059.80 789.90 711.60 5C2 68.51 1220.60 534.60 637.90 963.10 521.50 5C6 76.15 2007.20 2007.20 1157.20 750.10 636.60 1 Presented as mg/dL. 2 NT = not taken.

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141 Table A-20. IgG content of serum from CON foals1 Time Foal d0 36h d+7 d+28 d+56 d+84 5A54 76.15 2551.50 2007.20 1157.20 830.90 876.80 5A61 76.15 1753.50 1753.50 2138.30 674.20 637.90 5A64 NT2 NT 1273.20 1273.20 830.90 939.50 5B13 61.36 2846.30 2410.10 1273.20 830.90 578.60 5B18 102.20 3000.40 2551.50 1879.00 928.10 876.80 5B26 68.51 2846.30 2551.50 3000.40 711.60 602.50 5B29 68.51 3323.70 NT 1879.00 1273.20 695.30 5B36 61.36 2410.10 1879.00 1273.20 1500.20 636.60 5B41 122.40 2272.50 2272.50 1273.20 1042.30 815.20 5B45 76.15 2551.50 2272.50 1509.50 1003.60 636.60 5C4 93.00 3159.40 2551.50 1273.20 928.10 1069.10 1 Presented as mg/dL. 2 NT = not taken.

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142Fatty Acid Composition of Plasma from FISH Mares Table A-21. Fatty acid composition of FISH mare plasma at 28 d prior to expected foaling date Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.50 15.35 15.08 16.99 17.03 15.24 16.18 15.73 13.46 15.97 C16:1 1.60 1.15 1.69 1.68 1.49 1.11 1.44 1.16 1.24 1.18 C17:0 0.66 0.74 0.56 0.00 0.64 0.89 0.00 0.72 0.68 0.95 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 18.05 19.34 18.20 18.49 16.66 19.55 19.99 19.26 21.83 19.36 C18:1 10.50 12.15 10.41 12.05 12.04 10.47 10.91 10.21 10.57 12.38 C18:2 46.29 45.89 47.98 44.65 47.59 46.44 45.64 48.07 47.39 43.55 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 5.12 2.70 3.73 3.07 1.58 3.36 3.86 2.48 1.89 4.17 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.71 0.81 0.73 1.03 0.89 0.78 0.00 0.61 0.73 0.83 C20:4 1.57 1.88 1.63 2.04 2.09 2.17 1.98 1.77 2.21 1.61 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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143Table A-22. Fatty acid composition of FISH mare plasma at foaling Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 18.27 15.40 15.24 18.86 23.46 17.04 16.49 17.46 15.99 16.58 C16:1 1.62 0.96 1.30 1.72 2.53 1.01 1.28 1.33 1.63 1.46 C17:0 0.64 0.66 0.58 0.77 0.00 0.79 0.73 0.61 0.66 0.75 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 17.63 21.76 23.42 19.45 21.90 20.46 21.44 19.97 20.89 19.53 C18:1 11.94 9.61 9.71 11.69 18.64 9.07 9.68 9.13 10.77 8.79 C18:2 43.15 47.32 44.72 41.12 18.41 46.22 45.17 46.92 43.62 43.03 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 4.37 1.30 2.64 2.49 0.00 2.35 2.42 1.50 1.59 2.49 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.75 0.79 0.74 0.82 1.03 0.66 0.73 0.57 0.69 0.72 C20:4 1.63 2.21 1.66 1.94 10.00 2.41 2.06 1.93 1.90 2.11 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.66 2.47 C22:5 0.00 0.00 0.00 0.00 0.78 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 1.14 2.23 0.00 0.00 0.58 1.13 2.07 1 FA = fatty acid, presented as g FA per 100 g fat.

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144Table A-23. Fatty acid composition of FI SH mare plasma at 28 d post-foaling Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 16.42 16.55 15.90 16.69 18.17 17.23 16.35 17.91 14.34 16.35 C16:1 0.00 0.65 1.17 1.47 1.25 1.18 1.16 2.12 0.00 1.21 C17:0 0.91 0.81 0.75 0.73 0.91 1.06 0.73 0.62 0.00 0.89 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 22.27 21.43 21.27 20.49 19.15 20.03 19.98 19.33 23.61 19.56 C18:1 7.69 8.36 7.82 10.11 9.82 9.75 7.63 10.82 7.02 8.38 C18:2 44.60 46.15 44.66 43.32 44.52 42.63 46.92 41.36 48.21 43.29 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.57 C18:3 3.57 1.14 4.15 3.10 3.21 2.33 3.01 3.83 3.76 4.58 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.90 0.96 0.83 0.98 0.93 1.01 0.75 0.66 0.00 0.85 C20:4 1.33 1.39 1.40 1.28 1.18 1.65 1.68 1.47 1.65 1.30 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 1.25 1.39 1.12 0.85 0.00 1.63 0.92 0.88 1.41 1.90 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 1.06 1.17 0.93 0.98 0.86 1.51 0.86 1.00 0.00 1.11 1 FA = fatty acid, presented as g FA per 100 g fat.

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145Table A-24. Fatty acid composition of FI SH mare plasma at 56 d post-foaling Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 NA2 0.00 0.00 0.00 NA OT3 0.00 NA 0.00 C10:0 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C12:0 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C14:0 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C14:1 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C16:0 15.67 NA 15.32 16.19 16.68 NA OT 16.72 NA 16.18 C16:1 1.04 NA 0.71 1.43 0.86 NA OT 0.00 NA 0.00 C17:0 0.93 NA 0.82 0.68 0.82 NA OT 0.83 NA 1.03 C17:1 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C18:0 19.97 NA 20.40 21.00 20.72 NA OT 21.99 NA 22.14 C18:1 9.09 NA 7.59 10.03 8.19 NA OT 8.34 NA 7.91 C18:2 43.73 NA 46.87 44.42 47.25 NA OT 46.40 NA 44.60 C20:0 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C18:3 5.72 NA 3.98 3.96 3.36 NA OT 1.09 NA 2.20 C20:1 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C20:2 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C22:0 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C20:3 0.95 NA 0.95 0.99 0.86 NA OT 0.91 NA 0.99 C20:4 1.19 NA 1.37 1.29 1.27 NA OT 1.70 NA 1.49 C24:1 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C20:5 0.89 NA 1.06 0.00 0.00 NA OT 0.97 NA 2.04 C22:5 0.00 NA 0.00 0.00 0.00 NA OT 0.00 NA 0.00 C22:6 0.84 NA 0.92 0.00 0.00 NA OT 1.05 NA 1.43 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed. 3 OT = off trial.

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146Table A-25. Fatty acid composition of FI SH mare plasma at 84 d post-foaling Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 OT2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C16:0 16.00 15.13 16.20 16.41 25.51 16.25 OT 16.20 13.80 14.83 C16:1 0.68 0.81 1.45 1.66 0.00 0.82 OT 1.24 1.01 0.95 C17:0 0.98 0.61 0.68 0.87 1.45 1.00 OT 0.73 0.76 0.86 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C18:0 19.37 19.24 18.57 19.66 31.98 19.23 OT 19.90 19.81 20.58 C18:1 8.85 9.06 10.02 10.29 12.51 7.23 OT 8.38 7.97 8.02 C18:2 47.04 49.92 46.36 44.89 19.05 48.24 OT 45.67 50.05 46.71 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.55 0.00 0.00 C18:3 4.02 3.10 4.95 2.76 6.20 2.97 OT 3.75 3.81 4.24 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:3 1.04 0.86 0.78 1.18 1.29 0.75 OT 0.73 0.73 0.89 C20:4 0.81 1.27 0.99 1.38 2.00 1.67 OT 1.53 1.34 1.32 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.78 OT 0.56 0.72 0.76 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:6 1.20 0.00 0.00 0.91 0.00 1.05 OT 0.77 0.00 0.84 1 FA = fatty acid, presented as g FA per 100 g fat. 2 OT = off trial.

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147Fatty Acid Composition of Plasma from FLAX Mares Table A-26. Fatty acid composition of FLAX mare plasma at 28 d before expected foaling date Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.71 16.43 18.05 17.09 17.91 16.07 17.82 14.90 14.18 16.37 14.62 C16:1 0.75 1.84 1.77 0.00 0.81 1.50 0.73 1.58 0.00 1.29 1.34 C17:0 0.66 0.60 0.59 0.77 0.82 0.62 1.01 0.66 0.00 0.88 0.64 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 20.11 19.09 18.17 19.16 16.25 18.56 18.87 20.55 24.52 18.20 18.98 C18:1 10.45 10.86 12.72 11.36 12.25 10.95 10.87 11.60 10.78 10.99 11.28 C18:2 47.88 42.96 43.44 47.14 46.48 44.91 45.38 43.84 47.43 46.51 49.45 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 2.01 5.77 2.66 1.43 2.84 5.13 2.92 4.31 3.09 2.18 1.59 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.37 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.77 0.69 0.53 0.91 0.80 0.74 0.88 0.71 0.00 0.88 0.61 C20:4 1.66 1.77 1.70 2.14 1.84 1.54 1.52 1.86 0.00 2.69 1.47 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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148Table A-27. Fatty acid composition of FLAX mare plasma at foaling Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C16:0 15.06 17.83 17.98 16.68 17.00 17.07 17.88 NA 14.24 16.93 13.94 C16:1 1.39 1.95 1.61 1.04 1.08 1.72 1.14 NA 0.68 0.00 0.87 C17:0 0.63 0.71 0.60 0.58 0.73 0.61 0.81 NA 0.89 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:0 23.28 19.07 18.05 19.16 19.52 18.47 19.04 NA 20.78 20.50 23.12 C18:1 9.25 11.37 12.84 11.01 9.46 10.63 9.86 NA 10.19 10.49 9.68 C18:2 44.93 40.42 43.04 45.96 46.76 43.52 46.16 NA 46.90 49.27 49.55 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:3 3.01 6.55 3.70 2.91 2.89 6.04 2.65 NA 4.00 2.81 1.13 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:3 0.72 0.67 0.66 0.73 0.71 0.59 0.80 NA 0.75 0.00 0.00 C20:4 1.73 1.45 1.52 1.92 1.86 1.35 1.65 NA 1.57 0.00 1.72 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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149Table A-28. Fatty acid composition of FL AX mare plasma at 28 d post-foaling Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C16:0 15.35 16.57 16.26 16.63 18.02 NA 16.33 14.46 NA 16.53 15.42 C16:1 0.60 0.87 0.99 0.00 0.00 NA 0.97 0.87 NA 0.91 1.08 C17:0 0.73 0.77 0.72 0.81 0.83 NA 0.86 0.77 NA 0.90 0.74 C17:1 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C18:0 23.28 22.34 19.95 20.32 18.98 NA 18.82 22.35 NA 22.30 21.16 C18:1 7.21 7.74 9.73 8.46 9.10 NA 8.49 9.95 NA 7.77 9.97 C18:2 47.28 45.94 46.73 48.78 49.25 NA 47.13 46.57 NA 45.39 45.55 C20:0 0.57 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.61 C18:3 3.25 3.59 3.81 3.05 2.74 NA 5.41 2.69 NA 1.68 3.48 C20:1 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C20:3 0.71 0.88 0.68 0.82 0.00 NA 0.77 0.91 NA 0.85 0.81 C20:4 1.01 1.30 1.13 1.13 1.08 NA 1.21 1.43 NA 1.73 1.18 C24:1 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.96 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 NA 0.98 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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150Table A-29. Fatty acid composition of FL AX mare plasma at 56 d post-foaling Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C10:0 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C12:0 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C14:0 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C14:1 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C16:0 NA 16.13 15.79 15.68 17.99 NA NA 14.09 14.08 15.71 15.18 C16:1 NA 0.87 1.04 0.95 0.79 NA NA 0.00 0.00 1.23 1.13 C17:0 NA 0.82 0.60 0.83 0.82 NA NA 0.96 0.90 0.78 0.73 C17:1 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C18:0 NA 19.82 21.04 19.71 17.71 NA NA 21.59 23.21 21.51 22.45 C18:1 NA 8.36 9.63 9.78 10.73 NA NA 8.02 9.12 8.57 8.76 C18:2 NA 46.82 47.68 47.10 46.65 NA NA 48.33 47.37 47.58 45.88 C20:0 NA 0.00 0.00 0.00 0.00 NA NA 0.59 0.00 0.00 0.59 C18:3 NA 5.42 2.19 3.90 3.29 NA NA 4.39 3.31 2.43 3.67 C20:1 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C20:2 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C22:0 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C20:3 NA 0.72 0.81 0.87 0.87 NA NA 0.82 0.76 0.77 0.64 C20:4 NA 1.03 1.23 1.19 1.16 NA NA 1.21 1.26 1.42 0.97 C24:1 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C20:5 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C22:5 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 C22:6 NA 0.00 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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151Table A-30. Fatty acid composition of FL AX mare plasma at 84 d post-foaling Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 14.76 16.65 17.68 15.63 17.48 14.09 16.42 14.82 13.59 15.80 14.58 C16:1 0.84 1.49 1.22 0.51 0.90 1.01 0.58 0.56 0.00 0.59 0.68 C17:0 0.73 0.83 0.72 0.85 0.88 0.65 0.98 1.01 0.99 0.98 0.71 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 20.30 18.11 18.84 19.48 18.21 18.60 19.24 20.63 22.96 18.57 20.07 C18:1 7.75 10.44 11.56 9.69 9.93 7.65 8.60 10.18 8.45 8.69 9.42 C18:2 48.41 45.19 44.51 48.45 47.61 50.46 47.13 46.26 48.55 48.63 48.75 C20:0 0.58 0.00 0.00 0.00 0.00 0.00 0.00 0.57 0.00 0.44 0.00 C18:3 4.89 5.37 3.66 3.47 3.02 5.65 4.62 3.89 3.13 3.42 3.67 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.68 0.84 0.87 0.77 0.84 0.82 0.95 0.78 0.82 0.63 0.92 C20:4 1.06 1.08 0.95 1.16 1.13 1.07 1.47 1.30 1.50 1.25 1.20 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.45 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.55 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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152Fatty Acid Composition of Plasma from CON Mares Table A-31. Fatty acid composition of CON mare plasma at 28 d be fore expected foaling date Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 NA C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C16:0 14.71 14.82 16.35 16.24 15.86 17.72 15.11 15.14 16.36 NA NA C16:1 0.89 0.00 1.06 1.63 1.29 1.92 1.11 1.33 0.00 NA NA C17:0 0.81 0.70 0.82 0.76 0.80 0.63 0.71 0.63 0.92 NA NA C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C18:0 17.80 22.49 18.58 19.52 20.60 16.84 19.74 18.51 19.48 NA NA C18:1 10.79 9.43 12.79 12.24 10.78 11.28 11.51 9.97 10.82 NA NA C18:2 48.76 48.69 44.62 44.04 45.08 44.01 44.47 50.02 47.68 NA NA C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C18:3 2.94 1.10 2.83 3.21 2.92 5.40 5.29 1.82 2.63 NA NA C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C20:3 0.89 0.83 0.84 0.79 0.77 0.69 0.70 0.77 0.00 NA NA C20:4 2.40 1.96 2.11 1.56 1.91 1.50 1.35 1.79 2.10 NA NA C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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153Table A-32. Fatty acid composition of CON mare plasma at foaling Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C16:0 16.70 15.97 16.34 15.90 15.26 18.95 22.80 NA 17.29 16.84 15.84 C16:1 0.00 1.19 1.92 0.85 1.03 2.19 3.82 NA 1.29 1.40 0.68 C17:0 0.00 0.70 0.52 0.73 0.89 0.44 0.00 NA 0.70 0.64 0.82 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:0 19.13 22.53 19.33 21.75 22.07 17.05 20.33 NA 18.69 20.81 21.20 C18:1 12.26 10.51 10.71 9.06 10.55 10.88 27.20 NA 11.43 9.56 9.33 C18:2 46.22 43.44 45.84 48.84 45.76 44.62 15.27 NA 45.18 46.75 48.16 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 1.14 NA 0.00 0.00 0.00 C18:3 3.82 3.16 3.22 1.07 1.87 4.02 0.00 NA 3.11 1.53 1.30 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:3 0.00 0.77 0.57 0.00 0.70 0.58 0.73 NA 0.65 0.66 0.74 C20:4 1.87 1.73 1.55 1.80 1.88 1.28 6.13 NA 1.66 1.81 1.93 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.77 NA 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 1.83 NA 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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154Table A-33. Fatty acid composition of CO N mare plasma at 28 d post-foaling Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.68 17.09 15.11 15.84 16.76 16.97 15.25 14.53 17.87 15.88 13.94 C16:1 0.64 1.24 0.00 1.13 0.00 0.99 0.71 0.00 0.00 0.93 0.92 C17:0 0.96 0.00 0.71 0.70 0.00 0.73 0.83 0.00 0.91 0.68 0.90 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 21.47 22.06 23.53 20.01 20.75 20.19 20.93 22.29 21.17 21.49 20.31 C18:1 9.53 10.82 8.88 8.93 9.22 8.43 9.53 8.30 9.10 8.51 9.98 C18:2 45.92 43.75 47.87 47.66 48.15 48.02 46.46 50.40 45.82 49.99 48.97 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 3.70 3.66 1.93 3.76 3.64 2.68 4.38 2.29 2.89 0.00 2.63 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.83 0.00 0.82 0.83 0.00 0.86 0.73 0.96 0.94 0.94 0.93 C20:4 1.26 1.37 1.16 1.15 1.48 1.12 1.19 1.24 1.30 1.59 1.42 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

PAGE 175

155Table A-34. Fatty acid composition of CO N mare plasma at 56 d post-foaling Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 NA2 0.00 0.00 0.00 0.00 0.00 NA NA C10:0 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C12:0 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C14:0 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C14:1 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C16:0 15.31 15.37 15.60 NA 17.18 17.25 15.95 14.48 17.07 NA NA C16:1 0.95 0.88 1.24 NA 0.00 1.12 0.94 0.00 0.59 NA NA C17:0 0.90 0.87 0.68 NA 1.03 0.68 0.95 0.60 0.96 NA NA C17:1 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C18:0 20.94 19.95 21.35 NA 19.09 18.65 20.78 20.90 19.23 NA NA C18:1 10.25 9.01 9.59 NA 9.59 8.47 10.93 7.81 9.19 NA NA C18:2 46.75 47.15 46.33 NA 46.61 47.33 44.82 51.96 45.89 NA NA C20:0 0.00 0.00 0.51 NA 0.00 0.60 0.00 0.00 0.00 NA NA C18:3 4.01 4.64 2.95 NA 3.91 4.44 3.70 2.17 4.99 NA NA C20:1 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C20:2 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C22:0 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C20:3 0.00 0.96 0.77 NA 0.98 0.68 0.77 0.79 0.86 NA NA C20:4 0.90 1.17 0.98 NA 1.60 0.77 1.15 1.29 1.20 NA NA C24:1 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C20:5 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C22:5 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA C22:6 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 NA NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

PAGE 176

156Table A-35. Fatty acid composition of CO N mare plasma at 84 d post-foaling Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 14.72 15.95 15.71 15.73 15.56 16.88 16.00 14.93 16.40 16.29 16.06 C16:1 0.89 0.76 0.70 0.00 0.84 1.13 0.57 0.67 0.81 0.93 0.69 C17:0 0.94 0.84 0.82 0.90 0.98 0.71 0.95 0.70 1.01 0.92 0.83 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 17.09 20.43 19.95 18.91 18.08 18.25 19.52 20.80 18.25 18.92 19.59 C18:1 10.43 9.11 10.57 8.77 9.37 8.63 10.51 8.62 10.43 9.23 10.21 C18:2 49.57 45.74 46.95 49.28 47.76 48.29 46.93 50.25 46.47 47.72 47.12 C20:0 0.00 0.00 0.00 0.00 0.00 0.56 0.00 0.00 0.58 0.00 0.57 C18:3 4.37 4.97 2.63 4.32 4.99 4.01 3.66 2.08 3.70 4.04 3.04 C20:1 0.00 0.00 0.59 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.84 0.97 0.83 0.94 1.04 0.64 0.74 0.74 0.90 0.85 0.80 C20:4 1.15 1.24 1.24 1.15 1.39 0.89 1.11 1.19 1.46 1.09 1.08 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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157Fatty Acid Composition of Colost rum and Milk from FISH Mares Table A-36. Fatty acid compositi on of FISH mare colostrum Mare FA1 B24 A66 W69 B31 A59 B33 B46 B14 B01 B47 C8:0 3.16 3.05 3.94 5.26 2.84 3.05 5.25 3.69 6.11 4.19 C10:0 6.87 5.71 12.90 12.69 6.13 7.80 11.67 7.90 13.44 9.46 C12:0 5.29 3.42 11.37 9.29 4.12 5.42 9.18 6.11 10.36 6.52 C14:0 2.94 2.65 7.06 6.14 3.83 2.85 6.49 4.09 7.21 4.40 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 23.05 22.84 18.77 17.83 24.84 20.41 20.55 19.98 17.25 20.12 C16:1 4.11 4.91 3.88 3.22 5.97 4.03 5.32 5.22 4.22 3.89 C17:0 0.00 0.00 0.00 0.30 0.00 0.00 0.00 0.00 0.34 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 3.31 2.20 1.83 2.21 2.04 2.15 1.69 2.38 2.24 2.34 C18:1 20.86 22.22 16.00 14.51 22.17 20.51 17.78 20.27 12.98 18.10 C18:2 22.53 24.90 19.43 21.29 23.41 24.43 16.33 24.86 15.38 21.47 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 7.25 7.43 3.80 5.24 4.65 8.43 4.94 3.52 5.33 8.81 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.53 0.00 0.00 C20:2 0.63 0.66 1.03 0.76 0.00 0.91 0.79 0.72 0.61 0.69 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.34 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.41 0.00 0.00 0.00 0.33 1.53 0.00 C22:5 0.00 0.00 0.00 0.27 0.00 0.00 0.00 0.00 0.74 0.00 C22:6 0.00 0.00 0.00 0.58 0.00 0.00 0.00 0.40 1.92 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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158Table A-37. Fatty acid composition of FI SH mare milk at 36 h post-foaling Mare FA1 B24 A66 W69 B31 A59 B33 B46 B14 B01 B47 C8:0 5.46 3.89 5.90 3.05 5.00 6.07 4.99 6.38 5.27 6.95 C10:0 12.21 5.75 12.93 5.44 7.72 11.14 11.28 14.68 11.81 14.50 C12:0 11.96 3.71 12.37 3.90 5.09 9.11 10.47 13.59 10.77 12.15 C14:0 8.36 3.80 8.58 4.34 4.44 6.19 7.78 9.33 7.70 8.20 C14:1 0.77 0.31 0.97 0.26 0.23 0.53 0.19 0.53 0.48 0.67 C16:0 20.29 21.55 18.52 23.43 22.27 16.96 23.02 19.03 21.37 18.14 C16:1 5.21 5.65 5.15 6.18 6.75 4.89 5.63 4.99 4.96 4.59 C17:0 0.00 0.00 0.00 0.29 0.00 0.22 0.00 0.00 0.00 0.19 C17:1 0.00 0.00 0.00 0.48 0.00 0.27 0.00 0.00 0.38 0.19 C18:0 1.61 2.41 1.03 2.01 1.90 1.33 1.65 1.52 1.67 1.63 C18:1 13.53 21.08 13.26 22.45 21.53 15.66 16.05 10.59 14.15 12.53 C18:2 16.30 20.61 15.74 20.39 20.03 19.13 13.54 14.00 13.27 15.95 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 3.98 10.87 3.72 7.22 4.52 6.38 4.28 2.35 6.19 3.97 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.33 0.37 0.28 0.43 0.34 0.37 0.00 0.28 0.22 0.25 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.68 0.00 0.00 0.19 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.66 0.00 0.00 0.67 0.00 0.93 0.57 0.00 C22:5 0.00 0.00 0.28 0.00 0.00 0.29 0.00 0.27 0.33 0.00 C22:6 0.00 0.00 0.77 0.00 0.00 0.80 0.00 1.37 0.76 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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159Table A-38. Fatty acid composition of FI SH mare milk at 14 d post-foaling Mare FA1 B24 A66 W69 B31 A59 B33 B46 B14 B01 B47 C8:0 7.60 7.54 7.62 6.65 5.94 8.28 8.37 8.68 9.09 7.21 C10:0 14.91 12.16 9.62 9.76 8.54 16.68 13.77 17.76 16.70 13.43 C12:0 13.94 8.82 11.36 7.71 5.73 15.88 11.23 16.18 13.22 11.09 C14:0 9.40 5.51 7.78 5.55 4.29 10.42 7.21 10.75 7.65 7.13 C14:1 0.86 0.34 0.98 0.58 0.69 1.34 0.71 1.44 0.38 0.48 C16:0 19.44 15.03 17.31 15.50 17.32 19.53 16.31 18.91 18.40 16.84 C16:1 6.29 3.84 6.05 6.15 7.65 6.87 5.20 6.16 3.07 4.09 C17:0 0.18 0.20 0.00 0.00 0.16 0.28 0.00 0.16 0.30 0.24 C17:1 0.34 0.21 0.26 0.24 0.35 0.35 0.26 0.29 0.27 0.31 C18:0 1.26 1.99 1.03 1.52 1.42 1.19 1.43 1.32 1.82 1.60 C18:1 9.10 12.33 14.69 14.85 19.16 8.89 12.72 8.72 10.15 11.04 C18:2 8.77 13.16 14.84 17.39 20.39 6.95 12.14 6.33 7.34 10.94 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 5.60 17.23 8.45 10.64 5.46 1.49 7.87 1.50 9.62 13.36 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.26 0.33 0.34 0.36 0.36 0.24 0.32 0.19 0.00 0.29 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.32 0.23 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.32 0.30 0.30 0.37 0.41 0.33 0.39 0.34 0.39 0.36 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.49 0.32 0.48 0.87 0.95 0.53 0.75 0.59 0.78 0.55 C22:5 0.28 0.00 0.24 0.34 0.31 0.23 0.25 0.22 0.00 0.25 C22:6 0.95 0.37 0.68 1.56 1.13 0.85 1.24 1.00 0.82 0.79 1 FA = fatty acid, presented as g FA per 100 g fat.

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160Table A-39. Fatty acid composition of FI SH mare milk at 28 d post-foaling Mare FA1 B24 A66 W69 B31 A59 B33 B46 B14 B01 B47 C8:0 6.38 NA2 9.41 7.37 7.23 8.90 5.03 8.59 6.30 NA C10:0 10.91 NA 15.92 11.99 11.39 14.00 6.55 15.18 9.28 NA C12:0 10.06 NA 14.25 10.38 9.12 12.82 4.97 13.60 7.28 NA C14:0 6.82 NA 8.42 6.51 5.63 7.59 4.05 8.20 4.71 NA C14:1 0.83 NA 0.85 0.52 0.49 0.71 0.43 0.87 0.34 NA C16:0 16.99 NA 16.98 16.22 16.07 16.23 18.45 15.37 15.14 NA C16:1 5.89 NA 4.94 5.39 4.89 6.24 7.57 4.62 4.60 NA C17:0 0.30 NA 0.00 0.00 0.00 0.00 0.00 0.19 0.00 NA C17:1 0.00 NA 0.30 0.35 0.40 0.45 0.46 0.28 0.38 NA C18:0 1.42 NA 0.97 1.49 1.38 1.32 1.60 1.25 1.55 NA C18:1 11.46 NA 11.04 12.68 13.93 11.94 19.64 8.22 13.93 NA C18:2 12.52 NA 7.83 14.30 14.15 10.14 17.07 7.84 14.37 NA C20:0 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C18:3 13.83 NA 7.39 10.04 14.24 7.17 12.23 13.72 18.14 NA C20:1 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:2 0.32 NA 0.22 0.38 0.31 0.32 0.34 0.00 0.32 NA C22:0 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:3 0.27 NA 0.00 0.00 0.00 0.00 0.00 0.25 0.31 NA C20:4 0.36 NA 0.30 0.00 0.00 0.00 0.00 0.26 0.29 NA C24:1 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:5 0.61 NA 0.49 0.75 0.28 0.81 0.73 0.64 1.20 NA C22:5 0.24 NA 0.00 0.31 0.00 0.00 0.00 0.25 0.43 NA C22:6 0.88 NA 0.74 1.28 0.44 1.23 0.84 0.77 1.41 NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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161Table A-40. Fatty acid composition of FI SH mare milk at 56 d post-foaling Mare FA1 B24 A66 W69 B31 A59 B33 B46 B14 B01 B47 C8:0 OT2 6.35 NA3 6.56 7.03 7.47 NA 7.32 10.07 3.60 C10:0 OT 12.79 NA 8.43 11.29 9.72 NA 11.47 15.30 7.38 C12:0 OT 11.04 NA 6.90 9.91 9.13 NA 10.40 11.82 7.37 C14:0 OT 6.54 NA 4.66 5.97 5.32 NA 6.09 5.86 4.89 C14:1 OT 1.04 NA 0.56 0.66 0.77 NA 1.01 0.30 0.84 C16:0 OT 15.08 NA 16.03 16.25 14.64 NA 14.79 16.64 15.80 C16:1 OT 4.54 NA 6.90 5.13 5.82 NA 5.24 3.69 5.23 C17:0 OT 0.18 NA 0.00 0.00 0.00 NA 0.22 0.00 0.27 C17:1 OT 0.35 NA 0.39 0.36 0.44 NA 0.34 0.48 0.52 C18:0 OT 0.97 NA 1.16 1.32 1.17 NA 1.28 1.20 1.04 C18:1 OT 9.41 NA 16.40 12.97 11.85 NA 10.30 13.50 15.56 C18:2 OT 10.49 NA 17.01 14.85 14.37 NA 13.25 8.96 13.69 C20:0 OT 0.00 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:3 OT 19.64 NA 14.17 12.76 17.41 NA 16.34 9.99 22.42 C20:1 OT 0.00 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:2 OT 0.27 NA 0.33 0.36 0.36 NA 0.28 0.00 0.37 C22:0 OT 0.00 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:3 OT 0.00 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:4 OT 0.41 NA 0.00 0.50 0.42 NA 0.45 0.00 0.55 C24:1 OT 0.00 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:5 OT 0.49 NA 0.00 0.29 0.41 NA 0.66 0.86 0.29 C22:5 OT 0.21 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:6 OT 0.60 NA 0.45 0.41 0.73 NA 0.83 1.18 0.44 1 FA = fatty acid, presented as g FA per 100 g fat. 2 OT = off trial. 3 NA = not analyzed.

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162Table A-41. Fatty acid composition of FI SH mare milk at 84 d post-foaling Mare FA1 B24 A66 W69 B31 A59 B33 B46 B14 B01 B47 C8:0 OT2 6.32 5.94 4.70 NA3 6.67 6.47 6.55 5.17 6.19 C10:0 OT 8.90 8.43 6.81 NA 8.98 8.29 9.50 6.37 9.43 C12:0 OT 7.31 8.16 5.99 NA 9.03 7.25 8.73 5.23 9.12 C14:0 OT 4.52 5.21 4.68 NA 5.23 4.28 5.24 2.95 5.71 C14:1 OT 0.53 1.04 1.35 NA 1.20 0.66 0.84 0.37 0.99 C16:0 OT 15.98 16.02 16.16 NA 14.29 15.64 14.93 15.71 16.25 C16:1 OT 5.65 5.71 7.44 NA 6.18 7.07 6.16 5.01 6.01 C17:0 OT 0.00 0.00 0.16 NA 0.00 0.00 0.00 0.00 0.00 C17:1 OT 0.00 0.42 0.51 NA 0.48 0.40 0.54 0.56 0.51 C18:0 OT 1.36 1.17 0.94 NA 1.15 1.33 1.43 1.77 1.04 C18:1 OT 13.91 16.35 19.67 NA 11.49 16.21 13.54 16.41 12.85 C18:2 OT 14.99 14.12 19.12 NA 13.83 14.97 13.18 16.47 12.23 C20:0 OT 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 C18:3 OT 20.56 16.34 11.44 NA 19.74 15.78 17.58 22.76 19.80 C20:1 OT 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 C20:2 OT 0.00 0.44 0.43 NA 0.41 0.00 0.30 0.00 0.00 C22:0 OT 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 C20:3 OT 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 C20:4 OT 0.00 0.54 0.00 NA 0.00 0.59 0.55 0.00 0.00 C24:1 OT 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 C20:5 OT 0.00 0.00 0.41 NA 0.47 0.43 0.38 0.45 0.00 C22:5 OT 0.00 0.00 0.27 NA 0.30 0.00 0.00 0.00 0.00 C22:6 OT 0.00 0.44 0.65 NA 0.85 0.62 0.53 0.69 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 OT = off trial. 3 NA = not analyzed.

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163Fatty Acid Composition of Colo strum and Milk from FLAX Mares Table A-42. Fatty acid compositi on of FLAX mare colostrum Mare FA1 B21 B32 A62 C2 C6 A65 B44 B28 B19 B06 C1 C8:0 3.88 4.41 4.95 4.52 3.18 5.10 4.89 3.80 4.69 4.05 NA2 C10:0 10.96 9.73 10.04 9.34 6.83 10.67 11.87 7.34 9.75 10.03 NA C12:0 8.53 6.94 6.70 6.17 4.47 6.52 8.62 6.13 6.52 7.18 NA C14:0 5.35 4.54 4.27 3.92 3.44 3.81 4.95 4.52 4.42 4.73 NA C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C16:0 19.21 19.52 18.93 17.70 19.21 16.32 15.51 18.96 19.05 18.20 NA C16:1 3.78 3.64 4.90 3.44 2.89 3.11 2.38 5.81 3.51 2.67 NA C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C18:0 2.66 2.41 1.87 1.91 3.01 1.97 2.34 1.81 2.61 2.52 NA C18:1 17.84 18.46 16.31 18.90 18.34 16.07 16.08 18.95 18.56 16.86 NA C18:2 18.96 21.89 18.35 25.79 0.79 22.84 22.37 22.66 23.04 22.71 NA C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C18:3 7.81 7.80 13.26 7.26 10.42 12.30 10.14 9.44 7.31 10.08 NA C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:2 1.01 0.66 0.41 1.06 0.63 0.82 0.86 0.59 0.52 0.96 NA C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:3 0.00 0.00 0.00 0.00 0.00 0.46 0.00 0.00 0.00 0.00 NA C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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164Table A-43. Fatty acid composition of FL AX mare milk at 36 h post-foaling Mare FA1 B21 B32 A62 C2 C6 A65 B44 B28 B19 B06 C1 C8:0 4.40 3.41 6.64 6.60 3.92 5.66 6.03 4.24 6.45 4.93 NA2 C10:0 9.41 6.68 11.94 12.53 8.11 11.29 12.35 9.70 14.09 11.57 NA C12:0 8.07 5.16 9.45 9.77 6.70 9.06 10.60 9.50 11.87 10.86 NA C14:0 6.41 4.71 6.17 5.79 5.24 6.40 6.98 7.06 7.55 8.50 NA C14:1 0.44 0.35 0.38 0.39 0.24 0.33 0.42 0.72 0.34 0.54 NA C16:0 22.30 22.04 17.32 18.50 19.99 17.98 17.05 20.14 18.49 21.47 NA C16:1 5.57 5.18 5.90 1.05 4.07 4.18 3.35 4.80 3.10 4.33 NA C17:0 0.00 0.26 0.00 0.00 0.23 0.00 0.00 0.20 0.00 0.00 NA C17:1 0.00 0.31 0.34 0.00 0.31 0.00 0.00 0.30 0.00 0.23 NA C18:0 1.88 2.29 1.30 1.68 1.98 1.76 1.49 1.47 1.88 1.58 NA C18:1 19.09 22.03 15.31 16.68 18.20 14.37 14.64 15.28 12.91 13.11 NA C18:2 15.53 20.32 13.49 17.16 21.22 16.18 18.76 18.78 15.55 15.68 NA C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C18:3 6.54 6.46 11.33 6.41 9.35 12.05 7.82 7.50 6.95 6.87 NA C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:2 0.34 0.45 0.00 0.44 0.36 0.39 0.39 0.39 0.34 0.34 NA C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:3 0.00 0.00 0.30 0.00 0.00 0.33 0.00 0.00 0.00 0.00 NA C20:4 0.00 0.35 0.00 0.00 0.00 0.00 0.00 0.00 0.38 0.00 NA C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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165Table A-44. Fatty acid composition of FL AX mare milk at 14 d post-foaling Mare FA1 B21 B32 A62 C2 C6 A65 B44 B28 B19 B06 C1 C8:0 7.09 7.40 8.50 9.96 7.34 8.23 5.87 NA2 7.24 NA 6.63 C10:0 12.11 12.54 15.38 16.92 13.69 14.50 11.72 NA 13.11 NA 12.12 C12:0 10.48 11.03 13.23 14.74 12.30 12.80 11.83 NA 10.50 NA 10.05 C14:0 6.61 7.19 7.81 8.26 8.17 7.93 8.13 NA 6.90 NA 7.04 C14:1 0.63 1.18 0.80 0.75 0.83 1.09 0.88 NA 0.51 NA 0.50 C16:0 16.69 15.59 16.47 14.50 17.96 14.85 18.18 NA 18.36 NA 16.98 C16:1 5.84 4.86 5.01 4.41 4.88 7.38 6.42 NA 4.42 NA 5.00 C17:0 0.00 0.17 0.00 0.00 0.00 0.00 0.00 NA 0.29 NA 0.13 C17:1 0.38 0.31 0.26 0.37 0.29 0.22 0.38 NA 0.38 NA 0.27 C18:0 1.36 1.15 1.35 0.88 1.21 1.20 1.16 NA 1.82 NA 1.45 C18:1 16.20 11.31 10.09 9.87 12.44 8.80 10.90 NA 16.30 NA 14.78 C18:2 14.30 10.77 9.32 9.45 12.63 10.34 9.01 NA 13.07 NA 15.44 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 NA 0.00 C18:3 7.13 16.01 11.09 8.93 7.52 15.03 14.85 NA 6.40 NA 8.81 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 NA 0.00 C20:2 0.47 0.33 0.26 0.37 0.33 0.34 0.00 NA 0.37 NA 0.31 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 NA 0.00 C20:3 0.33 0.38 0.34 0.30 0.24 0.47 0.31 NA 0.00 NA 0.23 C20:4 0.37 0.26 0.27 0.27 0.30 0.25 0.31 NA 0.36 NA 0.27 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 NA 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 NA 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 NA 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 NA 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

PAGE 186

166Table A-45. Fatty acid composition of FL AX mare milk at 28 d post-foaling Mare FA1 B21 B32 A62 C2 C6 A65 B44 B28 B19 B06 C1 C8:0 5.87 NA2 9.00 8.51 8.33 9.78 5.11 7.48 7.58 NA 7.41 C10:0 9.20 NA 15.36 12.92 14.03 15.04 8.26 11.67 11.61 NA 13.03 C12:0 8.05 NA 13.22 11.59 13.38 12.74 6.54 10.15 9.58 NA 11.44 C14:0 5.48 NA 7.76 6.79 8.15 7.08 4.38 6.31 5.71 NA 7.05 C14:1 0.67 NA 0.76 1.34 1.00 0.69 0.34 0.71 0.42 NA 0.50 C16:0 15.86 NA 16.16 15.03 16.94 15.00 15.40 16.46 15.01 NA 16.84 C16:1 5.84 NA 4.46 5.23 5.48 7.70 4.51 6.12 4.49 NA 4.73 C17:0 0.00 NA 0.00 0.21 0.00 0.00 0.00 0.00 0.00 NA 0.00 C17:1 0.43 NA 0.22 0.38 0.37 0.25 0.37 0.36 0.43 NA 0.36 C18:0 1.43 NA 1.39 1.07 1.24 1.31 1.56 1.67 1.56 NA 1.57 C18:1 14.99 NA 8.82 11.26 10.17 10.24 17.15 14.40 15.01 NA 13.94 C18:2 15.05 NA 8.46 12.71 9.67 8.92 18.99 13.22 12.85 NA 11.69 C20:0 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 C18:3 15.80 NA 13.99 12.65 10.72 9.99 16.76 9.95 15.32 NA 10.71 C20:1 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 C20:2 0.56 NA 0.20 0.49 0.28 0.28 0.36 0.33 0.34 NA 0.38 C22:0 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 C20:3 0.58 NA 0.32 0.34 0.27 0.30 0.27 0.00 0.00 NA 0.29 C20:4 0.32 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 C24:1 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 C20:5 0.00 NA 0.00 0.00 0.00 0.33 0.00 0.49 0.00 NA 0.00 C22:5 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 C22:6 0.00 NA 0.00 0.00 0.00 0.40 0.00 0.66 0.00 NA 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

PAGE 187

167Table A-46. Fatty acid composition of FL AX mare milk at 56 d post-foaling Mare FA1 B21 B32 A62 C2 C6 A65 B44 B28 B19 B06 C1 C8:0 4.56 NA2 7.52 NA NA NA 5.58 5.67 6.83 7.23 7.43 C10:0 6.88 NA 11.44 NA NA NA 8.43 7.40 9.08 11.61 11.04 C12:0 5.93 NA 10.27 NA NA NA 7.95 6.39 7.41 10.63 9.87 C14:0 4.25 NA 5.91 NA NA NA 4.88 4.27 3.62 6.20 5.70 C14:1 0.85 NA 0.69 NA NA NA 0.63 0.55 0.64 1.17 0.60 C16:0 15.27 NA 15.71 NA NA NA 16.06 16.34 15.14 14.36 15.23 C16:1 6.23 NA 5.12 NA NA NA 4.78 7.42 4.53 4.36 4.32 C17:0 0.19 NA 0.00 NA NA NA 0.00 0.00 0.28 0.21 0.00 C17:1 0.53 NA 0.38 NA NA NA 0.46 0.51 0.47 0.34 0.38 C18:0 1.01 NA 0.86 NA NA NA 1.43 1.34 1.36 1.08 1.03 C18:1 17.94 NA 10.30 NA NA NA 14.56 18.71 16.10 9.47 10.56 C18:2 16.15 NA 10.58 NA NA NA 14.60 16.35 14.39 12.62 9.70 C20:0 0.00 NA 0.00 NA NA NA 0.00 0.00 0.00 0.00 0.00 C18:3 19.36 NA 20.68 NA NA NA 19.60 14.19 19.26 20.22 23.55 C20:1 0.00 NA 0.00 NA NA NA 0.00 0.00 0.00 0.00 0.00 C20:2 0.56 NA 0.00 NA NA NA 0.42 0.42 0.44 0.37 0.00 C22:0 0.00 NA 0.00 NA NA NA 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 NA 0.00 NA NA NA 0.00 0.00 0.00 0.00 0.00 C20:4 0.68 NA 0.56 NA NA NA 0.62 0.00 0.62 0.62 0.58 C24:1 0.00 NA 0.00 NA NA NA 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 NA 0.00 NA NA NA 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 NA 0.00 NA NA NA 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 NA 0.00 NA NA NA 0.00 0.39 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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168Table A-47. Fatty acid composition of FL AX mare milk at 84 d post-foaling Mare FA1 B21 B32 A62 C2 C6 A65 B44 B28 B19 B06 C1 C8:0 5.67 5.17 NA2 7.37 NA NA 4.20 NA 7.53 6.43 5.47 C10:0 8.56 6.42 NA 10.23 NA NA 6.96 NA 9.94 10.26 10.10 C12:0 8.25 5.74 NA 9.62 NA NA 6.94 NA 8.36 10.81 10.93 C14:0 5.33 3.64 NA 5.55 NA NA 5.30 NA 4.35 7.08 7.88 C14:1 1.26 0.60 NA 1.07 NA NA 2.26 NA 0.58 1.30 3.36 C16:0 14.86 15.43 NA 15.18 NA NA 16.47 NA 14.99 18.19 18.23 C16:1 5.86 6.60 NA 5.69 NA NA 5.72 NA 4.57 7.66 8.33 C17:0 0.00 0.00 NA 0.00 NA NA 0.29 NA 0.00 0.00 0.14 C17:1 0.49 0.38 NA 0.64 NA NA 0.64 NA 0.45 0.00 0.65 C18:0 0.90 1.29 NA 0.92 NA NA 1.06 NA 1.40 0.99 0.64 C18:1 12.77 18.59 NA 14.02 NA NA 17.73 NA 17.01 12.84 13.38 C18:2 12.68 20.19 NA 10.21 NA NA 13.88 NA 12.89 8.11 8.17 C20:0 0.00 0.00 NA 0.00 NA NA 0.00 NA 0.00 0.00 0.00 C18:3 22.81 15.41 NA 19.18 NA NA 19.11 NA 17.59 15.85 14.33 C20:1 0.00 0.00 NA 0.00 NA NA 0.00 NA 0.00 0.00 0.00 C20:2 0.49 0.46 NA 0.29 NA NA 0.48 NA 0.35 0.00 0.25 C22:0 0.00 0.00 NA 0.00 NA NA 0.00 NA 0.00 0.00 0.00 C20:3 0.00 0.00 NA 0.00 NA NA 0.00 NA 0.00 0.00 0.00 C20:4 0.58 0.00 NA 0.33 NA NA 0.53 NA 0.00 0.57 0.28 C24:1 0.00 0.00 NA 0.00 NA NA 0.00 NA 0.00 0.00 0.00 C20:5 0.00 0.00 NA 0.00 NA NA 0.00 NA 0.00 0.00 0.00 C22:5 0.00 0.00 NA 0.00 NA NA 0.00 NA 0.00 0.00 0.00 C22:6 0.00 0.00 NA 0.00 NA NA 0.00 NA 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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169Fatty Acid Composition of Colo strum and Milk from CON Mares Table A-48. Fatty acid compos ition of CON mare colostrum Mare FA1 B29 B36 B41 A64 B13 B45 A54 B18 C4 B26 A61 C8:0 3.99 3.35 4.75 1.52 3.33 3.44 3.20 3.30 5.47 5.75 5.49 C10:0 9.13 7.84 11.69 1.84 19.90 9.04 7.99 8.25 12.86 14.85 12.83 C12:0 8.89 6.16 7.73 1.40 5.19 7.91 5.79 6.49 9.22 11.09 9.06 C14:0 6.04 4.85 4.61 3.47 4.30 5.51 4.91 3.63 5.22 6.19 5.66 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 18.53 21.71 18.29 29.23 18.76 20.03 22.90 21.15 16.57 17.39 19.86 C16:1 5.42 3.74 3.51 8.13 5.36 3.58 6.19 3.73 2.41 2.84 3.33 C17:0 0.00 0.00 0.00 0.00 0.00 0.37 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 1.52 2.36 2.13 2.38 1.61 3.39 1.83 2.09 2.10 1.99 2.18 C18:1 16.34 19.02 19.41 25.52 16.37 18.67 18.93 19.28 15.88 15.17 16.90 C18:2 21.93 21.42 21.44 20.61 17.47 22.14 19.81 23.73 23.63 20.08 18.32 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 8.22 8.23 5.51 5.89 6.72 4.92 8.46 7.31 5.72 3.61 5.73 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.92 0.93 0.00 0.71 0.03 0.00 1.03 0.94 1.04 0.65 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.40 0.00 0.00 0.29 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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170Table A-49. Fatty acid composition of CON mare milk at 36 h post-foaling Mare FA1 B29 B36 B41 A64 B13 B45 A54 B18 C4 B26 A61 C8:0 NA2 5.26 5.35 2.63 NA 7.90 5.83 6.02 4.86 6.35 5.09 C10:0 NA 10.44 11.65 3.91 NA 14.66 13.06 11.59 9.38 13.85 11.01 C12:0 NA 9.39 10.72 2.97 NA 12.26 13.68 10.17 7.93 12.23 10.25 C14:0 NA 6.58 7.86 3.68 NA 8.09 9.35 6.43 5.99 8.61 8.03 C14:1 NA 0.34 0.73 0.29 NA 0.00 0.92 0.36 0.39 0.61 0.63 C16:0 NA 21.22 19.80 24.07 NA 19.23 20.77 18.22 19.01 20.55 21.93 C16:1 NA 5.54 5.29 7.98 NA 5.62 5.99 4.11 4.47 5.03 5.12 C17:0 NA 0.00 0.17 0.00 NA 0.20 0.00 0.00 0.00 0.00 0.00 C17:1 NA 0.00 0.28 0.00 NA 0.37 0.00 0.00 0.00 0.00 0.00 C18:0 NA 1.75 1.43 2.14 NA 1.59 1.19 1.79 1.57 1.25 1.40 C18:1 NA 17.40 15.85 26.14 NA 16.25 11.10 16.16 17.93 13.76 15.91 C18:2 NA 14.16 16.40 20.28 NA 13.84 14.70 20.25 21.26 14.54 15.01 C20:0 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 NA 7.65 4.15 5.31 NA 0.00 3.00 4.20 6.70 2.88 5.19 C20:1 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 NA 0.00 0.33 0.39 NA 0.00 0.21 0.54 0.42 0.35 0.27 C22:0 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.17 C20:4 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 NA 0.00 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

PAGE 191

171Table A-50. Fatty acid composition of CON mare milk at 14 d post-foaling Mare FA1 B29 B36 B41 A64 B13 B45 A54 B18 C4 B26 A61 C8:0 5.93 4.39 6.97 5.41 5.52 8.09 5.97 8.32 6.00 3.39 5.77 C10:0 8.96 7.14 12.12 8.52 9.01 14.32 9.90 14.46 9.69 4.34 10.37 C12:0 6.52 6.27 10.40 6.90 7.44 12.90 7.87 12.51 8.08 2.95 8.98 C14:0 4.43 5.14 6.49 5.35 5.24 8.38 5.89 7.47 5.35 3.32 6.88 C14:1 0.36 0.59 0.52 0.83 0.56 1.10 0.63 1.04 0.68 0.50 0.55 C16:0 16.99 18.43 16.06 18.37 18.45 17.74 18.06 15.91 15.19 19.32 19.51 C16:1 5.44 7.95 5.21 7.34 7.12 5.93 7.06 4.98 4.96 9.11 6.33 C17:0 0.00 0.00 0.00 0.00 0.00 0.18 0.00 0.17 0.00 0.00 0.00 C17:1 0.53 0.35 0.30 0.39 0.39 0.35 0.30 0.32 0.28 0.53 0.42 C18:0 1.97 1.29 1.44 1.50 1.20 1.39 1.28 1.35 1.30 1.36 1.69 C18:1 19.89 18.83 13.09 21.14 16.82 13.00 15.50 11.59 15.09 25.37 17.83 C18:2 18.58 15.51 13.90 18.69 15.53 9.33 14.40 10.07 18.61 21.38 13.64 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 9.54 13.02 12.73 4.95 11.68 6.70 11.63 11.17 13.82 7.52 7.30 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.45 0.37 0.31 0.49 0.35 0.35 0.25 0.38 0.46 0.57 0.33 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.37 0.00 0.00 0.34 0.22 0.00 0.35 0.31 0.00 0.00 C20:4 0.41 0.36 0.40 0.33 0.35 0.29 0.27 0.25 0.33 0.35 0.41 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.51 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.55 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

PAGE 192

172Table A-51. Fatty acid composition of CON mare milk at 28 d post-foaling Mare FA1 B29 B36 B41 A64 B13 B45 A54 B18 C4 B26 A61 C8:0 7.08 4.05 7.28 NA2 NA 7.11 9.29 9.83 4.82 NA 6.61 C10:0 10.65 5.67 10.32 NA NA 10.21 16.65 15.44 6.66 NA 12.03 C12:0 9.85 4.73 8.42 NA NA 9.09 14.57 13.80 5.66 NA 10.78 C14:0 5.91 3.80 4.74 NA NA 5.31 8.31 7.60 3.82 NA 7.61 C14:1 0.81 0.39 0.32 NA NA 0.71 0.88 0.87 0.53 NA 0.59 C16:0 14.41 18.82 14.43 NA NA 15.43 16.13 15.52 14.55 NA 19.56 C16:1 4.70 8.79 4.89 NA NA 5.26 5.45 5.25 5.31 NA 5.77 C17:0 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 NA 0.00 C17:1 0.45 0.57 0.34 NA NA 0.29 0.27 0.33 0.46 NA 0.43 C18:0 1.35 1.04 1.87 NA NA 1.40 1.19 1.33 1.55 NA 1.55 C18:1 11.64 21.87 15.44 NA NA 14.67 9.33 10.75 17.09 NA 14.09 C18:2 13.43 17.39 16.57 NA NA 13.88 9.85 7.42 19.25 NA 10.57 C20:0 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 NA 0.00 C18:3 18.74 12.26 14.83 NA NA 15.88 7.55 11.01 18.98 NA 10.15 C20:1 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 NA 0.00 C20:2 0.37 0.41 0.41 NA NA 0.41 0.27 0.25 0.53 NA 0.26 C22:0 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 NA 0.00 C20:3 0.44 0.00 0.00 NA NA 0.35 0.00 0.31 0.41 NA 0.00 C20:4 0.28 0.00 0.00 NA NA 0.00 0.00 0.31 0.37 NA 0.00 C24:1 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 NA 0.00 C20:5 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 NA 0.00 C22:5 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 NA 0.00 C22:6 0.00 0.00 0.00 NA NA 0.00 0.26 0.00 0.00 NA 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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173Table A-52. Fatty acid composition of CON mare milk at 56 d post-foaling Mare FA1 B29 B36 B41 A64 B13 B45 A54 B18 C4 B26 A61 C8:0 NA2 NA 7.43 5.30 6.01 NA 7.03 6.56 NA 4.78 NA C10:0 NA NA 11.36 7.64 8.37 NA 10.74 9.97 NA 6.54 NA C12:0 NA NA 10.41 7.14 6.59 NA 9.02 9.59 NA 5.08 NA C14:0 NA NA 6.24 5.07 4.32 NA 6.02 6.24 NA 3.56 NA C14:1 NA NA 1.06 1.33 0.58 NA 0.58 0.88 NA 0.44 NA C16:0 NA NA 16.49 15.91 16.77 NA 16.96 16.24 NA 16.98 NA C16:1 NA NA 4.89 6.78 7.00 NA 5.47 5.65 NA 6.50 NA C17:0 NA NA 0.30 0.17 0.00 NA 0.00 0.00 NA 0.00 NA C17:1 NA NA 0.50 0.45 0.38 NA 0.00 0.50 NA 0.38 NA C18:0 NA NA 1.15 0.85 1.15 NA 0.94 0.82 NA 1.49 NA C18:1 NA NA 14.15 18.55 17.43 NA 11.61 11.88 NA 19.57 NA C18:2 NA NA 11.86 15.26 17.15 NA 14.21 9.65 NA 19.00 NA C20:0 NA NA 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 NA C18:3 NA NA 13.70 15.25 13.26 NA 17.14 21.19 NA 14.34 NA C20:1 NA NA 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 NA C20:2 NA NA 0.39 0.46 0.47 NA 0.29 0.30 NA 0.36 NA C22:0 NA NA 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 NA C20:3 NA NA 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 NA C20:4 NA NA 0.46 0.41 0.59 NA 0.00 0.60 NA 0.48 NA C24:1 NA NA 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 NA C20:5 NA NA 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 NA C22:5 NA NA 0.00 0.00 0.00 NA 0.00 0.00 NA 0.00 NA C22:6 NA NA 0.00 0.00 0.00 NA 0.00 0.00 NA 0.46 NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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174Table A-53. Fatty acid composition of CON mare milk at 84 d post-foaling Mare FA1 B29 B36 B41 A64 B13 B45 A54 B18 C4 B26 A61 C8:0 5.19 5.05 4.73 NA2 6.20 5.64 NA NA 6.49 NA NA C10:0 6.77 7.27 8.19 NA 11.36 7.69 NA NA 9.61 NA NA C12:0 5.79 8.05 8.06 NA 11.07 7.36 NA NA 9.53 NA NA C14:0 3.70 5.24 5.58 NA 7.22 4.65 NA NA 6.08 NA NA C14:1 0.65 0.95 3.03 NA 3.24 1.13 NA NA 2.79 NA NA C16:0 13.86 16.92 15.25 NA 15.91 14.18 NA NA 15.20 NA NA C16:1 5.75 8.07 5.87 NA 6.14 6.11 NA NA 6.19 NA NA C17:0 0.00 0.00 0.26 NA 0.20 0.00 NA NA 0.26 NA NA C17:1 0.60 0.46 0.59 NA 0.58 0.67 NA NA 0.80 NA NA C18:0 1.05 1.15 0.89 NA 0.65 1.02 NA NA 0.64 NA NA C18:1 15.36 13.47 15.05 NA 14.98 14.11 NA NA 15.06 NA NA C18:2 17.47 12.83 13.25 NA 10.61 12.82 NA NA 11.08 NA NA C20:0 0.00 0.00 0.00 NA 0.00 0.00 NA NA 0.00 NA NA C18:3 23.51 20.44 20.39 NA 13.46 24.30 NA NA 17.24 NA NA C20:1 0.00 0.00 0.00 NA 0.00 0.00 NA NA 0.00 NA NA C20:2 0.38 0.00 0.43 NA 0.39 0.30 NA NA 0.43 NA NA C22:0 0.00 0.00 0.00 NA 0.00 0.00 NA NA 0.00 NA NA C20:3 0.00 0.00 0.00 NA 0.00 0.00 NA NA 0.00 NA NA C20:4 0.00 0.00 0.69 NA 0.30 0.32 NA NA 0.41 NA NA C24:1 0.00 0.00 0.00 NA 0.00 0.00 NA NA 0.00 NA NA C20:5 0.00 0.00 0.00 NA 0.00 0.00 NA NA 0.00 NA NA C22:5 0.00 0.00 0.00 NA 0.00 0.00 NA NA 0.00 NA NA C22:6 0.00 0.00 0.00 NA 0.00 0.00 NA NA 0.00 NA NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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175Fatty Acid Composition of Plasma from FISH Foals Table A-54. Fatty acid composition of FISH foal plasma at birth Foal FA1 5B24 5A66 5W69 5B31 5A59 5B14 5B33 5B46 5B01 5B47 C8:0 NA2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 NA 0.56 0.59 0.00 0.77 0.64 0.00 0.84 0.00 0.00 C14:0 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.65 0.00 0.00 C14:1 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 NA 15.86 17.56 17.08 17.03 15.02 16.07 18.32 17.13 16.70 C16:1 NA 2.08 1.59 1.46 1.60 1.55 1.26 2.82 1.57 1.41 C17:0 NA 0.48 0.53 0.00 0.58 0.54 0.57 0.54 0.63 0.72 C17:1 NA 0.00 0.46 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 NA 18.10 19.13 20.61 21.08 22.63 21.14 18.12 20.41 20.51 C18:1 NA 8.28 8.30 7.36 7.09 6.92 6.38 8.95 8.30 7.23 C18:2 NA 44.60 41.21 45.51 43.17 42.93 44.78 36.87 40.32 45.85 C20:0 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 NA 5.63 3.99 2.39 4.44 3.97 2.34 6.12 4.37 3.43 C20:1 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 NA 0.51 0.63 0.61 0.81 0.53 0.56 0.62 0.55 0.00 C22:0 NA 0.80 0.81 0.00 0.00 0.95 0.00 0.78 0.80 0.00 C20:3 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 NA 1.76 2.20 2.44 2.52 2.40 2.88 2.11 2.51 2.17 C24:1 NA 0.00 0.54 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 NA 0.46 0.56 0.80 0.00 0.63 1.52 0.84 0.96 0.69 C22:5 NA 0.00 0.59 0.00 0.00 0.00 0.60 0.66 0.53 0.00 C22:6 NA 0.88 1.32 1.74 0.90 1.29 1.90 1.76 1.91 1.29 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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176Table A-55. Fatty acid composition of FISH foal plasma at 14 d of age Foal FA1 5B24 5A66 5W69 5B31 5A59 5B14 5B33 5B46 5B01 5B47 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.38 0.57 0.54 0.42 0.00 0.00 0.00 0.65 0.39 0.42 C12:0 1.21 1.10 1.32 0.89 0.64 0.64 0.62 1.77 0.84 1.03 C14:0 1.70 1.19 1.61 1.06 0.86 0.93 0.92 1.99 1.23 1.12 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 19.22 15.93 18.42 16.98 19.21 17.13 17.50 17.87 18.11 17.80 C16:1 2.61 1.79 2.07 2.37 3.97 1.83 2.14 2.39 1.50 1.57 C17:0 0.51 0.56 0.48 0.42 0.47 0.56 0.52 0.50 0.84 0.69 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.43 C18:0 21.51 20.87 21.01 20.97 18.69 24.59 21.87 20.72 22.92 22.05 C18:1 7.03 8.38 7.85 9.26 12.81 6.77 7.60 8.29 8.21 7.20 C18:2 36.04 39.76 39.03 38.49 37.27 38.07 38.60 36.17 35.33 36.57 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.42 C18:3 1.29 3.22 1.36 2.19 1.51 0.00 0.00 1.85 1.41 2.19 C20:1 0.00 0.00 0.40 0.00 0.40 0.00 0.00 0.00 0.00 0.00 C20:2 0.50 0.66 0.62 0.60 0.63 0.48 0.51 0.65 0.45 0.58 C22:0 1.03 0.77 0.66 0.82 0.51 0.89 0.92 0.65 0.91 0.77 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 2.96 2.55 1.54 1.69 1.32 3.39 3.67 2.55 2.06 3.18 C24:1 0.00 0.00 0.00 0.40 0.00 0.39 0.00 0.00 0.00 0.00 C20:5 1.46 0.92 1.08 1.04 0.63 1.46 1.56 1.42 2.25 1.32 C22:5 0.62 0.46 0.48 0.48 0.00 0.54 0.73 0.59 0.68 0.52 C22:6 1.92 1.28 1.54 1.92 1.09 2.32 2.85 1.95 2.87 2.14 1 FA = fatty acid, presented as g FA per 100 g fat.

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177Table A-56. Fatty acid composition of FISH foal plasma at 28 d of age Foal FA1 5B24 5A66 5W69 5B31 5A59 5B14 5B33 5B46 5B01 5B47 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.54 0.59 0.61 0.00 0.00 0.45 0.00 0.45 0.00 0.00 C12:0 1.63 1.38 1.60 0.69 0.78 1.24 0.95 1.13 0.94 1.20 C14:0 1.77 1.11 1.17 0.75 0.73 1.23 0.94 1.16 0.95 0.76 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 18.45 15.64 18.59 17.44 17.32 17.14 17.56 17.95 16.76 17.79 C16:1 2.63 1.94 1.97 1.71 1.59 1.99 2.00 3.13 1.89 1.47 C17:0 0.51 0.59 0.58 0.49 0.63 0.55 0.55 0.54 0.64 0.63 C17:1 0.00 0.56 0.48 0.00 0.00 0.00 0.87 0.00 0.00 0.58 C18:0 19.45 20.44 20.62 21.52 23.71 22.53 21.86 18.51 20.43 22.32 C18:1 6.72 7.00 7.89 6.69 6.79 6.12 7.02 9.94 8.19 7.02 C18:2 35.69 36.01 36.50 41.68 39.76 36.57 37.17 34.37 34.70 38.31 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 4.50 6.01 1.20 1.22 1.97 3.60 0.73 4.61 5.57 1.82 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.62 0.66 0.60 0.57 0.62 0.56 0.57 0.61 0.55 0.54 C22:0 0.90 0.74 0.90 0.93 0.78 0.99 1.03 0.88 0.94 1.07 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 2.64 2.56 2.82 2.74 2.84 3.05 3.44 2.66 2.93 3.07 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 1.36 1.93 1.68 1.05 0.83 1.38 1.93 1.16 1.88 1.37 C22:5 0.60 0.66 0.63 0.56 0.00 0.57 0.77 0.68 0.80 0.00 C22:6 1.98 2.19 2.16 1.97 1.65 2.02 2.61 2.23 2.83 2.06 1 FA = fatty acid, presented as g FA per 100 g fat.

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178Table A-57. Fatty acid composition of FISH foal plasma at 56 d of age Foal FA1 5B24 5A66 5W69 5B31 5A59 5B14 5B33 5B46 5B01 5B47 C8:0 OT2 NA3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 OT NA 0.40 0.00 0.46 0.42 0.00 0.73 0.44 0.00 C12:0 OT NA 0.79 0.99 1.15 0.91 0.47 2.09 1.02 0.00 C14:0 OT NA 0.70 0.00 0.85 0.84 0.39 1.51 0.58 0.00 C14:1 OT NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 OT NA 16.91 16.81 17.12 16.31 17.16 18.86 16.73 16.27 C16:1 OT NA 1.74 2.23 2.10 1.86 1.69 2.91 1.18 1.40 C17:0 OT NA 0.57 0.00 0.50 0.55 0.46 0.50 0.68 0.74 C17:1 OT NA 0.38 0.68 0.41 0.45 0.49 0.00 0.00 0.65 C18:0 OT NA 19.46 20.60 19.60 19.28 18.29 18.23 20.34 20.85 C18:1 OT NA 8.40 7.79 7.16 6.65 6.57 8.71 7.22 7.31 C18:2 OT NA 39.45 39.95 40.52 40.50 43.35 36.19 39.89 41.66 C20:0 OT NA 0.36 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 OT NA 4.95 4.06 4.23 4.68 3.04 3.70 2.76 4.02 C20:1 OT NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 OT NA 0.67 0.63 0.74 0.68 0.52 0.57 0.74 0.63 C22:0 OT NA 0.64 1.04 0.77 0.76 0.82 0.71 0.90 0.90 C20:3 OT NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 OT NA 2.10 2.76 2.34 2.59 2.64 2.18 3.10 2.48 C24:1 OT NA 0.00 0.00 0.00 0.00 0.49 0.00 0.00 0.00 C20:5 OT NA 0.66 0.66 0.58 1.17 1.17 0.97 1.52 1.03 C22:5 OT NA 0.51 0.00 0.47 0.54 0.45 0.48 0.66 0.50 C22:6 OT NA 1.31 1.81 1.00 1.81 2.00 1.67 2.22 1.57 1 FA = fatty acid, presented as g FA per 100 g fat. 2 OT = off trial. 3 NA = not analyzed.

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179Table A-58. Fatty acid composition of FISH foal plasma at 84 d of age Foal FA1 5B24 5A66 5W69 5B31 5A59 5B14 5B33 5B46 5B01 5B47 C8:0 OT2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 OT 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 OT 0.56 0.59 0.00 0.77 0.64 0.00 0.84 0.00 0.00 C14:0 OT 0.00 0.00 0.00 0.00 0.00 0.00 0.65 0.00 0.00 C14:1 OT 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 OT 15.86 17.56 17.08 17.03 15.02 16.07 18.32 17.13 16.70 C16:1 OT 2.08 1.59 1.46 1.60 1.55 1.26 2.82 1.57 1.41 C17:0 OT 0.48 0.53 0.00 0.58 0.54 0.57 0.54 0.63 0.72 C17:1 OT 0.00 0.46 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 OT 18.10 19.13 20.61 21.08 22.63 21.14 18.12 20.41 20.51 C18:1 OT 8.28 8.30 7.36 7.09 6.92 6.38 8.95 8.30 7.23 C18:2 OT 44.60 41.21 45.51 43.17 42.93 44.78 36.87 40.32 45.85 C20:0 OT 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 OT 5.63 3.99 2.39 4.44 3.97 2.34 6.12 4.37 3.43 C20:1 OT 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 OT 0.51 0.63 0.61 0.81 0.53 0.56 0.62 0.55 0.00 C22:0 OT 0.80 0.81 0.00 0.00 0.95 0.00 0.78 0.80 0.00 C20:3 OT 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 OT 1.76 2.20 2.44 2.52 2.40 2.88 2.11 2.51 2.17 C24:1 OT 0.00 0.54 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 OT 0.46 0.56 0.80 0.00 0.63 1.52 0.84 0.96 0.69 C22:5 OT 0.00 0.59 0.00 0.00 0.00 0.60 0.66 0.53 0.00 C22:6 OT 0.88 1.32 1.74 0.90 1.29 1.90 1.76 1.91 1.29 1 FA = fatty acid, presented as g FA per 100 g fat. 2 OT = off trial.

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180Fatty Acid Composition of Plasma from FLAX Foals Table A-59. Fatty acid composition of FLAX foal plasma at birth Foal FA1 5B21 5B32 5C2 5A62 5B28 5C 6 5A65 5B44 5C1 5B19 5B06 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.42 0.00 0.44 0.00 0.00 0.00 0.00 0.00 C12:0 0.88 0.00 0.86 1.07 0.51 1.12 0.00 0.00 1.02 0.58 0.00 C14:0 0.53 0.00 0.48 0.93 0.00 0.45 0.00 0.00 0.92 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.65 17.24 16.38 17.62 16.83 17.06 14.18 16.14 17.89 15.21 15.75 C16:1 2.04 1.85 1.73 2.72 1.66 1.77 1.56 1.49 2.60 1.21 1.78 C17:0 0.57 0.00 0.62 0.56 0.60 0.53 0.53 0.68 0.68 0.51 0.52 C17:1 0.41 0.00 0.60 0.00 0.00 0.00 0.00 0.52 0.00 0.00 0.00 C18:0 19.01 18.89 20.06 18.71 21.32 20.23 22.30 22.19 20.71 21.43 23.77 C18:1 8.53 9.46 8.61 8.32 7.75 8.14 7.08 8.02 8.26 7.99 6.63 C18:2 40.85 46.29 40.84 41.05 43.07 42.88 44.95 43.10 39.37 46.42 44.11 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 7.92 4.47 6.08 6.46 3.49 4.26 5.97 4.19 4.23 3.92 3.03 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.76 0.00 0.63 0.65 0.60 0.72 0.64 0.68 0.61 0.52 0.53 C22:0 0.57 0.00 0.67 0.00 0.00 0.00 0.85 0.72 0.65 0.00 0.83 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 1.80 1.81 2.01 1.50 2.06 1.93 1.93 2.25 2.17 2.20 2.43 C24:1 0.46 0.00 0.42 0.00 0.50 0.48 0.00 0.00 0.45 0.00 0.62 C20:5 0.00 0.00 0.00 0.00 0.37 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.48 0.00 0.00 0.00 0.45 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.76 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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181Table A-60. Fatty acid composition of FLAX foal plasma at 14 d of age Foal FA1 5B21 5B32 5C2 5A62 5B28 5C 6 5A65 5B44 5C1 5B19 5B06 C8:0 0.00 0.00 NA2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.53 0.59 NA 0.99 0.50 0.00 0.40 0.54 0.25 0.00 0.53 C12:0 1.17 1.42 NA 1.88 1.14 0.80 1.03 1.14 0.44 0.63 1.17 C14:0 1.34 1.49 NA 1.73 1.28 1.00 1.06 1.40 0.75 0.81 1.34 C14:1 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 16.49 17.45 NA 16.30 16.87 16.70 15.21 16.58 17.30 17.94 16.49 C16:1 2.24 2.02 NA 2.21 2.17 1.29 1.53 2.08 2.21 1.35 2.24 C17:0 0.51 0.52 NA 0.42 0.57 0.46 0.53 0.63 0.53 0.55 0.51 C17:1 0.00 0.00 NA 0.00 0.37 0.38 0.00 0.00 0.18 0.00 0.00 C18:0 21.81 22.61 NA 22.70 21.98 23.19 24.66 22.56 23.05 22.52 21.81 C18:1 9.97 8.62 NA 8.24 7.92 7.40 6.67 7.95 11.00 8.92 9.97 C18:2 39.92 38.54 NA 39.37 39.26 42.94 41.43 39.85 36.37 38.65 39.92 C20:0 0.39 0.00 NA 0.00 0.31 0.39 0.38 0.32 0.22 0.38 0.39 C18:3 1.73 3.74 NA 3.76 1.73 1.27 2.96 3.26 1.59 1.12 1.73 C20:1 0.00 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.30 0.00 0.00 C20:2 0.80 0.71 NA 0.67 0.58 0.64 0.79 0.65 0.57 0.56 0.80 C22:0 0.45 0.53 NA 0.39 0.51 0.40 0.63 0.46 0.65 0.93 0.45 C20:3 0.00 0.00 NA 0.00 0.00 0.00 0.00 2.26 0.00 0.00 0.00 C20:4 2.29 1.30 NA 0.90 2.61 2.33 1.35 0.00 3.45 3.93 2.29 C24:1 0.35 0.45 NA 0.00 0.00 0.37 0.00 0.32 0.42 0.00 0.35 C20:5 0.00 0.00 NA 0.00 0.75 0.00 0.37 0.00 0.00 0.34 0.00 C22:5 0.00 0.00 NA 0.00 0.37 0.00 0.37 0.00 0.27 0.38 0.00 C22:6 0.00 0.00 NA 0.45 1.05 0.44 0.63 0.00 0.46 1.01 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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182Table A-61. Fatty acid composition of FLAX foal plasma at 28 d of age Foal FA1 5B21 5B32 5C2 5A62 5B28 5C 6 5A65 5B44 5C1 5B19 5B06 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.53 0.62 1.00 0.57 0.71 0.60 0.00 0.30 0.62 0.45 C12:0 0.82 1.56 1.63 2.33 1.42 2.01 1.45 0.65 0.67 1.34 1.25 C14:0 0.95 1.27 1.35 1.99 1.33 1.91 1.32 0.80 0.93 1.39 0.96 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 16.32 16.78 16.38 17.04 17.67 17.90 16.33 15.17 17.01 17.25 16.21 C16:1 2.34 2.39 2.04 2.37 2.33 2.35 2.23 2.00 1.94 1.54 1.74 C17:0 0.00 0.49 0.50 0.49 0.49 0.00 0.44 0.47 0.57 0.59 0.46 C17:1 0.48 0.00 0.44 0.43 0.35 0.00 0.00 0.45 0.21 0.41 0.48 C18:0 20.51 18.76 21.22 19.97 19.52 18.87 21.13 20.69 22.55 18.43 22.98 C18:1 8.72 9.39 7.66 7.21 8.47 7.91 7.30 8.38 9.64 8.51 7.02 C18:2 42.53 39.38 41.96 37.59 38.60 40.42 40.40 40.44 39.63 39.92 39.55 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.30 0.31 0.00 0.00 C18:3 3.20 5.69 2.50 5.85 2.36 5.00 2.42 5.66 1.81 5.36 5.11 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.79 0.71 0.82 0.59 0.54 0.00 0.72 0.67 0.76 0.56 0.76 C22:0 0.83 0.68 0.70 0.63 0.74 0.64 0.72 0.66 0.58 0.58 0.81 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 2.50 2.37 2.19 0.49 2.47 2.29 2.38 2.22 2.50 2.32 2.20 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.60 0.88 0.00 0.87 0.54 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.47 0.58 0.00 0.51 0.34 0.34 0.39 0.00 C22:6 0.00 0.00 0.00 0.96 1.68 0.00 1.18 0.56 0.24 0.80 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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183 Table A-62. Fatty acid composition of FLAX foal plasma at 56 d of age Foal FA1 5B21 5B32 5C2 5A62 5B28 5C 6 5A65 5B44 5C1 5B19 5B06 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 C10:0 0.00 0.00 0.00 0.65 0.00 0.41 0.58 0.00 0.53 0.00 NA C12:0 0.46 0.00 0.50 1.63 0.62 1.24 1.36 0.55 1.24 0.51 NA C14:0 0.00 0.00 0.00 0.94 0.00 1.11 0.89 0.00 0.97 0.50 NA C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C16:0 16.26 16.01 16.08 16.74 16.18 17.68 15.61 15.20 16.00 15.87 NA C16:1 1.76 1.74 1.71 2.23 2.01 2.09 1.71 1.29 1.98 1.30 NA C17:0 0.55 0.00 0.56 0.51 0.50 0.42 0.44 0.58 0.54 0.53 NA C17:1 0.52 0.83 0.67 0.00 0.55 0.43 0.00 0.58 0.42 0.36 NA C18:0 20.72 20.92 20.15 19.53 20.90 17.84 20.94 22.29 20.52 18.88 NA C18:1 8.91 9.54 8.35 7.35 8.31 8.23 7.59 7.74 7.31 8.45 NA C18:2 41.80 43.14 41.23 38.77 40.50 43.01 42.32 43.74 39.23 45.51 NA C20:0 0.36 0.00 0.36 0.00 0.37 0.00 0.38 0.00 0.33 0.00 NA C18:3 4.59 2.49 6.12 7.96 3.51 3.66 4.97 4.11 6.59 5.18 NA C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:2 0.88 0.73 0.85 0.64 0.73 0.55 0.62 0.61 0.68 0.46 NA C22:0 0.68 1.02 0.68 0.62 0.79 0.66 0.75 0.68 0.62 0.59 NA C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:4 2.12 2.89 2.33 1.91 2.43 2.22 1.83 2.20 2.10 2.08 NA C24:1 0.40 0.70 0.41 0.00 0.52 0.46 0.00 0.43 0.53 0.40 NA C20:5 0.00 0.00 0.00 0.00 0.39 0.00 0.00 0.00 0.00 0.00 NA C22:5 0.00 0.00 0.00 0.00 0.51 0.00 0.00 0.00 0.39 0.38 NA C22:6 0.00 0.00 0.00 0.52 1.17 0.00 0.00 0.00 0.00 0.00 NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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184Table A-63. Fatty acid composition of FLAX foal plasma at 84 d of age Foal FA1 5B21 5B32 5C2 5A62 5B28 5C 6 5A65 5B44 5C1 5B19 5B06 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.42 0.00 0.44 0.00 0.00 0.00 0.00 0.00 C12:0 0.88 0.00 0.86 1.07 0.51 1.12 0.00 0.00 1.02 0.58 0.00 C14:0 0.53 0.00 0.48 0.93 0.00 0.45 0.00 0.00 0.92 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.65 17.24 16.38 17.62 16.83 17.06 14.18 16.14 17.89 15.21 15.75 C16:1 2.04 1.85 1.73 2.72 1.66 1.77 1.56 1.49 2.60 1.21 1.78 C17:0 0.57 0.00 0.62 0.56 0.60 0.53 0.53 0.68 0.68 0.51 0.52 C17:1 0.41 0.00 0.60 0.00 0.00 0.00 0.00 0.52 0.00 0.00 0.00 C18:0 19.01 18.89 20.06 18.71 21.32 20.23 22.30 22.19 20.71 21.43 23.77 C18:1 8.53 9.46 8.61 8.32 7.75 8.14 7.08 8.02 8.26 7.99 6.63 C18:2 40.85 46.29 40.84 41.05 43.07 42.88 44.95 43.10 39.37 46.42 44.11 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 7.92 4.47 6.08 6.46 3.49 4.26 5.97 4.19 4.23 3.92 3.03 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.76 0.00 0.63 0.65 0.60 0.72 0.64 0.68 0.61 0.52 0.53 C22:0 0.57 0.00 0.67 0.00 0.00 0.00 0.85 0.72 0.65 0.00 0.83 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 1.80 1.81 2.01 1.50 2.06 1.93 1.93 2.25 2.17 2.20 2.43 C24:1 0.46 0.00 0.42 0.00 0.50 0.48 0.00 0.00 0.45 0.00 0.62 C20:5 0.00 0.00 0.00 0.00 0.37 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.48 0.00 0.00 0.00 0.45 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.76 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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185Fatty Acid Composition of Plasma from CON Foals Table A-64. Fatty acid composition of CON foal plasma at birth Foal FA1 5B29 5B36 5A64 5B41 5B13 5B 45 5A54 5B18 5C4 5B26 5A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 1.05 0.00 0.00 1.03 0.00 0.53 0.65 0.73 0.00 0.00 C14:0 0.00 0.57 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.42 18.10 16.14 16.13 16.63 14.85 16.41 16.75 16.57 16.47 16.32 C16:1 1.66 3.15 1.36 1.23 1.65 1.44 1.20 1.82 1.61 1.40 1.30 C17:0 0.70 0.00 0.57 0.61 0.00 0.00 0.49 0.57 0.63 0.00 0.63 C17:1 0.00 0.00 0.00 0.00 0.00 0.65 0.00 0.00 0.00 0.53 0.00 C18:0 21.17 17.02 20.26 22.44 22.68 21.99 22.03 21.84 21.01 21.54 21.50 C18:1 7.65 9.30 9.09 8.28 7.99 7.04 6.37 7.22 8.11 7.70 9.23 C18:2 45.74 40.90 44.98 44.04 44.12 47.20 46.88 44.45 44.47 45.63 43.74 C20:0 4.70 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 7.57 4.39 3.52 3.08 4.13 3.00 3.56 3.95 2.92 3.63 C20:1 0.66 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.79 0.68 0.69 0.65 0.00 0.53 0.59 0.78 0.65 0.00 C22:0 0.00 0.00 0.62 0.00 0.00 0.00 0.00 0.00 0.00 0.88 0.77 C20:3 2.30 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 1.54 1.91 2.42 2.16 2.70 1.97 2.06 2.13 2.29 2.33 C24:1 0.00 0.00 0.00 0.64 0.00 0.00 0.57 0.50 0.00 0.00 0.55 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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186Table A-65. Fatty acid composition of CON foal plasma at 14 d of age Foal FA1 5B29 5B36 5A64 5B41 5B13 5B 45 5A54 5B18 5C4 5B26 5A61 C8:0 NA2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 NA 0.00 0.57 0.65 0.00 0.00 0.54 0.80 0.50 0.00 0.81 C12:0 NA 0.76 1.28 1.57 0.84 0.84 1.14 1.89 1.19 0.00 1.56 C14:0 NA 1.05 1.76 1.75 0.92 1.17 1.34 2.00 1.37 0.53 2.09 C14:1 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 NA 17.78 18.82 16.55 17.05 17.04 18.04 17.47 16.30 16.75 18.44 C16:1 NA 2.81 2.98 2.19 2.32 1.93 2.21 2.12 1.79 2.50 2.61 C17:0 NA 0.42 0.39 0.44 0.00 0.61 0.45 0.51 0.53 0.47 0.61 C17:1 NA 0.00 0.28 0.00 0.00 0.36 0.00 0.26 0.33 0.40 0.19 C18:0 NA 21.92 18.61 21.24 22.91 23.85 22.01 22.30 21.99 22.22 19.89 C18:1 NA 9.92 13.00 8.70 9.07 7.57 7.22 8.14 9.33 10.90 10.89 C18:2 NA 39.83 37.54 38.97 42.49 40.98 39.27 37.06 40.63 40.41 36.97 C20:0 NA 0.35 0.00 0.39 0.00 0.35 0.00 0.33 0.00 0.00 0.29 C18:3 NA 2.68 1.22 3.91 2.12 1.16 2.20 3.08 3.36 1.06 1.70 C20:1 NA 0.00 0.36 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 NA 0.76 0.71 0.65 0.66 0.68 0.50 0.76 0.82 0.83 0.65 C22:0 NA 0.51 0.50 0.75 0.48 0.63 0.67 0.47 0.50 0.88 0.66 C20:3 NA 0.00 0.00 1.97 0.00 0.00 0.00 0.29 0.00 0.00 0.00 C20:4 NA 1.21 1.42 0.00 1.15 2.83 1.52 2.20 1.34 2.65 2.15 C24:1 NA 0.00 0.30 0.28 0.00 0.00 0.42 0.33 0.00 0.41 0.24 C20:5 NA 0.00 0.00 0.00 0.00 0.00 0.86 0.00 0.00 0.00 0.00 C22:5 NA 0.00 0.00 0.00 0.00 0.00 0.49 0.00 0.00 0.00 0.25 C22:6 NA 0.00 0.27 0.00 0.00 0.00 1.13 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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187Table A-66. Fatty acid composition of CON foal plasma at 28 d of age Foal FA1 5B29 5B36 5A64 5B41 5B13 5B 45 5A54 5B18 5C4 5B26 5A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.70 0.00 0.77 0.00 0.76 0.59 0.00 0.57 0.71 C12:0 0.00 0.64 1.41 0.36 1.89 1.18 1.75 1.62 0.70 1.60 1.99 C14:0 0.49 0.69 1.47 0.38 1.55 1.15 1.76 1.48 0.78 1.41 2.07 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.99 17.82 16.59 16.09 18.03 16.66 18.70 16.88 14.90 17.80 19.33 C16:1 1.30 2.82 2.16 1.53 2.23 2.16 1.91 2.32 2.17 2.72 2.79 C17:0 0.61 0.00 0.46 0.49 0.00 0.48 0.48 0.38 0.51 0.39 0.54 C17:1 0.49 0.63 0.00 0.50 0.48 0.43 0.00 0.00 0.68 0.36 0.00 C18:0 22.51 21.61 19.06 21.67 22.31 20.48 20.04 22.59 19.74 21.44 19.24 C18:1 6.92 10.18 9.50 9.19 8.56 8.12 6.89 7.70 9.27 10.76 9.33 C18:2 46.02 39.29 41.19 43.94 38.65 39.93 41.65 40.39 41.71 37.88 37.64 C20:0 0.39 0.00 0.27 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 1.85 2.21 4.02 1.91 1.96 5.37 1.60 3.03 5.28 0.86 2.59 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.74 0.70 0.79 0.76 0.64 0.70 0.57 0.61 0.63 0.76 0.57 C22:0 0.00 0.78 0.53 0.74 0.66 0.75 0.77 0.00 0.84 0.68 0.66 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 2.69 2.64 1.84 2.44 2.26 2.60 2.16 2.13 2.79 2.36 2.54 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.95 0.00 0.00 0.40 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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188Table A-67. Fatty acid composition of CON foal plasma at 56 d of age Foal FA1 5B29 5B36 5A64 5B41 5B13 5B 45 5A54 5B18 5C4 5B26 5A61 C8:0 0.00 NA2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.59 C12:0 0.00 NA 0.76 0.66 0.66 1.00 0.66 0.62 0.80 0.34 1.26 C14:0 0.00 NA 0.59 0.00 0.00 0.97 0.47 0.00 0.56 0.47 1.31 C14:1 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.29 NA 17.36 16.93 16.72 15.70 16.92 14.69 17.09 17.18 18.24 C16:1 1.53 NA 1.93 1.39 2.11 2.47 1.44 1.52 1.93 2.09 2.36 C17:0 0.68 NA 0.46 0.54 0.00 0.47 0.52 0.55 0.56 0.48 0.48 C17:1 0.67 NA 0.00 0.00 0.00 0.50 0.00 0.00 0.00 0.42 0.00 C18:0 21.06 NA 20.16 21.98 21.25 20.10 20.39 22.96 20.61 18.62 19.11 C18:1 8.21 NA 8.36 8.55 8.85 7.96 6.84 6.63 9.07 9.12 8.87 C18:2 43.84 NA 42.84 42.53 42.73 41.15 43.62 44.23 40.59 43.72 39.96 C20:0 0.38 NA 0.00 0.00 0.00 0.00 0.40 0.00 0.00 0.00 0.00 C18:3 3.88 NA 3.78 3.46 3.40 5.14 4.27 3.98 4.22 1.77 4.03 C20:1 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.77 NA 0.73 0.71 0.71 0.56 0.65 0.67 0.78 0.57 0.42 C22:0 0.67 NA 0.57 0.83 0.71 0.76 0.79 0.87 0.81 0.75 0.64 C20:3 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 2.56 NA 1.96 2.43 2.33 2.79 2.05 2.65 2.43 2.38 2.33 C24:1 0.45 NA 0.49 0.00 0.54 0.43 0.48 0.62 0.54 0.00 0.40 C20:5 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.48 0.00 C22:5 0.00 NA 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.49 0.00 C22:6 0.00 NA 0.00 0.00 0.00 0.00 0.49 0.00 0.00 1.12 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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189Table A-68. Fatty acid composition of CON foal plasma at 84 d of age Foal FA1 5B29 5B36 5A64 5B41 5B13 5B 45 5A54 5B18 5C4 5B26 5A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 1.05 0.00 0.00 1.03 0.00 0.53 0.65 0.73 0.00 0.00 C14:0 0.00 0.57 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 15.42 18.10 16.14 16.13 16.63 14.85 16.41 16.75 16.57 16.47 16.32 C16:1 1.66 3.15 1.36 1.23 1.65 1.44 1.20 1.82 1.61 1.40 1.30 C17:0 0.70 0.00 0.57 0.61 0.00 0.00 0.49 0.57 0.63 0.00 0.63 C17:1 0.00 0.00 0.00 0.00 0.00 0.65 0.00 0.00 0.00 0.53 0.00 C18:0 21.17 17.02 20.26 22.44 22.68 21.99 22.03 21.84 21.01 21.54 21.50 C18:1 7.65 9.30 9.09 8.28 7.99 7.04 6.37 7.22 8.11 7.70 9.23 C18:2 45.74 40.90 44.98 44.04 44.12 47.20 46.88 44.45 44.47 45.63 43.74 C20:0 4.70 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 7.57 4.39 3.52 3.08 4.13 3.00 3.56 3.95 2.92 3.63 C20:1 0.66 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.79 0.68 0.69 0.65 0.00 0.53 0.59 0.78 0.65 0.00 C22:0 0.00 0.00 0.62 0.00 0.00 0.00 0.00 0.00 0.00 0.88 0.77 C20:3 2.30 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 1.54 1.91 2.42 2.16 2.70 1.97 2.06 2.13 2.29 2.33 C24:1 0.00 0.00 0.00 0.64 0.00 0.00 0.57 0.50 0.00 0.00 0.55 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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190Fatty Acid Composition of Red Blood Cells from FISH Mares Table A-69. Fatty acid composition of FISH mare red blood cells at 28 d before expected foaling date Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 36.31 34.40 35.64 41.46 41.78 38.40 42.53 39.76 35.58 38.03 C16:1 1.36 0.00 1.12 0.00 0.89 0.00 0.00 1.46 0.00 0.00 C17:0 1.51 0.00 0.78 0.00 0.72 0.00 1.21 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 28.07 27.93 31.50 32.67 31.75 27.01 30.05 26.66 29.82 32.13 C18:1 27.16 27.29 23.15 22.23 21.56 26.59 22.30 26.68 25.60 25.07 C18:2 5.58 10.37 7.81 3.63 3.30 8.00 3.92 5.43 9.00 4.77 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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191Table A-70. Fatty acid composition of FI SH mare red blood cells at foaling Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 36.50 39.54 18.90 41.48 28.46 45.04 38.00 45.39 42.75 35.99 C16:1 0.00 0.00 1.23 0.00 2.92 0.00 0.00 0.79 0.00 4.54 C17:0 1.21 0.00 0.64 0.00 0.35 1.52 1.74 1.55 1.43 1.42 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 26.40 30.72 17.60 29.66 16.85 25.92 28.09 25.89 28.61 25.87 C18:1 29.63 24.40 22.99 24.24 33.25 22.76 26.92 21.31 22.41 25.36 C18:2 6.27 5.34 38.64 4.62 18.16 4.77 5.25 5.06 4.80 6.82 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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192Table A-71. Fatty acid composition of FISH mare red blood cells at 28 d post-foaling Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 37.06 41.49 27.50 41.43 41.99 41.70 41.47 41.91 42.72 39.81 C16:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 25.27 28.00 21.91 29.53 33.92 26.02 28.90 25.65 29.69 29.68 C18:1 30.52 25.42 25.50 25.06 21.14 26.93 25.02 27.05 24.37 24.37 C18:2 7.15 5.09 25.09 3.98 2.95 5.34 4.61 5.39 3.22 6.15 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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193Table A-72. Fatty acid composition of FISH mare red blood cells at 56 d post-foaling Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 OT2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C16:0 39.97 43.51 26.25 38.66 42.46 45.16 OT 47.13 43.29 38.41 C16:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C18:0 24.60 26.18 17.14 26.65 31.52 26.53 OT 27.00 28.59 27.55 C18:1 29.42 25.22 20.64 24.86 22.86 24.52 OT 23.09 24.60 27.98 C18:2 6.01 5.09 35.98 9.82 3.15 3.78 OT 2.78 3.51 6.07 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 OT = off trial.

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194Table A-73. Fatty acid composition of FISH mare red blood cells at 84 d post-foaling Mare FA1 B47 W69 A66 B31 A59 B33 B24 B46 B14 B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 OT2 0.00 0.00 NA3 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C12:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C14:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C14:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C16:0 37.20 43.41 34.88 42.89 42.56 44.01 OT 45.73 46.00 NA C16:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C17:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C17:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C18:0 23.47 28.63 24.69 27.32 28.53 22.39 OT 26.81 29.70 NA C18:1 29.84 22.54 26.95 23.74 22.36 21.38 OT 23.90 24.30 NA C18:2 9.49 5.42 13.48 6.04 6.55 12.22 OT 3.56 0.00 NA C20:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C18:3 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C20:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C20:2 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C22:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C20:3 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C20:4 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C24:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C20:5 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C22:5 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA C22:6 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 OT = off trial. 3 NA = not analyzed.

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195Fatty Acid Composition of Re d Blood Cells from FLAX Mares Table A-74. Fatty acid composition of FLAX mare red blood cells at 28 d before expected foaling date Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 40.27 40.26 43.51 43.75 46.31 35.36 35.70 40.02 35.46 42.09 32.74 C16:1 0.00 0.00 0.67 0.00 0.00 1.37 0.00 0.00 1.46 0.00 1.49 C17:0 0.00 0.00 0.68 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.95 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 32.74 30.75 32.62 30.62 29.27 27.00 24.06 32.00 28.99 33.70 28.21 C18:1 23.48 25.35 19.05 23.03 21.33 27.82 25.43 23.73 26.92 21.13 24.11 C18:2 3.51 3.64 3.46 2.59 3.10 8.44 14.81 4.25 7.17 3.08 12.50 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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196Table A-75. Fatty acid composition of FL AX mare red blood cells at foaling Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C16:0 37.71 36.31 42.21 42.32 48.96 29.40 47.08 NA 38.97 37.68 42.97 C16:1 2.54 0.00 0.00 1.86 0.00 1.60 0.00 NA 0.00 2.21 0.00 C17:0 1.26 1.67 1.32 1.64 1.24 1.04 1.71 NA 1.42 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:0 28.72 31.15 28.54 28.64 25.18 24.67 24.85 NA 28.48 29.31 30.95 C18:1 25.39 27.01 23.22 21.73 21.31 25.27 22.47 NA 24.57 25.24 21.14 C18:2 4.36 3.86 4.72 3.80 3.31 18.02 3.90 NA 6.56 5.56 4.94 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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197Table A-76. Fatty acid composition of FLAX mare red blood cells at 28 d post-foaling Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 44.13 40.75 41.27 45.81 45.32 40.44 43.21 38.43 39.97 41.75 39.81 C16:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 30.84 28.58 27.45 25.17 26.94 30.23 25.56 30.72 31.88 30.78 30.89 C18:1 22.13 25.82 25.86 23.98 23.73 25.27 25.87 25.87 24.48 23.41 23.88 C18:2 2.90 4.85 5.43 5.04 4.01 4.07 5.36 4.98 3.67 4.06 5.42 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

PAGE 218

198Table A-77. Fatty acid composition of FLAX mare red blood cells at 56 d post-foaling Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 45.97 32.68 42.37 48.00 50.33 39.28 46.37 39.68 39.32 53.79 43.24 C16:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 30.94 21.34 28.87 28.47 26.03 29.09 24.85 27.98 30.22 35.86 28.21 C18:1 23.09 28.73 24.17 23.53 23.65 27.65 24.98 26.35 26.65 5.60 24.97 C18:2 0.00 17.25 4.59 0.00 0.00 3.98 3.80 5.99 3.80 4.75 3.58 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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199Table A-78. Fatty acid composition of FLAX mare red blood cells at 84 d post-foaling Mare FA1 B21 A62 B32 C2 C6 A65 B06 C1 B44 B28 B19 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C16:0 40.47 38.78 36.96 46.98 46.48 38.12 45.57 NA 36.21 42.62 35.07 C16:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:0 29.08 24.59 25.63 26.79 24.75 29.02 25.86 NA 27.89 29.42 26.34 C18:1 24.47 27.66 27.95 22.95 23.74 27.11 23.91 NA 29.48 23.48 28.44 C18:2 5.98 8.97 9.46 3.29 5.03 5.75 4.66 NA 6.43 4.48 10.15 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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200Fatty Acid Composition of Re d Blood Cells from CON Mares Table A-79. Fatty acid composition of CON mare red blood cells at 28 d before expected foaling date Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 44.05 47.94 41.03 32.81 50.39 45.04 36.77 42.78 42.15 37.59 35.88 C16:1 0.00 0.97 0.00 1.43 1.05 0.00 0.00 1.48 0.00 1.95 1.30 C17:0 0.00 1.44 0.00 1.07 1.71 0.00 0.00 1.22 0.00 0.00 1.36 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 29.84 38.63 32.87 27.69 34.36 29.09 31.15 29.98 32.99 27.69 29.63 C18:1 23.58 7.30 22.62 26.69 7.36 21.93 26.28 21.52 21.76 25.52 24.55 C18:2 2.54 3.71 3.48 10.31 5.14 3.94 5.80 3.02 3.11 7.25 7.28 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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201Table A-80. Fatty acid composition of CON mare red blood cells at foaling Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C16:0 39.73 40.84 39.47 42.14 36.04 45.00 45.03 NA 40.81 39.32 36.17 C16:1 0.00 0.00 0.00 0.00 1.45 1.36 5.05 NA 0.00 4.25 2.21 C17:0 1.38 1.26 1.54 1.44 1.40 1.28 0.00 NA 1.59 0.64 1.47 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:0 27.23 31.34 31.86 24.69 28.79 25.93 17.65 NA 30.54 17.41 27.41 C18:1 26.69 22.43 23.51 24.62 26.83 19.70 30.50 NA 23.98 32.08 26.02 C18:2 4.97 4.13 3.63 7.10 5.49 6.73 1.76 NA 3.08 6.29 6.71 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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202Table A-81. Fatty acid compos ition of CON mare red blood cells at 28 d post-foaling Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 41.84 41.31 37.11 39.50 41.12 42.73 40.43 40.78 41.81 44.04 39.24 C16:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 29.35 30.84 31.04 28.48 29.33 25.64 32.74 29.13 30.28 28.88 27.47 C18:1 25.55 24.17 27.33 26.56 25.22 25.16 23.35 26.04 25.02 21.99 27.72 C18:2 3.26 3.68 4.53 5.45 4.34 6.47 3.48 4.05 2.89 5.08 5.57 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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203Table A-82. Fatty acid compos ition of CON mare red blood cells at 56 d post-foaling Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 41.52 41.50 38.15 37.78 43.13 42.30 40.38 48.30 50.47 46.87 49.18 C16:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 29.47 30.10 30.86 27.39 28.67 27.40 31.29 29.47 25.72 28.59 24.26 C18:1 24.29 23.99 25.96 29.46 23.41 23.92 24.17 22.24 23.81 21.05 22.18 C18:2 4.73 4.41 5.03 5.36 4.79 6.39 4.16 0.00 0.00 3.48 4.38 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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204Table A-83. Fatty acid compos ition of CON mare red blood cells at 84 d post-foaling Mare FA1 B29 B36 B13 B41 B45 A54 C4 A64 B18 B26 A61 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 39.00 38.26 39.83 38.69 36.35 43.91 42.27 41.91 41.50 46.16 45.23 C16:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 25.50 24.82 29.62 26.29 23.78 27.09 29.04 27.38 25.44 29.21 26.71 C18:1 27.78 29.26 25.90 29.42 28.54 22.23 25.72 24.08 26.35 20.82 23.70 C18:2 7.72 7.66 4.65 5.59 11.34 6.77 2.97 6.63 6.71 3.82 4.36 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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205Fatty Acid Composition of Red Blood Cells from FISH Foals Table A-84. Fatty acid composition of FISH foal red blood cells at birth Foal FA1 5B47 5W69 5A66 5B31 5A59 5B33 5B24 5B46 5B14 5B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1.18 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 41.10 38.53 22.45 37.99 41.96 25.87 27.04 36.20 39.10 37.91 C16:1 6.30 2.70 2.73 2.25 4.13 4.27 2.32 2.34 2.89 5.24 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 16.47 15.18 14.07 15.81 28.25 12.92 12.95 19.71 18.77 20.36 C18:1 32.60 32.70 34.09 36.40 20.78 36.71 35.74 32.17 35.99 31.50 C18:2 1.90 3.60 25.12 3.51 3.23 15.33 5.40 2.30 1.57 3.31 C20:0 1.64 3.03 0.97 2.05 1.65 1.33 1.51 1.58 1.69 1.68 C18:3 0.00 0.00 0.57 0.00 0.00 0.89 0.91 0.00 0.00 0.00 C20:1 0.00 4.27 0.00 2.00 0.00 2.68 12.47 4.53 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 1.65 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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206Table A-85. Fatty acid com position of FISH foal red blood cells at 14 d of age Foal FA1 5B47 5W69 5A66 5B31 5A59 5B33 5B24 5B46 5B14 5B01 C8:0 0.00 0.00 0.00 NA2 NA 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C16:0 37.42 31.63 19.03 NA NA 19.88 35.15 25.94 26.29 30.06 C16:1 2.74 2.93 3.16 NA NA 3.38 4.20 3.45 2.03 1.68 C17:0 0.00 0.83 0.59 NA NA 0.00 0.94 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C18:0 21.19 17.88 15.64 NA NA 13.95 18.16 19.63 17.96 20.35 C18:1 30.28 29.56 28.64 NA NA 31.08 32.85 29.66 30.16 29.14 C18:2 3.49 8.22 31.41 NA NA 24.68 7.14 8.53 5.22 6.13 C20:0 2.98 2.13 1.52 NA NA 0.00 1.55 1.48 1.76 1.26 C18:3 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 5.02 0.00 NA NA 5.69 0.00 11.32 14.80 9.79 C20:2 1.89 1.80 0.00 NA NA 1.33 0.00 0.00 1.78 1.59 C22:0 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 NA NA 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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207Table A-86. Fatty acid com position of FISH foal red blood cells at 28 d of age Foal FA1 5B47 5W69 5A66 5B31 5A59 5B33 5B24 5B46 5B14 5B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 55.63 39.02 33.48 50.39 39.35 33.79 51.56 38.40 37.88 33.94 C16:1 3.78 3.09 4.33 5.81 3.88 4.96 5.50 3.62 3.13 2.64 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 24.02 21.97 24.47 22.56 22.56 21.25 25.58 21.68 21.28 20.41 C18:1 7.73 27.50 3.68 4.26 29.37 32.33 7.23 31.66 27.91 33.04 C18:2 8.83 5.42 34.04 16.98 4.84 7.67 10.13 4.64 6.67 9.97 C20:0 0.00 3.00 0.00 0.00 0.00 0.00 0.00 0.00 3.13 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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208Table A-87. Fatty acid com position of FISH foal red blood cells at 56 d of age Foal FA1 5B47 5W69 5A66 5B31 5A59 5B33 5B24 5B46 5B14 5B01 C8:0 0.00 NA2 0.00 0.00 0.00 0.00 OT3 0.00 0.00 0.00 C10:0 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C12:0 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C14:0 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C14:1 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C16:0 39.04 NA 25.16 30.52 36.66 36.35 OT 42.90 43.25 24.44 C16:1 2.21 NA 2.15 2.12 2.41 2.51 OT 0.00 0.00 1.73 C17:0 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C17:1 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C18:0 20.98 NA 18.21 16.66 23.73 16.10 OT 21.39 23.28 14.34 C18:1 30.28 NA 28.25 30.58 28.88 33.83 OT 30.68 31.22 31.36 C18:2 7.49 NA 26.22 20.14 8.32 8.58 OT 5.03 2.26 28.13 C20:0 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C18:3 0.00 NA 0.00 0.00 0.00 2.63 OT 0.00 0.00 0.00 C20:1 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:2 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:0 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:3 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:4 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C24:1 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:5 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:5 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:6 0.00 NA 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed. 3 OT = off trial.

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209Table A-88. Fatty acid com position of FISH foal red blood cells at 84 d of age Foal FA1 5B47 5W69 5A66 5B31 5A59 5B33 5B24 5B46 5B14 5B01 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 OT2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C16:0 33.44 26.20 24.82 23.64 35.66 27.91 OT 39.07 38.30 23.89 C16:1 0.00 17.87 0.00 1.76 1.92 0.00 OT 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C17:1 0.00 0.00 5.42 0.00 0.00 0.00 OT 0.00 0.00 5.97 C18:0 20.97 23.69 28.11 14.92 24.25 11.90 OT 23.23 22.49 23.72 C18:1 32.93 21.96 27.25 28.53 29.29 29.66 OT 31.93 31.29 28.33 C18:2 12.66 10.28 14.40 31.15 8.88 30.53 OT 5.77 7.93 18.08 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 OT 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 OT = off trial.

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210Fatty Acid Composition of Re d Blood Cells from FLAX Foals Table A-89. Fatty acid composition of FLAX foal red blood cells at birth Foal FA1 5B21 5A62 5B32 5C2 5C6 5A65 5B06 5B44 5B28 5B19 5C1 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C16:0 33.93 29.79 36.93 44.22 31.45 24.80 40.11 29.89 27.17 37.09 NA C16:1 3.69 4.14 2.58 2.25 3.11 3.01 2.89 2.53 2.33 7.00 NA C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.98 0.00 0.00 0.00 NA C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C18:0 18.45 12.73 16.33 18.19 14.35 14.81 18.52 14.67 12.64 17.35 NA C18:1 37.04 31.49 34.29 31.36 32.01 34.56 33.15 31.90 31.72 34.06 NA C18:2 5.00 5.60 2.92 1.84 4.38 9.42 2.49 3.59 1.94 3.04 NA C20:0 1.88 12.25 1.58 2.15 1.72 0.96 1.87 1.78 1.87 1.45 NA C18:3 0.00 4.01 0.00 0.00 0.86 0.73 0.00 0.00 0.00 0.00 NA C20:1 0.00 0.00 5.36 0.00 12.11 11.69 0.00 15.63 22.32 0.00 NA C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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211Table A-90. Fatty acid composition of FLAX foal red blood cells at 14 d of age Foal FA1 5B21 5A62 5B32 5C2 5C6 5A65 5B06 5B44 5B28 5B19 5C1 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 32.20 28.97 33.76 37.95 29.92 33.25 25.42 31.82 31.14 33.81 19.14 C16:1 4.31 4.12 3.77 4.93 4.43 3.22 2.26 2.18 2.92 3.52 9.38 C17:0 0.00 0.92 0.00 0.00 1.10 0.00 0.00 0.00 1.10 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 21.31 20.24 21.15 22.31 19.26 26.62 17.68 20.49 21.03 22.21 18.01 C18:1 35.46 34.05 34.48 30.02 35.63 33.16 29.44 32.31 28.72 33.13 25.12 C18:2 5.63 6.74 3.82 2.01 5.81 3.75 4.66 5.78 2.79 6.20 4.89 C20:0 0.00 2.40 3.02 2.78 1.73 0.00 1.39 0.00 2.80 0.00 11.24 C18:3 0.00 0.86 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 3.47 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 17.14 5.55 7.66 0.00 3.49 C20:2 1.10 1.71 0.00 0.00 2.11 0.00 2.01 1.86 1.84 1.12 5.26 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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212Table A-91. Fatty acid composition of FLAX foal red blood cells at 28 d of age Foal FA1 5B21 5A62 5B32 5C2 5C6 5A65 5B06 5B44 5B28 5B19 5C1 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 53.87 53.08 49.36 54.67 55.73 36.14 38.45 35.70 53.14 39.02 52.83 C16:1 6.43 4.94 5.47 6.02 4.51 2.20 3.17 2.65 6.45 3.29 3.96 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 26.51 28.53 26.84 26.74 25.16 24.19 22.11 26.37 27.51 22.57 25.75 C18:1 6.82 5.11 3.51 7.79 6.74 32.45 31.05 26.39 5.16 27.41 4.95 C18:2 6.37 8.34 14.82 4.79 4.75 5.02 5.22 5.83 7.75 7.72 12.51 C20:0 0.00 0.00 0.00 0.00 3.12 0.00 0.00 3.05 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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213Table A-92. Fatty acid composition of FLAX foal red blood cells at 56 d of age Foal FA1 5B21 5A62 5B32 5C2 5C6 5A65 5B06 5B44 5B28 5B19 5C1 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 38.57 33.52 39.54 29.77 39.47 37.55 37.98 39.89 41.05 35.24 30.58 C16:1 2.70 0.00 2.25 11.17 0.00 2.86 1.61 2.02 0.00 0.00 2.35 C17:0 0.00 0.00 0.00 5.56 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 7.08 0.00 0.00 0.00 0.00 0.00 7.31 0.00 C18:0 21.91 21.03 24.50 22.64 22.28 25.14 23.77 23.33 23.11 20.06 16.96 C18:1 30.84 32.02 28.56 19.15 30.52 30.67 31.59 28.87 30.09 30.07 29.52 C18:2 5.97 13.43 5.14 4.63 7.73 3.78 2.26 5.89 5.76 7.32 20.59 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 2.78 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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214Table A-93. Fatty acid composition of FLAX foal red blood cells at 84 d of age Foal FA1 5B21 5A62 5B32 5C2 5C6 5A65 5B06 5B44 5B28 5B19 5C1 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 35.45 40.13 35.70 44.63 43.37 37.09 38.19 34.58 39.40 34.17 39.01 C16:1 1.90 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 13.18 0.00 0.00 0.00 C18:0 23.78 23.10 22.78 22.86 23.78 26.90 22.71 24.72 23.67 21.95 23.83 C18:1 32.10 31.26 33.18 28.15 29.04 31.89 30.72 22.48 31.02 32.74 31.77 C18:2 6.77 5.51 8.34 4.36 3.81 4.13 8.39 5.04 5.91 11.14 5.39 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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215Fatty Acid Composition of Re d Blood Cells from CON Foals Table A-94. Fatty acid composition of CON foal red blood cells at birth Foal FA1 5B29 5B36 5B13 5B41 5B45 5A54 5C4 5B18 5B26 5A61 5A64 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C16:0 40.50 36.66 35.52 24.43 32.16 42.54 40.82 21.76 39.10 38.22 NA C16:1 4.19 3.63 5.38 2.28 2.50 6.80 0.00 2.60 1.56 5.25 NA C17:0 1.02 0.00 1.06 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C18:0 17.84 15.42 17.94 15.31 13.19 19.65 31.41 12.09 29.21 14.39 NA C18:1 32.93 34.79 35.60 36.65 28.13 27.99 23.94 33.17 23.22 36.39 NA C18:2 1.76 2.96 3.14 20.72 2.03 1.78 3.83 15.32 5.07 4.50 NA C20:0 1.76 1.24 1.37 0.61 1.55 1.25 0.00 1.13 1.84 1.25 NA C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.77 0.00 0.00 NA C20:1 0.00 5.31 0.00 0.00 20.44 0.00 0.00 13.17 0.00 0.00 NA C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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216Table A-95. Fatty acid composition of CO N foal red blood cells at 14 d of age Foal FA1 5B29 5B36 5B13 5B41 5B45 5A54 5C4 5B18 5B26 5A61 5A64 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C16:0 38.00 32.86 32.48 23.08 38.58 39.55 33.23 NA 23.38 37.14 40.83 C16:1 2.55 4.56 3.54 2.34 4.10 3.29 3.50 NA 2.49 2.26 4.93 C17:0 0.00 0.00 0.00 0.66 0.00 1.29 1.06 NA 0.65 1.10 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 2.59 C18:0 20.45 19.66 25.20 17.91 19.15 26.42 24.30 NA 17.95 18.93 19.42 C18:1 33.43 36.85 33.95 31.10 31.41 26.45 30.18 NA 28.56 28.87 25.57 C18:2 4.29 3.82 4.83 24.90 3.25 3.01 2.59 NA 15.62 5.64 2.80 C20:0 0.00 2.24 0.00 0.00 3.51 0.00 2.98 NA 0.76 0.00 2.57 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 10.59 4.80 0.00 C20:2 1.29 0.00 0.00 0.00 0.00 0.00 2.16 NA 0.00 1.26 1.28 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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217Table A-96. Fatty acid composition of CO N foal red blood cells at 28 d of age Foal FA1 5B29 5B36 5B13 5B41 5B45 5A54 5C4 5B18 5B26 5A61 5A64 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA2 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C16:0 38.00 32.86 32.48 23.08 38.58 39.55 33.23 NA 23.38 37.14 40.83 C16:1 2.55 4.56 3.54 2.34 4.10 3.29 3.50 NA 2.49 2.26 4.93 C17:0 0.00 0.00 0.00 0.66 0.00 1.29 1.06 NA 0.65 1.10 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 2.59 C18:0 20.45 19.66 25.20 17.91 19.15 26.42 24.30 NA 17.95 18.93 19.42 C18:1 33.43 36.85 33.95 31.10 31.41 26.45 30.18 NA 28.56 28.87 25.57 C18:2 4.29 3.82 4.83 24.90 3.25 3.01 2.59 NA 15.62 5.64 2.80 C20:0 0.00 2.24 0.00 0.00 3.51 0.00 2.98 NA 0.76 0.00 2.57 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 10.59 4.80 0.00 C20:2 1.29 0.00 0.00 0.00 0.00 0.00 2.16 NA 0.00 1.26 1.28 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 NA 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat. 2 NA = not analyzed.

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218Table A-97. Fatty acid composition of CO N foal red blood cells at 56 d of age Foal FA1 5B29 5B36 5B13 5B41 5B45 5A54 5C4 5B18 5B26 5A61 5A64 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 43.78 36.70 39.48 32.69 41.96 44.46 38.00 36.93 34.70 39.13 31.16 C16:1 3.17 2.63 2.63 0.00 0.00 0.00 0.00 2.19 1.94 0.00 2.37 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 21.84 21.31 23.12 19.76 23.42 25.23 25.40 21.30 24.26 21.06 19.61 C18:1 27.98 32.22 29.75 32.52 29.28 25.49 30.70 31.32 33.85 34.18 27.92 C18:2 3.24 7.14 5.02 15.03 5.33 4.82 5.91 8.26 5.25 5.64 18.94 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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219Table A-98. Fatty acid composition of CO N foal red blood cells at 84 d of age Foal FA1 5B29 5B36 5B13 5B41 5B45 5A54 5C4 5B18 5B26 5A61 5A64 C8:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C10:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C12:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C14:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C16:0 35.47 35.31 41.74 29.73 30.76 42.27 39.77 30.81 36.44 44.32 35.88 C16:1 0.00 2.62 0.00 0.00 0.00 0.00 0.00 1.97 9.00 0.00 2.08 C17:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C17:1 6.27 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:0 30.71 21.69 27.83 20.70 21.12 26.61 27.35 20.62 29.93 24.38 21.52 C18:1 27.56 33.46 26.10 32.78 31.87 22.39 28.24 31.60 24.63 28.01 28.90 C18:2 0.00 6.93 4.33 16.80 16.25 8.73 4.64 15.00 0.00 3.30 11.62 C20:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C18:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:2 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:0 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:3 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:4 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C24:1 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C20:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:5 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 C22:6 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 1 FA = fatty acid, presented as g FA per 100 g fat.

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220Response of Mares during an Intradermal Skin Test Table A-99. Skin thickness values of FISH mares during an intradermal skin test1 Time2 Mare 0h 2h 4h 6h 8h 12h 24h 48h A61 3.93 11.39 16.71 17.47 14.48 15.98 18.33 11.83 B26 4.42 11.68 18.05 16.78 22.09 19.44 15.91 19.50 B41 3.91 9.83 13.59 11.17 16.79 13.98 10.09 15.52 C4 4.23 11.03 15.43 10.33 14.68 12.51 14.79 12.24 A54 3.78 13.52 22.67 23.52 24.36 23.94 19.63 23.87 B13 4.78 13.28 16.68 15.47 16.25 15.86 14.78 20.07 B18 5.37 12.92 13.84 15.78 13.61 14.69 18.63 13.43 B29 3.18 10.56 15.57 14.73 13.69 14.21 15.34 14.87 B45 4.25 9.75 12.16 11.73 12.21 11.97 10.79 11.01 B36 3.93 11.39 16.71 17.47 14.48 15.98 18.33 11.83 1 Presented in mm. 2 Measured as h post injection.

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221Table A-100. Skin thickness values of FL AX mares during an intradermal skin test1 Time2 Mare 0h 2h 4h 6h 8h 12h 24h 48h B06 3.78 11.71 10.17 10.94 14.54 18.57 16.56 14.82 B19 3.83 16.46 12.78 14.62 18.55 17.56 18.06 22.46 A65 4.45 7.45 6.84 7.15 14.29 13.30 13.80 17.74 B44 4.00 10.51 12.59 11.55 12.46 13.19 12.83 13.27 C1 4.35 14.51 14.21 14.36 16.13 16.54 16.33 18.62 A62 5.88 12.53 12.37 12.45 14.77 13.73 14.25 12.81 B21 4.54 7.84 7.97 7.91 9.88 11.03 10.45 9.10 C2 4.09 10.90 10.11 10.51 14.89 14.27 14.58 18.25 B28 4.52 13.81 10.92 12.36 17.72 12.45 15.08 19.97 C6 4.91 12.79 12.07 12.43 15.62 18.22 16.92 15.81 B32 4.68 11.54 10.46 11.00 11.34 11.45 11.40 9.73 1 Presented in mm. 2 Measured as h post injection.

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222Table A-101. Skin thickness values of C ON mares during an intradermal skin test1 Time2 Mare 0h 2h 4h 6h 8h 12h 24h 48h A61 4.61 11.29 11.52 11.41 15.11 16.80 15.96 16.18 B26 4.59 9.88 9.13 9.51 19.80 18.25 19.03 20.17 B41 5.03 12.68 9.56 11.12 15.73 10.08 12.90 18.14 C4 4.38 13.56 10.84 12.20 12.78 12.36 12.57 12.68 A54 4.82 11.58 11.55 11.57 13.23 12.62 12.93 15.94 B13 4.81 13.34 11.42 12.38 17.89 17.45 17.67 21.08 B18 5.35 16.36 13.85 15.11 21.19 20.00 20.59 21.20 B29 4.80 13.78 10.58 12.18 16.78 12.09 14.43 15.95 B45 3.92 10.54 10.46 10.50 12.80 13.48 13.14 10.30 B36 4.37 12.95 14.99 13.97 15.55 18.14 16.85 14.75 1 Presented in mm. 2 Measured as h post injection.

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223Response of Foals during an Intradermal Skin Test Table A-102. Skin thickness values of FI SH foals during an intradermal skin test1 Time2 Foal 0h 2h 4h 6h 8h 12h 24h 48h 5W69 4.76 4.55 4.66 9.81 9.15 9.48 11.02 10.30 5B33 3.60 3.83 3.72 8.34 9.79 9.07 11.21 11.34 5B14 4.57 4.38 4.48 9.66 10.35 10.01 12.14 14.92 5B46 4.22 3.78 4.00 10.86 7.86 9.36 14.61 12.56 5B1 4.66 4.54 4.60 10.01 10.48 10.25 13.55 15.53 5A59 4.69 4.36 4.52 12.64 10.63 11.63 15.87 16.40 5B31 3.63 3.52 3.57 10.50 9.85 10.17 13.13 13.28 5B47 3.81 4.17 3.99 10.99 8.45 9.72 15.25 10.42 5A66 3.76 3.82 3.79 7.95 11.27 9.61 10.23 16.50 1 Presented in mm. 2 Measured as h post injection.

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224Table A-103. Skin thickness values of FL AX foals during an intradermal skin test1 Time2 Foal 0h 2h 4h 6h 8h 12h 24h 48h 5B06 4.00 3.06 3.53 11.45 11.92 11.69 14.85 14.26 5B19 3.75 4.45 4.10 10.46 13.54 12.00 13.79 16.67 5A65 3.58 3.56 3.57 9.26 11.18 10.22 12.13 15.00 5B44 3.29 3.49 3.39 8.68 9.84 9.26 11.66 13.77 5B28 4.56 4.42 4.49 11.02 10.71 10.86 14.00 12.07 5C1 4.61 3.62 4.11 11.48 9.94 10.71 15.30 17.30 5C6 4.72 3.36 4.04 9.24 9.26 9.25 13.55 12.01 5A62 4.29 3.80 4.05 9.76 9.04 9.40 14.62 12.13 5B21 3.60 3.47 3.54 7.55 7.38 7.46 13.30 13.55 5C2 3.92 4.22 4.07 12.53 11.68 12.10 15.13 14.95 5B32 3.76 3.49 3.63 10.41 9.46 9.94 14.28 14.32 1 Presented in mm. 2 Measured as h post injection.

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225Table A-104. Skin thickness values of C ON foals during an intradermal skin test1 Time2 Foal 0h 2h 4h 6h 8h 12h 24h 48h 5A61 5.12 4.94 5.03 11.37 10.25 10.81 13.90 12.50 5B26 4.01 3.99 4.00 8.07 7.66 7.87 12.60 10.47 5B41 4.73 4.63 4.68 8.80 9.15 8.97 9.16 13.65 5B13 4.62 4.59 4.60 12.09 9.72 10.91 15.61 13.51 5A54 5.35 4.35 4.85 13.50 10.71 12.10 13.29 12.37 5C4 4.67 4.75 4.71 12.89 12.83 12.86 14.34 17.64 5B18 3.82 4.11 3.96 10.35 9.61 9.98 14.99 14.23 5B29 4.21 3.87 4.04 12.51 8.28 10.39 16.78 7.97 5B45 3.14 2.88 3.01 10.63 9.45 10.04 12.74 12.40 5B36 4.21 4.17 4.19 9.30 8.95 9.13 10.57 14.66 1 Presented in mm. 2 Measured as h post injection.

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226 APPENDIX B PROCEDURE FOR IMMUNOGLOBULIN G ANALYSIS Immunoglobulin G (IgG) content was an alyzed using a single radial immunodiffusion (SRID) kit (VMRD, Inc., Pu llman, WA) with a de tection range of 200 to 1600 mg/dL. The kit included four SR ID plates (12 wells each) containing monospecific antisera in buffered agarose, four reference standards (d escribed at the end of this appendix) preserved with 0.09% s odium azide and a 3 L precision pipette and plunger. SRID plates were shipped and st ored upside down in mylar pouches. The mechanism at work in this analysis is as fo llows: the antigen in the sample added to the plate diffuses into the gel containing the anti body, and a precipitation ring forms that is proportional to the concentration of the antige n. This analysis is time and temperature dependent. The procedure used for IgG determination was as follows: 1. Samples were allowed to come to room temperature and vortexed thoroughly. 2. Samples with high expected IgG values were diluted with deionized water (diH2O) to ensure that readings w ould be within measurable levels. Samples were diluted by pipetting 250 L of sample into a clean vial and adding th e appropriate amount of diH20. Samples were vortexed thoroughly af ter dilution. Dilutions were as follows: Colostrum: 1 part sample, 15-17 parts diH2O Mare serum (d0): 1 part sample, 3 parts diH2 O Foal serum (36h through d+84): 1 part sample, 3 parts diH2 O Mare milk (36h through d+84, foal serum (d0): No dilution 3. Three L of Standards A through D were pipetted (using the included precision pipette and plunger) into wells 1 through 4 of plate 1. Once the filling process had begun, the pipette was lifted off the bottom of the well to ensure the liquid did not overflow the well.

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227 4. The remaining wells of all plates were filled with 3 L of each sample to be tested, following the same pipetting technique as a bove. Identification and dilution rate of the sample in each well were recorded on the data sheet included in the kit. 5. Plate covers were firmly reattached and pl ates were left undisturbed, rightside up at room temperature for 18-24 hours outside of their mylar pouches. 6. After 18-24 hours, ring diameter was read in mm using a monocular comparator (VMRD, Inc., Pullman, WA). Diameter r eadings were recorded on the data sheet included in the kit. Used plates were i nverted, returned to their mylar pouches and stored at 4-8C. 7. To determine IgG concentrations, standard and sample diameters and dilution rates were entered into the co mputer program MetraFIT (Metra Biosystems, Inc., Mountain View, CA). Concentrations were calculated using a 4 parameter model using a standard equation provided by the pr ogram. The equation used was IgG concentration = (a d) / (1 + (RD / c) ^ b) + d, where a = 2.968, b = 1.245, c = 1278.2, d = 9.829 and RD = ring diameter. STANDARDS Standard A : 200 mg IgG/dL Standard B : 400 mg IgG/dL Standard C : 800 mg IgG/dL Standard D : 1600 mg IgG/dL

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228 APPENDIX C PROCEDURE FOR FATTY ACID ANALYSIS Fatty acids were extracted from plasma, milk or red blood cells as described by Folch et al. (1957). The fatty acid extraction procedure was as follows: 8. Colostrum, milk and plasma samples were dried in a freeze dryer in preparation for fatty acid (FA) extraction. Colostrum and milk samples were dried for 5 days and plasma samples were dried for 24-48 hours. Every 48-72 hours, samples were removed from the freeze dryer and stor ed at -20C while the freeze dryer was defrosted. At the end of defrosting (a pproximately 30 minutes), samples were placed back into the freeze dryer to continue drying. Grass, hay, and concentrate samples were dried in a 60C oven for 3 days in preparation for FA analysis. 9. After drying, colostrum and milk samples were weighed in their sample cups to determine dry sample weights. These weights were then used to calculate colostrum and milk dry matter. Afte r weighing, the dry milk samples were transferred from the samples cups to plas tic Whirl Pack bags. Blood samples were kept in their original vial s. All samples were stored at -20C until extraction. 10. To prepare for FA extraction, 40 mL screw cap vials were wei ghed without caps to determine a tare weight used later to calculate the amount of tota l fat extracted. These vials were labeled as “T-Tubes.” Special care was taken to not allow bare skin to touch these vials as skin oils could add additional weight. After weighing, Teflon lined caps were placed on the vials and the vials were set aside for later use. 11. Weighted or measured sample amounts we re placed into another set of 40 mL screw cap vials and the we ights/volumes of samples was recorded. Target weights/volumes used were: 1 g freeze dried milk 2 g freeze dried colostrum 2 mL freeze dried plasma 2 mL freeze dried red blood cells 2-3 g dried hay or grass 1-3 g dried concentrate 0.3 g fish oil or flaxseed supplement 12. Twenty mL of Folch 1 and 50 L of a C19:0 internal st andard were added to all samples (see end of appendix for reagent e xplanation). Vials were then vortexed for 2 minutes.

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229 13. Samples were left at room temper ature over night (at least 16 hours). 14. The next morning, a nitrogen gas evapor ator apparatus was prepared by adding distilled water (dH2O) to the water bath and heating it with a heating rod to 37C. The water bath in the methylation tank was also filled and heated to 90C. 15. Samples were vortexed and filtered through #40 Whatman filter paper (150 mm) into the T-Tubes. 16. To recover any FA remaining in the orig inal sample vial, 10-20 mL of Folch 1 were added to the original vial. Vials were again vortexed and filtered. The filter paper was then rinsed with 1-2 mL of clean Folch 1. 17. Once the samples were finished filteri ng, 0.1 mL of 10% BHT was pipetted into each sample and the vials were gently swirled to mix. 18. Samples were dried under nitrogen gas fl ow in a 37C water bath until all liquid had disappeared (approximately 1.5-2 hours). 19. Vials were removed from the drying a pparatus, dried with a paper towel and allowed to cool completely. 20. When the tubes were cool, they were wei ghed to determine the amount of fat in the original sample. This was accomplished using a digital scale. A small beaker was placed on the scale, its weight tared and the vials were placed in the beaker and weighed without their caps. The original T-Tube weights were subtracted from these weights to give the wei ght of actual fat recovered. 21. Teflon tape was wrapped around the threads of each vial to prevent evaporation during methylation. 22. Two mL of 4% H2SO4 in methanol were added to each vial containing the dried fat. Caps were replaced and checked for tightness of fit. 23. Samples were heated in a 90C bath for 15 minutes to permit methylation of the fatty acid. 24. Samples were allowed to cool completely after methylation before being uncapped. The Teflon tape was removed from the vi al threads and 1.0 mL hexane was added to the sample by pipet. Caps were quick ly replaced to avoid hexane evaporation. 25. Samples were vortexed and transferred to 8 mL glass vials with Teflon septa screw caps. 26. Two mL of double di stilled water (ddH2O) were added to the vials via needle and syringe. Vials were vortexed, inverted and left at room temperature for at least 30 minutes to allow for layer separation.

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230 27. The bottom layer (made up of water and chemicals) was removed using a needle and syringe. Great care was taken not to remove any of the top layer (made of hexane and fat). Therefore, a small amount of water was left after each removal to ensure no hexane was accidentally removed. 28. Two mL ddH2O was again added to the vials via needle and syringe and the vials were vortexed, inverted and left to stand at room temperature for at least 30 minutes. 29. The removal of the water layer was repeat ed, again leaving a small amount of water to ensure no hexane removal. 30. Steps 19-22 were repeated, for a total of three washes. 31. Two mL of ddH2O was added to the sample. Th e sample was vortexed and left standing upright for at least 30 minutes at r oom temperature. (Note: If the hexane did not separate from the water or wa s cloudy, samples were stored at 4-8C overnight to ensure separation). 32. The hexane layer was transferred by glass pi pet into a 2 ml glass GC vial for FA analysis. If less than 0.5 mL of hexane was recovered, the hexane was transferred to a 200 L polypropylene tube FA analysis. 33. Samples were stored at -20C and allowe d to come to room temperature before being placed on the GC autosampler. After analysis, samples were stored at -20C. Gas Chromatograph Information Gas chromatography (GC) was performed us ing a CP-3800 Gas Chromatograph (Varian, Inc., Palo Alto, CA). A WCOT fused sili ca column (CP-SIL 88, le ngth 100 m, internal diameter 0.25 mm, flow rate 5.0 mL/min, Vari an, Inc., Palo Alto, CA) was used. The carrier gas was helium with a pressure of 29.5 psi (one minute), 35.4 psi (0.42 psi/min, total of 45 minutes) and 37.9 psi (0.17 psi/min, held for 50 minutes, total of 110 minutes). The temperature program was 120C for one minute, increased to 190C at 5C/minute and held at 190C for 30 minutes (total of 45 minutes), increased to 220C at 2C/minute and held at 220C for 50 minutes, giving a total run time of 110 mi nutes. Fatty acids were identified by comparison of peak re tention times for samples and reference standards (Nu-Chek Prep, Inc., Elysian, MN).

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231 REAGENTS 10% BHT : 20 g butylated hydrototulene in 200 mL total volume with methanol; antioxidant 4% H2SO4: 8.33 mL H2SO4 in 200 mL total volume with methanol; for methylation Folch 1 : 1 part methanol, 2 parts chloroform; for fat homogenization Double distilled water (ddH2O) : replaced daily; for washing

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243 BIOGRAPHICAL SKETCH Elizabeth Lindsay Stelzleni was born in Ga inesville, Florida, on March 2, 1982. She was raised a strict Gator fan and alwa ys knew she would attend the University of Florida. Elizabeth loved horses from a ve ry young age and was given riding lessons for her seventh birthday. It was then that her devotion to horses truly began. Elizabeth graduated fourth in her class from Gainesville High School in 2000 with a GPA of 4.5. During her high school years she bought Handsome Slew, her Thoroughbred gelding whom she proceeded to win many area and national awards on in the sport of eventing. In he r senior year of high school, Elizabeth began training young horses and retraining problem horses in the sports of eventing, dressage and hunter/jumper. Elizabeth entered Santa Fe Community College in the fa ll of 2000 and achieved her Associate of Arts degree in 2002. She then m oved to the University of Florida to begin her Bachelor of Science degree program in animal sciences (equine science specialization) and graduated cum laude in 2004. At graduation, she was honored as a Two-Year Scholar by the Univer sity. Around the same time th at Elizabeth was preparing to graduate, Dr. Lori Warren had just come to the University as a professor of equine nutrition. Dr. Warren agreed to take Elizabet h on as a graduate student, and Elizabeth began her Master of Science degree in the fall of 2004. During her time as a graduate student, Elizabeth worked as a teaching assi stant for many equine science classes and continued to train young and problem horses for various sports.

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244 During the first year of her graduate program, Elizabeth married Alexander Stelzleni on December 18, 2004. Alexander was working on his doctoral degree in meat science and beef production when the two met and plans on graduating with his degree in May of 2006. Upon graduation, Alexander plan s on pursuing his goal of securing a job as a professor of meat science and animal production classes, while Elizabeth will pursue her goal of working for a feed co mpany as an equine specialist.


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Copyright Date: 2008

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EFFECT OF DIETARY n-3 FATTY ACID SOURCE ON PLASMA, RED BLOOD
CELL AND MILK COMPOSITION AND IMMUNE STATUS OF MARES AND
FOALS














By

ELIZABETH LINDSAY STELZLENI


A THESIS PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
MASTER OF SCIENCE

UNIVERSITY OF FLORIDA


2006



























Copyright 2006

by

Elizabeth Lindsay Stelzleni


































This document is dedicated to my mother and step-father, Melanie and Jim Eisenhour, for
their unconditional love and support even when they had no idea what I was doing, and to
my husband Alex, who I could not have survived graduate school without.
















ACKNOWLEDGMENTS

First and foremost I want to thank my husband Alex for his never ending patience,

love and understanding through these first years of our marriage. His faith in me has

oftentimes exceeded the faith I have in myself, and without his constant encouragement I

could not have completed this work. I am so proud of him for completing his doctoral

degree this summer, while at the same time walking me through my first experiences of

graduate school. I am extremely lucky to have a husband who is also my best friend.

I owe great gratitude to Dr. Lori Warren, my committee chair. Her guidance and

wisdom have been invaluable to me, both inside the classroom and out. She has been

instrumental in my choices of future paths, and I thank her for this direction. I would

also like to thank Drs. Lokenga Badinga and Steeve Giguere, who served on my

committee and dedicated their time to improving my proj ect and thesis. Joel McQuagge

also deserves my appreciation for his encouragement, humor and friendship.

My sample analysis could not have been completed had it not been for the

supervision and instruction of Jan Kivipelto. Jan also receives my debt of gratitude for

being a shoulder to lean on and an open ear to talk to. I owe thanks as well to Steve

Vargas and the employees of the University of Florida Horse Research Center, especially

Cher Jackson. Their help, both in taking samples and organizing data, was crucial to this

proj ect. I would also like to thank the horses of the Horse Research Center and Horse

Teaching Unit. Without their cooperation and patience I could not have completed this

work. A special thank you goes to "Buster Buckley," who always made me smile.









I am fortunate enough to have friends throughout the department willing to offer

help and smiles during the past few years. Many thanks go to Sarah Dilling, Kelly

Spearman, Drew Cotton, Aimee Holton, Sarah White and Liz Greene for their assistance.

I also appreciate the support of the crew at the Horse Teaching Unit, especially Justin

Calahan and Kristin Detweiler.

Last, but most definitely not least, I would like to thank my grandmother, Lois

VanNatta; my "Baba," Dena Lovacheff; my sister- and brother-in-law, Jennifer and Todd

Schwent; and the rest of Alex' s and my family. I would like to lend a special thank you

to my in-laws, Lynne and Michael Stelzleni, for their unconditional love, support and

encouragement of Alex and me. Most importantly, I want to thank my mother, Melanie

Eisenhour, for showing me the kind of woman I want to be and my step-father, Jim

Eisenhour, for taking me in and loving me like his own daughter. They have offered me

nothing but undying love and support and have been my biggest fans. I am forever

indebted to them for all they have done.




















TABLE OF CONTENTS


page

ACKNOWLEDGMENT S .............. .................... iv


LI ST OF T ABLE S ............ ..... .__ ...............x....


LI ST OF FIGURE S .............. .................... xvii


AB STRAC T ................ .............. xix


CHAPTER


1 INTRODUCTION ................. ...............1.......... ......


2 REVIEW OF LITERATURE ................. ...............3.......... .....


Fatty Acid Structure, Digestion and Metabolism .............. ...............3.....
Fatty Acid Structure .............. ...............3.....
Fatty Acid Digestion............... ...............4
De novo Fatty Acid Synthesis .............. ...............7.....
Fatty Acid Degradation .............. ...............8.....
Polyunsaturated Fatty Acids ............... ... ............ ...............9......
n-6 and n-3 Polyunsaturated Fatty Acids .............. ....... ...............
Elongation of and Competition Between n-6 and n-3 Families .......................... 13
Eicosanoid Production and Function ................. ...............16................
The Immune System ................. ...............17........... ....
Acquired Immunity .............. ...............17....
Immunoglobulins .................. ...............17.................
Passive Immunity in the Foal .............. ...............20....
Failure of Passive Transfer............... ...............22
Innate Immunity .............. ...............24....
Inflam m ation ............... ..... ..... .. .. ... ..........2
Effects of Dietary PUFA Supplementation on Inflammation and Immune
Function .............. .... .. ... .. .............. ...............2
Blood and Tissue Responses to Experimental Feeding of n-3 PUFA .................26
Effects of PUFA supplementation on the acquisition of passive immunity
in the foal ................ ............ ... .......3
Effects of PUFA supplementation on the inflammatory response ...............3 3
Effects of PUFA supplementation on disease resistance and survival.........3 5
Characteristics of Mare Milk ................. ...............39........... ...












Mare Colostrmm .................. .... ...... ... ...... ........___..........3
Factors Affecting Mare Colostrmm IgG Content............... ...............39
Composition of Mare Milk ........._......... ....__ ........._.._ ...........4
Effect of Diet on Fat and Fatty Acid Composition of Milk .........._... ..............43
Fatty Acid Transfer across the Placenta .............. ...............46....
Conclusions............... ..............4


3 MATERIALS AND METHODS .............. ...............51....


Animals................ ...............51
Diets and Treatments .............. ...............52....

Bodyweights .............. .... .... ..............5
Blood Sample Collection and Processing .................._...... .........._. .......5
Colostrmm and Milk Collection and Processing ........._..._......_._ .........._.... 56
Fatty Acid Analysis .............. ...............57....
Intradermal Skin Test ................ .. ...............58.

Supplement and Feed Sample Analysis............... ...............59
Statistical Analysis............... ...............59

4 RE SULT S .............. ...............61....


Feed and Supplement Analysis............... ...............61
M are Fatty Acid Intake ............ ..... ._ ...............62...
Mare and Foal Bodyweight .............. ...............63....
Mare Plasma Fatty Acid Composition............... ..............6
Omega-6 Fatty Acids............... ...............63.
Omega-3 Fatty Acids...................... ..............6
Omega-6:Omega-3 Fatty Acid Ratios ................ ................................98
Mare Colostrmm and Milk Fatty Acid Composition............... ..............6
Foal Plasma Fatty Acid Composition ................. ...............66........... ...
Omega-6 Fatty Acids............... ...............66.
Omega-3 Fatty Acids...................... ..............6
Omega-6:Omega-3 Fatty Acid Ratios ................ ................................68
Fatty Acid Correlations................ ..................6
Fatty Acid Composition of Red Blood Cells ................. .............. ......... .....69
Mare Red Blood Cell Fatty Acids .............. ...............69....
Foal Red Blood Cell Fatty Acids............... ...............69.
Mare Serum, Colostrmm and Milk IgG............... ...............70..
Foal Serum IgG ........ ........._ .... ...... ... .......__ _.........7
Mare and Foal Responses to the Intradermal Skin Test ................. ............. .......71
Mare Response to PHA .............. ...............71....
Foal Response to PHA. .............. ... .............. ...............72......
Comparing Mare and Foal Responses to PHA ................. ................ ....._.72

5 DI SCUS SSION ................. ................. 105........ ....


Fatty Acid Composition of Feeds and Supplements ................. .......................105











Mare and Foal Bodyweight .............. ...............108....
Mare Plasma Fatty Acid Content ................. ...............109........... ...
Mare Milk Fatty Acid Content ................. ......... ...............111 ....
Foal Plasma Fatty Acid Content ................. ........... ......... ........ ....... 11
Mare and Foal Red Blood Cell Fatty Acid Content .........__.. .... ._.__............114
Effect of n-3 Supplementation on IgG. ....._._._ ....... .....__...........1
Mare and Foal Inflammatory Response .....__.....___ ........... .............1

6 IMPLICATIONS ............ ..... .__ ...............121...

APPENDIX

A RAW DATA ............ ..... ._ ...............123...

Mare Expected and Actual Foaling Dates and Dates Started on Trial .....................123
Fatty Acid Composition of Monthly Pasture Samples ............_.. ........_........126
Mare Fatty Acid Intake ................. ...............127...............
M are Bodyweight .............. ...............128....
F oal B odywei ght............... ............. 13
M are Serum IgG .............. ...... .._ ...............134..
Mare Colostrmm and Milk IgG ............ .....__ ...............136
Foal Serum IgG. .............. ...... ...__ ......... .._.. ..........13
Fatty Acid Composition of Plasma from FISH Mares ............_.. ........_........142
Fatty Acid Composition of Plasma from FLAX Mares. ............_.. ........._.......147
Fatty Acid Composition of Plasma from CON Mares. ............_.. ........_.........152
Fatty Acid Composition of Colostrmm and Milk from FISH Mares ........................ 157
Fatty Acid Composition of Colostrum and Milk from FLAX Mares............._._... ....163
Fatty Acid Composition of Colostrum and Milk from CON Mares............._._... ......169
Fatty Acid Composition of Plasma from FISH Foals ........._.._....... ._._............175
Fatty Acid Composition of Plasma from FLAX Foals ............ ... ......_.........180
Fatty Acid Composition of Plasma from CON Foals ......___ ....... ...._..........185
Fatty Acid Composition of Red Blood Cells from FISH Mares ............. .............190
Fatty Acid Composition of Red Blood Cells from FLAX Mares ...........................195
Fatty Acid Composition of Red Blood Cells from CON Mares. ............. ..............200
Fatty Acid Composition of Red Blood Cells from FISH Foals ............... ..............205
Fatty Acid Composition of Red Blood Cells from FLAX Foals ............................210
Fatty Acid Composition of Red Blood Cells from CON Foals ............... .... ...........215
Response of Mares during an Intradermal Skin Test ................. ......._._. .........220
Response of Foals during an Intradermal Skin Test.................. ...............22

B PROCEDURE FOR IMMUNOGLOBULIN G ANALYSIS ........._..... ..............226

C PROCEDURE FOR FATTY ACID ANALYSIS .............. ...............228....
















LIST OF REFERENCES ................. ...............232................


BIOGRAPHICAL SKETCH .............. ...............243....


















LIST OF TABLES


Table pg

2-1 Fatty acid composition of common feeds and fat supplements fed to horses .....12

2-2 Fatty acid composition of common forages fed to horses ................. ................13

2-1 Immunoglobulin concentrations of serum and milk in mature horses ................18

3-1 Nutrient composition of the grain mix concentrate and the milled flaxseed
and encapsulated fish oil supplements .............. ...............53....

3-2 Nutrient composition of the bahiagrass pasture (by month) and Coastal
bermudagrass hay .............. ...............54....

4-1 Fatty acid composition of the grain mix concentrate and the milled flaxseed
and encapsulated fish oil supplements .............. ...............73....

4-2 Fatty acid composition of winter and spring bahiagrass pasture and Coastal
bermudagrass hay .............. ...............74....

4-3 Mare average daily fatty acid intake from December-March............................7

4-4 Mare average daily fatty acid intake from April-June............... ...............7

4-5 M are bodyweights .............. ...............77....

4-6 Foal bodyweights............... ..............7

4-7 Overall effect of treatment on the fatty acid composition of mare plasma ........78

4-8 Omega-6 fatty acid content of mare plasma ................. ................ ........ .79

4-9 Omega-3 fatty acid content of mare plasma ................. ................. ........ 80

4-10 Omega-6:omega-3 fatty acid ratios in mare and foal plasma and mare milk......81

4-11 Overall effect of treatment on the total fat content of mare colostrmm and
m ilk ................. ...............82.................

4-12 Overall effect of treatment on the fatty acid composition of mare colostrmm
and m ilk ................ ...............8.. 2..............











4-13 Omega-6 fatty acid content of mare colostrum and milk ................. ................83

4-14 Omega-3 fatty acid content of mare colostrum and milk ................. ................84

4-15 Overall effect of treatment on the fatty acid composition of foal plasma..........85

.4-16 Omega-6 fatty acid content of foal plasma. ................ ............................86

4-17 Omega-3 fatty acid content of foal plasma. ................ ............................87

4-18 Correlations between mare milk and mare plasma fatty acid concentrations
and mare milk and foal plasma fatty acid concentrations .............. ..................88

4-19 Overall effect of treatment on the fatty acid content of mare red blood cells ....89

4-20 Linoleic acid content of mare red blood cells ................. ......... ...............90

4-22 Linoleic and alpha-linolenic acid contents of foal red blood cells ................... ...91

4-21 Overall treatment effect on the fatty acid composition of foal red blood cells ..92

4-23 Overall effect of treatment on mare serum and colostrmm IgG content at
foaling ................. ...............93.................

4-24 IgG content of mare milk ......._.........._.. ........___ ........._. ...._93

4-25 Correlations between IgG content of mare and foal serum, colostrum, and
m are age............... ...............94..

4-26 IgG content of foal serum ................. ...............95...............

4-27 Skin thickness of mares in response to an intradermal inj section of
phytohemagglutinin ........._._.._......_.. ...............95.....

4-28 Skin thickness of foals in response to an intradermal inj section of
phytohemagglutinin ........._.__........__. ...............96....

4-29 Skin response of mares and foals pooled across treatments to an intradermal
skin test using phytohemagglutinin as the stimulant............._ ........._._. .....97

A-1 FISH mare expected foaling dates, actual foaling dates and dates started on
trial ................ ............... 123........ .....

A-2 FLAX mare expected foaling dates, actual foaling dates and dates started on
trial ................ ............... 124........ .....

A-3 CON mare expected foaling dates, actual foaling dates and dates started on
trial ................ ............... 125........ .....











A-4 Fatty acid composition of bahiagrass pasture (by month) and Coastal
bermudagrass hay .............. ...............126....

A-5 Mare daily intake of forage, grain and supplement by month. ................... .......127

A-6 FISH mare bodyweights ................ ...............128...............

A-7 FLAX mare bodyweights .............. ...............129....

A-8 CON mare bodyweights .............. ...............130....

A-9 FISH foal bodyweights ................. ...............131...............

A-10 FLAX foal bodyweights ................. ...............132...............

A-11 CON foal bodyweights ................. ...............133...............

A-12 Serum IgG content of FISH mares at foaling ................. ........................134

A-13 Serum IgG content of FLAX mares at foaling ................. ........... ...........134

A-14 Serum IgG content of CON mares at foaling ................. ................. ......135

A-15 IgG content of colostrmm and milk from FISH mares............... ..................136

A-16 IgG content of colostrum and milk from FLAX mares ................. .................1 37

A-17 IgG content of colostrmm and milk from CON mares ............... ................138

A-18 IgG content of serum from FISH foals............... ...............139.

A-19 IgG content of serum from FLAX foals .....__ ................ ................ ...140

A-20 IgG content of serum from CON foals ....._____ .... ......... ..........__.....14

A-21 Fatty acid composition of FISH mare plasma at 28 d prior to expected foaling
date .............. ...............142....

A-23 Fatty acid composition of FISH mare plasma at 28 d post-foaling .................144

A-24 Fatty acid composition of FISH mare plasma at 56 d post-foaling .................145

A-26 Fatty acid composition of FLAX mare plasma at 28 d before expected foaling
date .............. ...............147....

A-27 Fatty acid composition of FLAX mare plasma at foaling ........._.._... ...............148

A-28 Fatty acid composition of FLAX mare plasma at 28 d post-foaling ...............149










A-29 Fatty acid composition of FLAX mare plasma at 56 d post-foaling ...............150

A-30 Fatty acid composition of FLAX mare plasma at 84 d post-foaling ...............15 1

A-31 Fatty acid composition of CON mare plasma at 28 d before expected foaling
date .............. ...............152....

A-32 Fatty acid composition of CON mare plasma at foaling ................. ................153

A-33 Fatty acid composition of CON mare plasma at 28 d post-foaling .................154

A-34 Fatty acid composition of CON mare plasma at 56 d post-foaling .................155

A-3 5 Fatty acid composition of CON mare plasma at 84 d post-foaling .................156

A-36 Fatty acid composition of FISH mare colostrum ................. ........__. ........157

A-37 Fatty acid composition of FISH mare milk at 36 h post-foaling .....................158

A-3 8 Fatty acid composition of FISH mare milk at 14 d post-foaling .....................159

A-39 Fatty acid composition of FISH mare milk at 28 d post-foaling .....................160

A-40 Fatty acid composition of FISH mare milk at 56 d post-foaling .....................161

A-41 Fatty acid composition of FISH mare milk at 84 d post-foaling .....................162

A-42 Fatty acid composition of FLAX mare colostrm ................. ............. .......163

A-43 Fatty acid composition of FLAX mare milk at 36 h post-foaling .............. .....164

A-44 Fatty acid composition of FLAX mare milk at 14 d post-foaling .............. .....165

A-45 Fatty acid composition of FLAX mare milk at 28 d post-foaling .............. .....166

A-46 Fatty acid composition of FLAX mare milk at 56 d post-foaling .............. .....167

A-47 Fatty acid composition of FLAX mare milk at 84 d post-foaling .............. .....168

A-48 Fatty acid composition of CON mare colostrm ................. ............ .........169

A-49 Fatty acid composition of CON mare milk at 36 h post-foaling .....................170

A-50 Fatty acid composition of CON mare milk at 14 d post-foaling .....................171

A-51 Fatty acid composition of CON mare milk at 28 d post-foaling .....................172

A-52 Fatty acid composition of CON mare milk at 56 d post-foaling .....................173

A-53 Fatty acid composition of CON mare milk at 84 d post-foaling .....................174










A-54 Fatty acid composition of FISH foal plasma at birth ................. ................. .175

A-55 Fatty acid composition of FISH foal plasma at 14 d of age .............. ..... ...........176

A-56 Fatty acid composition of FISH foal plasma at 28 d of age .............. ..... ...........177

A-57 Fatty acid composition of FISH foal plasma at 56 d of age .............. ..... ...........178

A-58 Fatty acid composition of FISH foal plasma at 84 d of age .............. .... ...........179

A-59 Fatty acid composition of FLAX foal plasma at birth ................. .........._.._.. .180

A-60 Fatty acid composition of FLAX foal plasma at 14 d of age ........._.._................181

A-61 Fatty acid composition of FLAX foal plasma at 28 d of age ........._.._................182

A-62 Fatty acid composition of FLAX foal plasma at 56 d of age ........._.._................183

A-63 Fatty acid composition of FLAX foal plasma at 84 d of age ........._.._................184

A-64 Fatty acid composition of CON foal plasma at birth ................. ................ ...185

A-65 Fatty acid composition of CON foal plasma at 14 d of age .............. ............... 186

A-66 Fatty acid composition of CON foal plasma at 28 d of age .............. ............... 187

A-67 Fatty acid composition of CON foal plasma at 56 d of age .............. ............... 188

A-68 Fatty acid composition of CON foal plasma at 84 d of age .............. ............... 189

A-69 Fatty acid composition of FISH mare red blood cells at 28 d before expected
foaling date ..... ._ ................ ...............190......

A-70 Fatty acid composition of FISH mare red blood cells at foaling............._.._.. ....191

A-71 Fatty acid composition of FISH mare red blood cells at 28 d post-foaling....... 192

A-72 Fatty acid composition of FISH mare red blood cells at 56 d post-foaling....... 193

A-73 Fatty acid composition of FISH mare red blood cells at 84 d post-foaling....... 194

A-74 Fatty acid composition of FLAX mare red blood cells at 28 d before expected
foaling date ................. ...............195......... ......

A-75 Fatty acid composition of FLAX mare red blood cells at foaling ................... ..196

A-76 Fatty acid composition of FLAX mare red blood cells at 28 d post-foaling ..... 197

A-77 Fatty acid composition of FLAX mare red blood cells at 56 d post-foaling ..... 198










A-78 Fatty acid composition of FLAX mare red blood cells at 84 d post-foaling ..... 199

A-79 Fatty acid composition of CON mare red blood cells at 28 d before expected
foaling date .............. ...............200....

A-80 Fatty acid composition of CON mare red blood cells at foaling ................... ....201

A-81 Fatty acid composition of CON mare red blood cells at 28 d post-foaling .......202

A-82 Fatty acid composition of CON mare red blood cells at 56 d post-foaling .......203

A-83 Fatty acid composition of CON mare red blood cells at 84 d post-foaling .......204

A-84 Fatty acid composition of FISH foal red blood cells at birth ................... .........205

A-85 Fatty acid composition of FISH foal red blood cells at 14 d of age ........._........206

A-86 Fatty acid composition of FISH foal red blood cells at 28 d of age ........._........207

A-87 Fatty acid composition of FISH foal red blood cells at 56 d of age ........._........208

A-88 Fatty acid composition of FISH foal red blood cells at 84 d of age ........._........209

A-89 Fatty acid composition of FLAX foal red blood cells at birth ................... .......210

A-90 Fatty acid composition of FLAX foal red blood cells at 14 d of age ................21 1

A-91 Fatty acid composition of FLAX foal red blood cells at 28 d of age ................212

A-92 Fatty acid composition of FLAX foal red blood cells at 56 d of age ................213

A-93 Fatty acid composition of FLAX foal red blood cells at 84 d of age ................214

A-94 Fatty acid composition of CON foal red blood cells at birth ............................215

A-95 Fatty acid composition of CON foal red blood cells at 14 d of age ..................216

A-96 Fatty acid composition of CON foal red blood cells at 28 d of age ..................217

A-97 Fatty acid composition of CON foal red blood cells at 56 d of age ..................218

A-98 Fatty acid composition of CON foal red blood cells at 84 d of age ..................219

A-99 Skin thickness values of FISH mares during an intradermal skin test ........._....220

A-100 Skin thickness values of FLAX mares during an intradermal skin test ............221

A-101 Skin thickness values of CON mares during an intradermal skin test .........._...222

A-102 Skin thickness values of FISH foals during an intradermal skin test ................223










A-103 Skin thickness values of FLAX foals during an intradermal skin test .............224

A-104 Skin thickness values of CON foals during an intradermal skin test ................225

















LIST OF FIGURES


Figure pg

2-1 Essential fatty acid metabolism. ............. ...............14.....

4-1 Total omega-6 fatty acid content in mare plasma from 28 d pre-partum to 84
d post-foaling. ........._.__ ..... ._ ...............97....

4-2 Total omega-3 fatty acid content in mare plasma from 28 d pre-partum to 84
d post foaling. ............. ...............98.....

4-3 Total omega-6 fatty acid content of mare milk from foaling (dO) through 84 d
post-foaling. ........... ..... .._ ...............98....

4-4 Total omega-3 FA content of mares milk from foaling (dO) through 84 d post-
foaling ................. ...............99.................

4-5 Total omega-6 fatty acid content of foal plasma from birth (dO) through 84 d
of age. ............. ...............99.....

4-6 Total omega-3 fatty acid content of foal plasma from birth (dO) through 84 d
of age. ............. .....................100

4-7 Linoleic acid content of mare red blood cells from 28 d pre-partum to 84 d
post-foaling. ........... ..... .._ ...............100...

4-8 Linoleic acid content of foal red blood cells from birth (dO) to 84 d of age. ....101

4-9 Alpha-linolenic acid content of foal red blood cells from birth (dO) to 84 d of
age............... ...............101..

4-10 Correlation between mare serum IgG concentration at foaling (dO) and foal
serum IgG concentration 36 h post-foaling. ................... ................0

4-11 Foal serum IgG concentration at birth and before nursing. .............. ..............102

4-12 Foal serum IgG content after colostrmm ingestion from 36 h to 84 d post-
foaling ................. ...............103................

4-13 Skin thickness of mares in response to an intradermal inj section of
phytohemagglutinin. ........... ..... .___ ...............103....











4-14 Skin thickness of foals in response to an intradermal inj section of
phytohemagglutinin. ........... ..... ._ __ ...............104....

4-15 Skin thickness of mares and foals in response to an intradermal inj section of
phytohemagglutinin. ........... ..... ._ __ ...............104....


XV111
















Abstract of Thesis Presented to the Graduate School
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Master of Science

EFFECT OF DIETARY n-3 FATTY ACID SOURCE ON PLASMA, RED BLOOD
CELL AND MILK COMPOSITION AND IMMUNE STATUS OF MARES AND
FOALS

By

Elizabeth Lindsay Stelzleni

August 2006

Chair: Lori K. Warren
Major Department: Animal Sciences

Supplementing the diets of horses with fat is a popular trend in today's equine

industry. However, little focus has been given to the effect of supplementing with

omega-3 fatty acids (FA) in the broodmare and her suckling foal. To study these effects,

36 Thoroughbred and Quarter Horse mares with an average bodyweight of 580.9 & 3.5 kg

(mean & SE) were randomly assigned to one of three treatment groups: 1) basal diet with

no supplementation (CON, n = 12); 2) basal diet plus milled flaxseed supplementation

(FLAX, n = 12); or 3) basal diet plus encapsulated fish oil supplementation (FISH, n =

12) from 28 days prior to expected foaling date until 84 days after foaling. The flaxseed

and fish oil supplements were fed to mares in amounts to provide 6 g total n-3 FA/100 kg

BW per day. The basal diet consisted of a commercial grain-based concentrate, Coastal

bermudagrass hay and bahiagrass pasture.









Blood samples were obtained from mares at 28 d pre-partum and milk and blood

samples were obtained from mares and foals at foaling, 36 h and 14, 28, 56 and 84 d

post-partum to determine FA and IgG content. On d 84, mares and foals received paired

intradermal inj sections of phytohemagluttinin (PHA) and skin thickness was determined

over a 48 h period as a measure of the inflammatory response. Bodyweights were

obtained from mares and foals at 14 d intervals throughout the trial.

Treatment had no effect on gestation length (P = 0.84), mare bodyweight (P = 0.80)

or foal bodyweight (P = 0.76). Mares fed FLAX had higher plasma alpha-linolenic acid

(ALA) (P=0.06) than mares fed FISH or CON mares. Mares fed FISH had higher plasma

eicosapentaenoic acid (EPA), docosahexanoic acid (DHA) and total n-3 (P=0.03) than

FLAX and CON mares. Across treatments, total milk n-3 increased (P=0.0005) and total

n-6 decreased (P=0.0001) from foaling to d 84. Milk from FLAX mares had higher ALA

(P=0.01) than milk from FISH and CON mares. Milk from FISH mares had higher EPA

and DHA and a lower n-6:n-3 ratio (P=0.007) than milk from FLAX and CON mares.

Foals suckling FLAX mares had higher plasma ALA (P=0.04) than foals suckling FISH

and CON mares. Foals suckling FISH mares had higher plasma EPA, DHA and total n-3

and a lower plasma n-6:n-3 ratio (P=0.002) than FLAX and CON foals. Treatment did

not affect colostrum, milk or foal serum IgG. Response to PHA inj section was greater

(P=0.0001) in mares compared to foals but similar between treatments. Although the

addition of n-3 FA to the mare's diet altered the FA content of mare milk and mare and

foal plasma, changes in total IgG and PHA intradermal responses were not detected..















CHAPTER 1
INTTRODUCTION

Supplementing the diet with fat is a popular trend in the horse industry. Fat is

commonly fed to horses to improve the hair coat, improve body condition and increase

the energy density of the diet. However, most of the research that has examined fat

supplementation of the horse has been performed with little regard to the type of fatty

acids (FA) provided. In addition, most of this research has focused on mature

performance horses; relatively little information is available on fat supplementation of

mares and the effects on the suckling foal.

Corn oil, soybean oil, and rice bran are common sources of fat added to horse

rations; however, these feeds are high in omega-6 FA. High levels of n-6 FA have been

associated with more pronounced inflammatory responses in humans (Meydani et al.,

1993; Simopoulos, 1999); therefore, potential exists for such diets to also have negative

biological effects in the horse.

Based on the immunomodulatory effects of n-3 FA in humans and other animals

(Simopoulos, 1999; Anderson and Fritsche, 2002), there is interest in determining

whether n-3 FA supplementation can modify inflammatory and immune responses in

horses. In addition, the dietary source of n-3 FA may be important for eliciting the

desired health benefits. Flaxseed is an excellent source of alpha-linolenic acid (ALA),

whereas Hish oil is a good source of eicosapentaenoic acid (EPA) and docosahexaenoic

acid (DHA). Although both are rich in total n-3 FA, fish oil may be a more effective

means of providing biologically active n-3 FA than flax.










The immune status of foals is a vital concern for horse breeders, as suckling foals

are susceptible to many health problems including diarrhea and septicemia. These health

problems can cause significant veterinary expense, as well as endanger the life of the

foal. Previous research has shown that supplementation of broodmares. with linseed oil or

a mix of corn and linseed oil increases the n-3 content of her milk and the n-3 content of

her foal's blood (Duvaux-Ponter et al, 2004; Spearman et al., 2005). Therefore, it seems

possible to enhance the concentration of n-3 FA in the foal by manipulation of the mare's

diet.

The obj ectives of this research were to 1) examine the effect of dietary n-3

supplementation on the FA composition of mare milk and mare and foal plasma; 2)

examine the efficiency with which ground flaxseed or encapsulated fish oil augment the

presence of EPA and DHA in the mare and foal; 3) examine the effects of

supplementation with flaxseed vs. Eish oil on increasing colostrum, milk and foal plasma

IgG; and 4) examine the effects of feeding flaxseed vs. fish oil on the inflammatory

response in the mare and foal. We hypothesize that supplementing the mare with Hish oil

will increase the EPA and DHA concentrations in mare milk and mare and foal blood to a

higher extent than will flaxseed, will increase the IgG in mare colostrum and foal blood,

and will decrease the inflammatory response in mares and foals.















CHAPTER 2
REVIEW OF LITERATURE

Fatty Acid Structure, Digestion and Metabolism

Fatty Acid Structure

Fatty acids (FA) consist of carbon (C), hydrogen (H) and oxygen (0) arranged in

a carbon chain with a carboxyl group (-COOH) at one end and a methyl group (-CH3) at

the other. FA are classified and named by their chain lengths and their degree of

unsaturation, or number of double bonds. Unsaturated FA can be monounsaturated (only

one double bond) or polyunsaturated (two or more double bonds), whereas saturated fatty

acids have no double bonds. Fatty acids are also classified as short, medium or long

chain, with short chain FA having less than 8 carbons, medium chain FA having 8 to 16

carbons and long chain FA having greater than 16 carbons. The numbering sequence of

the carbons in a fatty acid chain begins at the carboxyl end, with the carboxyl carbon

being C1. An older system used Greek letters to identify carbon atoms. In this system,

C2 (the first carbon after the carboxyl carbon) was the ot-carbon, C3 was the P-carbon

and so on, ending with the last carbon in the chain at the methyl end as the co-carbon

(Gurr et al., 2002).

Currently, the numbering system is the preferred method of naming individual FA.

In this system, the number of carbon atoms in the FA chain is given followed by a colon

and the number of double bonds. For example, stearic acid, a saturated FA of 18C, is

identified as C18:0. Linoleic acid, a polyunsaturated FA of 18C with two double bonds,

is identified as C18:2. While the current numbering system is preferred, the older system









is used to identify co-6 and co-3 fatty acids, where the last double bond in the fatty acid

chain is six and three carbons away from the co-carbon, respectively (Greene, 2006).

Newer research may substitute the ao with an n, but the meaning does not change.

The presence of double bonds in a fatty acid chain also allows for positional and

geometric isomerism. Positional isomerism refers to a different location of double bonds

in the carbon chain. Geometric isomerism refers to the orientation of the hydrogen

atoms around the carbon-carbon double bond. A cis configuration results when both

hydrogen atoms are on the same side of the bond, while a trans configurations results

when hydrogen atoms are on opposite sides of the bond. Most natural unsaturated FA are

in the cis configuration (Spallholz et al., 1999).

Fatty Acid Digestion

Dietary fats exist mostly as triglycerides (TG) which are made up of three FA

attached to a glycerol backbone (Mu and Hoy, 2004). The digestion of these TG begins

in the stomach by the action of gastric lipase released from the gastric mucosa. In

humans and rats, lingual lipase from the von Ebner glands, a group of serious glands on

the tongue, also aids in FA digestion in the stomach. This lipase is transferred with the

food bolus into the stomach where its activity begins (Mu and Hoy, 2004). Secretion of

the lingual lipase occurs continuously but is stimulated by dietary (high fat) and

mechanical (suckling) factors (Carey et al., 1983; Tso, 1989). Digestion by both lipases

produces free FA and diglycerides (Carey et al., 1983; Tso, 1989). The lingual lipase is

especially important in the newborn, as pancreatic lipase activity is not fully developed at

birth. In addition, the short and medium-chain TG present in milk fat are readily

hydrolyzed by the lingual lipase (Tso, 1989). Horse saliva, however, does not possess









this lingual lipase (Frape, 1998; Ellis and Hill, 2005). In fact, it is currently thought that

equine saliva does not contain any enzyme activity (Ellis and Hill, 2005). Therefore,

equine saliva is not as important in beginning digestion but is vital in providing feed

lubrication (Frape, 1998) and buffering of the feed-saliva mixture (Ellis and Hill, 2005).

While only 10-30% of dietary fat is hydrolyzed in the stomach, the maj ority of FA

digestion takes places in the small intestine, especially in the duodenum. In animals with

a gall bladder, the action of the food bolus entering the duodenum stimulates gall bladder

emptying, secretion of pancreatic lipase and the release of cholecystokinin (CCK). Bile

acids are also released from the gall bladder or directly from the liver to emulsify the fat

(Mu and Hoy, 2004). The horse, however, does not have a gall bladder, but this does not

seem to affect the digestion of fat (Cunha, 1991). In the horse, bile continuously drains

from the liver into the small intestine to facilitate the emulsion of fat (Frape, 1998).

Furthermore, the peristaltic and segmental contractions present in the intestine supply

mechanical energy to reduce the fat particle size and increase the interfacial area of the

fat droplets (Carey et al., 1983). The action of pancreatic lipase on a triglyceride

molecule releases two free FA and a 2-monoglyceride. These compounds, along with

biliary salts, form micelles that are absorbed into the intestinal mucosal cells by passive

diffusion (Doreau and Chilliard, 1997). In the horse, pancreatic lipase is secreted in high

amounts and increases as fat is added to the diet (Frank et al., 2004). Therefore, the horse

is able to digest high amounts of fat in the diet. Horses have been fed diets with 20% of

the DE provided by oil with good results and no negative effect on digestibility (Cunha,

1991).









Once the monoglycerides and free FA are absorbed into the intestinal cell, the long-

chain fatty acids (LCFA) must be transported to the endoplasmic reticulum, the maj or site

of absorbed lipid metabolism. One explanation for how the LCFA reach the endoplasmic

reticulum is by the action of fatty acid-binding protein (FABP). FABP is present in the

intestinal mucosa, liver, kidney, and adipose tissue and has no affinity for short or

medium-chain FA (Tso, 1985). It has been postulated that FABP may be responsible for

removing LCFA acids from their binding to the cytosolic side of the luminal membrane

and transferring them to the endoplasmic reticulum (Carlier et al., 1991). Unlike LCFA,

short and medium-chain FA are transferred directly from the intestinal cell into the portal

blood as free FA bound to albumin (Carlier et al., 1991).

Once inside the endoplasmic reticulum, LCFA and monoglycerides are recombined

into triglycerides by the monoglyceride pathway. The enzyme complex that makes up

this pathway is known as "triglyceride synthetase." This complex consists of three

enzymes: acyl-CoA synthetase, MG transacylase and diglyceride transacylase. The acyl-

CoA synthetase, in the presence of CoA, activates the LCFA to form acyl-CoA. The

acyl-CoA is then used for the reacylation of monoglyceride to diglycerides and finally to

triglycerides (Tso, 1985). The resulting triglycerides are then packaged with cholesterol

esters and phospholipids into chylomicrons, which are large lipoproteins that act as

carriers of dietary triglycerides. Chylomicron formation is activated by the addition of

apoproteins, which are proteins that play an important role in the formation and secretion

of chylomicrons by the enterocytes. Once chylomicrons are formed, they are released by

exocytosis into the lymphatic system where they can enter the blood stream via the

thoracic duct and be transported to the rest of the body (Carlier et al., 1991).









De novo Fatty Acid Synthesis

There are two primary sources of FA in the body: FA provided by the diet and FA

made by the animal via de novo synthesis (Lehner and Kuksis, 1996). The pathways for

de novo FA synthesis exist in the animal during the well-fed state and in monogastrics

occur primarily in the liver. Most of the carbon used for de novo FA formation is

supplied through the pyruvate pool and from the end product of glycolysis. There are

three substances needed for FA synthesis: acetyl CoA, malonyl CoA and NADPH. The

first step in the synthesis of FA is the formation of acetyl CoA from pyruvate in the

mitochondrial matrix by the action of pyruvate dehydrogenase. The acetyl CoA must

then be moved out of the mitochondria and into the cytosol where FA synthesis takes

place. Because the inner mitochondrial membrane is not permeable to acetyl CoA, the

acetyl CoA is combined with oxaloacetate to form citrate. Citrate is then translocated to

the cytosol where it is cleaved back to oxaloacetate and acetyl CoA by ATP:citrate lyase

(Gurr et al., 2002). This mechanism of moving acetyl CoA into the cytosol in the form of

citrate is called the citrate shuttle.

Once acetyl CoA reaches the cytosol, de novo FA synthesis begins. The first

reaction of this mechanism, which is also the rate limiting reaction, involves the

formation of malonyl CoA by the enzyme acetyl-CoA carboxylase (ACC) (Knowles,

1989). The malonyl CoA forms the source of the vast maj ority of the carbons of a FA

chain. The enzyme complex that synthesizes LCFA from acetyl and malonyl CoA is

fatty acid synthase (FAS). This enzyme complex has synthase, reductase and dehydrase

actions. The typical end product of animal FAS action is palmitic acid (C16:0) (Greene,

2006).









Once produced, palmitic acid can be elongated and desaturated. Type III synthases

(commonly called elongases) lengthen FA preformed in the animal 2C at a time. The

principal elongation reactions occur in the endoplasmic reticulum membranes and

involve acyl-CoA as a primer, malonyl-CoA as a donor of 2C units and NADPH as the

reducing coenzyme. This system is capable of producing FA chain with an excess of 20

carbons (Suneja et al., 1990). Desaturation, or the addition of double bonds, occurs

mainly by oxidative desaturation, a process by which a double bond is introduced directly

into the LCFA with 02 and NADH as cofactors (Scheuerbrandt and Bloch, 1962).

Mammalian desaturases are only able to introduce double bonds in the A9, A6 and A5

positions. Plant desaturases can introduce additional double bonds at the Al2 and Al5

positions, therefore creating n-6 and n-3 FA. All double bonds introduced by the process

of oxidative desaturation are in the cis configuration (Lehner and Kuksis, 1996).

Fatty Acid Degradation

The mobilization and oxidation of FA occur primarily during fasting, physical

exercise and stress in the animal in order to break down dietary or stored TG into FA to

provide energy. The mobilization of FA occurs via lipolysis in the adipose tissue, in

which FA are cleaved from their glycerol backbone mainly by hormone sensitive lipase

(HSL) and released into circulation (Johnson and Greenwood, 1998). The main forms of

FA oxidation are termed alpha (ot), beta (P) and omega (co), referring to which carbon on

the acyl chain is attacked. Of these three, P-oxidation is the most prevalent. In P-

oxidation, there is a stepwise removal of 2C units from the carboxyl end of the FA

(Greene, 2006).









The mitochondria and microbodies (peroxisomes and glyoxysomes) are capable of

performing P-oxidation. The process begins by converting the FA into fatty acyl-CoA as

soon as it enters the cytosol of the cell. The inner mitochondrial membrane, however, is

impermeable to fatty acyl-CoA. In order to move this molecule across the membrane, the

enzyme carnitine:palmitoyl transferase (CPT1), located on the outer mitochondrial

membrane, combines the fatty acyl-CoA with carnitine. The resulting acyl carnitine is

then transported across the membrane, crossing the inner membrane by a

carnitine: acylcarnitine translocase (Pande, 1975). Once the acyl carnitine is inside the

mitochondrial matrix, CPT2 transfers the acyl group from carnitine to CoA, therefore

reforming acyl-CoA as a substrate for further P-oxidation (Bieber, 1988).

The process of P-oxidation involves a repeated sequence of four reactions resulting

in the removal of 2C from the acyl chain. First, acyl-CoA dehydrogenase acts on the

acyl-CoA to form trans-3,3-enoyl-CoA. Enoyl hydratase then acts on the product of the

first reaction to form 3-hydroxy acyl-CoA. The third reaction is catalyzed by the enzyme

3-hydroxy acyl-CoA dyhyrogenase which works with NAD+ to form 3-oxoacyl-CoA.

The final reaction involves 3-oxoacyl-CoA thiolase which produces a shorter fatty acyl-

CoA and acetyl-CoA (Bieber, 1988). The resulting acyl-CoA is recycled back into P-

oxidation for the removal of additional 2 carbon units, while the acetyl-CoA can be used

in the TCA cycle to produce energy (Gurr et al., 2002).

Polyunsaturated Fatty Acids

n-6 and n-3 Polyunsaturated Fatty Acids

By definition, n-6 polyunsatured fatty acids (PUFA) have the last double bond in

the FA chain six carbons from the methyl (omega) end. The two most physiologically









import n-6 PUFA are linoleic acid (LA; C18:2) and arachidonic acid (AA; C20:4). Of

these, LA is considered a dietary essential fatty acid because it cannot be synthesized by

mammals. Sources of LA include vegetable oils such as corn, sunflower, peanut, and soy

oils (Carlier et al., 1991). Linoleic acid can be elongated and desaturated in the body to

produce AA in a mechanism that is discussed later in this chapter. Omega-6 PUFA, with

AA as the principal component, predominate in organs and tissues performing storage

functions (adipose tissue), chemical processing (liver), excretion (kidney) and mechanical

work (muscle) (Innis, 1991). In addition, plasma lipoproteins contain high amounts of

LA in triglycerides, cholesterol esters and phospholipids (Innis, 1992a). A very

important feature of n-6 PUFA is their effect on the body. In general, n-6 PUFA have

proinflammatory, prothrombotic and proaggregatory effects, characterized by increases in

blood viscosity, vasospasm, vasoconstriction and decreases in bleeding time

(Simopoulos, 1999).

Omega-3 PUFA have the last double bond in their carbon chains three carbons

from the methyl end. The dietary essential PUFA from the n-3 family is ot-linolenic acid

(ALA; 18:3), but other physiologically important n-3 PUFA include eicosapentaenoic

acid (EPA; 20:5) and docosahexaenoic acid (DHA; 22:6) (Innis, 1992a). Using elongase

and desaturase actions similar to those in n-6 PUFA, ALA can be transformed into EPA,

which can be further transformed into DHA. Alpha-linolenic acid is found primarily in

the chloroplast of green leafy vegetables and in seeds of flax, linseed and walnuts. Fatty

fish and fish oils, however, are the main sources of EPA and DHA (Benatti et al., 2004).

The primary sites of n-3 PUFA accumulation in the body include the nervous tissue,

reproductive organs and retina membranes (Innis, 1991). Unlike the plasma









concentrations of LA, tissue and plasma triglyceride and cholesterol ester levels of ALA

are usually quite low (<1-2% FA) (Innis, 1992a). Polyunsaturated FA of the n-3 family

are known to have anti-inflammatory, antithrombotic, antiarrhythmic, hypolipidemic and

vasodilatory effects on the body (Simopoulos, 1999). To obtain optimal health, it is

important to have adequate dietary amounts of PUFA of both the n-6 and n-3 families,

but it may also be important to have a proper ratio between the two. A ratio of 4-5: 1 of

n-6:n-3 has been suggested as most beneficial for humans, but most investigation in this

area has been conducted in lab animals (Wiseman, 1997).

The efficiency at which the horse converts ALA to EPA and DHA is unknown. In

addition, while a recommendation for a beneficial n-6:n-3 ratio exists for humans, the

optimal ratio for horses is unknown. Most horse feeds today are high in n-6 FA, with the

horse' s maj or n-3 FA intake obtained from forages. The FA composition of common

grains and fat supplements fed to horses are presented in Table 2-1 and the FA

composition of common forages fed to horses are presented in Table 2-2.










Table 2-1. Fatty acid composition of common feeds and fat supplements fed to horses
Feed


Rice
Bran
Oil6
0.43

16.27

1.84

41.92


Textured
Grain2

0.14

NA


COrn Flaxseed
Oil4 Oil"


Fish
Oil4

5.6

21.6

9.0

15.5


Soybean
Meal3

Trace

10.7


Oats


Trace

22.1


Fatt
acid
C14:0

C16:0

C18:0

C18:1


0.2

10.8


NA

NA


1.3 20.6


1.5

21.4

14.2


38.1

24.9

2.1

NA

NA

NA


10.2

54.8


C18:2n-6 38.82

C18:3n-3 3.72

C20:4n-6 0.03

C20:5n-3 0.08

C22:6n-3 0.06


15.2


1.5 35.44

1.4 1.24


1.1 53.6


NA

13.5

11.5


SPresented as g fatty acid/100 g fat
2 COmmercial grain mix (Hallway Feeds, Lexington,


KY) containing barley, corn,


soybean meal, molasses, oats and supplemental pellet; 14.8% CP, 6.5% fat; from
O' Connor et al., 2004.
3 From Ellis and Hill, 2005.
4 From Chen et al., 2006.
SFrom Francois et al., 2003.
6 From Sierra et al., 2005.
SNA information not available.









Table 2-2. Fatty acid composition of common forages fed to horses
Forage

Fatty Fresh Fresh Perennial Bermudag:rass .ioh Ha4
acidly Bahiagrass2 Rye Grass3 Hay
C14:0 0.00 0.4 0.00 1.63

C16:0 22.56 14.6 39.14 NA

C18:0 4.28 1.2 6.72 NA

C18:1 3.00 1.7 7.05 NA

C18:2n-6 21.32 10.6 23.35 15.76

C18:3n-3 46.21 68.4 15.93 26.68

C20:4n-6 0.00 NA5 0.00 0.35

C20:5n-3 0.00 NA 0.00 0.36

C22:6n-3 0.00 NA 0.00 0.25
Presented as g fatty acid/100 g fat.
2 From the present study.
3 From Elgersma et al., 2003.
4 From O'Connor et al., 2004.
SNA information not available.


Elongation of and Competition Between n-6 and n-3 Families

As stated earlier, both LA and ALA can be elongated and desaturated to form their

longer chain derivatives (Figure 2-1). This conversion happens in the endoplasmic

reticulum (Benatti et al., 2004). The first step of the mechanism converting LA to AA is

catalyzed by A6-desaturase, the rate-limiting step of the pathway. This enzyme acts on

LA to insert a double bond between carbons 6 and 7. This product is then elongated by

the addition of two carbon units to form dihomo-y-linoleic acid (C20:3). Further

desaturation by A'-desaturase inserts a double bond between carbons 5 and 6, thereby

creating AA. Arachidonic acid can then be elongated to form adrenic acid (C22:4). The

enzyme A6-desaturase inserts a double bond between carbons 4 and 5 of adrenic acid to

form co6-docosapentaenoic acid (C22:5) (Innis, 1991).









Diet
(Vegetable fats and oils)

C18:2n-6 C18:3n-3
A6-desaturation
1 ~elongation
C20:3n-6 C20:4n-3

(animal fat) 1 ASdesaturation I
"IC20:4n-6 C20:5n-3
I I\
1 elongation \
Diet
C22:4n-6 C22:5n-3 (fish fat)
A6-desaturation I
elongation
C22:5n-6 C22:6n-3



Figure 2-1. Essential fatty acid metabolism. Adapted from Innis, 1992a.


The conversion of ALA to its longer chain derivatives uses the same pathway and

enzymes as LA. The enzyme A6-desaturase acts first on ALA to form stearidonic acid

(C18:4). This acid is then elongated and desaturated by A'-desaturase to form EPA. To

form DHA, EPA is elongated to form co3-docosapentaenoic acid (DPA; C22:5), which is

then desaturated by A6-desaturase to form DHA (Innis, 1991). However, there is a

marked inefficiency of conversion of ALA to EPA, with only about 0.2% of plasma ALA

fated for synthesis of EPA in human blood (Pawlosky et al., 2001). There is 10-fold

greater rate of transfer, however, of EPA to DHA than there is from ALA to EPA,

showing that the initial desaturation/elongation to EPA is the most restrictive (Pawlosky

et al., 2001). The difficulty of conversion of ALA to DHA has been shown in rats, where

maternal rats were fed a diet high made in ALA by the addition of flaxseed oil (Bowen

and Clandinin, 2000). Maternal rats were started on the experimental diet on the day of









parturition and their pups were sacrificed at two weeks of age. Bowen and Clandinin

(2000) showed that supplementing maternal rats with a high ALA diet did not increase

the DHA content of the whole body, skin, epididymal fat pads or muscles in rat pups,

therefore suggesting that the conversion of ALA to DHA is inefficient in the rat.

However, the efficiency at which the horse converts ALA to EPA and DHA is unknown.

Therefore, providing animals with a dietary source of EPA and DHA (such as fish or fish

oil) may be a better way to ensure incorporation of these FA into the body than feeding a

source of ALA.

Because the n-6 and n-3 families use the same enzymes in the process of

desaturation to their longer chain derivatives, there is competition between them. The

maj or site of competition occurs at the site of A6-desaturase action, the rate limiting

reaction for PUFA desaturation. There is a strong preferential substrate affinity of the A6-

desaturase for n-3 PUFA, especially ALA over LA (Innis, 1991; Drevon, 1992).

Therefore, feeding animals a source of n-3 PUFA will often decrease the amount of n-6

PUFA processed in the body, as more of the A6-desaturase will act on the n-3 PUFA and

less on the n-6. Studies have shown, in both animals and humans, that providing a

dietary source of n-3 PUFA reduces the amount of AA found in the blood (Fritsche et al.,

1993; Sauerwald et al., 1996). This competition between n-3 and n-6 PUFA has been

established in sows assigned to diets containing 7% added fat where menhaden fish oil

was substituted for lard at 0, 3.5 and 7% of the total dietary fat (Fritsche et al., 1993).

Sows were fed from 107 days of gestation to 28 days of lactation. The substitution of

fish oil for lard at both 3.5 and 7% decreased serum levels of AA by approximately 50%

in sow serum (Fritsche et al., 1993). However, the opposite phenomenon has been









documented as well. Extensive research has shown that providing a diet rich in LA but

poor in ALA will result in the accumulation of AA and very little EPA and DHA

(Wiseman, 1997).

Eicosanoid Production and Function

Eicosanoids are a large family of oxygenated 20-carbon FA (Smith, 1989) that act

as local hormones to modulate the intensity and duration of inflammatory and immune

responses (Yaqoob, 2004). The family is made up of three groups: the prostanoids

(prostaglandins and thromboxanes) which are synthesized by cyclooxygenase (COX), the

leukotrienes which are synthesized by lipoxygenase (LOX) and the epoxides synthesized

by epoxygenase. Eicosanoids are produced from 20-carbon PUFA containing three to

five cis, methylene-interrupted double bonds. These PUFA include AA, a member of the

n-6 family, and EPA, a member of the n-3 family. Linoleic acid (18 carbons) and DHA

(22 carbons) can be converted to eicosanoid homologues, but these are not actual

eicosanoids and are thought to have limited biological function. Because AA is the most

abundant C20 pOlyunsaturate in mammalian systems, it is the maj or precursor of

eicosanoids (Smith, 1989). Macrophages and monocytes are important sources of

eicosanoids, as their membranes typically contain large amounts of AA (Yaqoob, 2004).

Arachidonic acid and EPA each produce eicosanoids of a different series.

Arachidonic acid is a substrate for the 2-series prostaglandins (PG), namely prostaglandin

E2 (PGE2) and prostaglandin F2 (PGF2) and the 4-series leukotrienes (LT), namely

leukotriene B4 (LTB4). Prostaglandin E2 and LTB4 have powerful proinflammatory

actions (James et al., 2000). Prostaglandin E2 induces fever and increases vascular

permeability, vasodilation, pain and edema. However, PGE2 alSo suppresses the

production of inflammatory cytokines TNF-ot, IL-1 and IL-6 by macrophages and T cells.









Leukotriene B4 inCreaSCS Vascular permeability and blood flow, is a chemotactic agent for

leukocytes, induces the release of neutrophil lysosomal enzymes, and enhances the

generation of reactive oxygen species. Leukotriene B4 alSo increases production of TNF-

ce, IL-1 and IL-6 by macrophages (Calder, 2001; Yaqoob, 2004). In contrast to AA, EPA

is a substrate for the 3-series PG, namely PGE3, and the 5-series LT, namely LTBS.

These eicosanoids have the same types of inflammatory effects as those generated from

AA, but they are far less biologically potent (Calder, 2001). Therefore, production of

eicosanoids from EPA could modulate the immune response.

The Immune System

Acquired Immunity

The acquired immune system is capable of recognizing and selectively inhibiting

specific foreign antigens (Goldsby et al., 2003). T cells, B cells, antigen-presenting cells,

the maj or histocompatibility complex (MHC), and immunoglobulins all play important

roles in the acquired immune system. This system of immunity is classified as acquired

because the immune cells must be exposed to an antigen once to develop, or acquire,

memory for that antigen. A second exposure to the same antigen will trigger an enhanced

state of immune reactivity (Goldsby et al., 2003).

Immunoglobulins

Along with playing an important role in acquired immunity, immunoglobulins are

also an important part of humoral immunity, or the type of immunity pertaining to

extracellular fluids including the plasma and lymph (Goldsby et al., 2003). Humoral

immunity is driven by B cells, which originate and mature in the bone marrow (Kuby,

1992). Immunoglobulins are a group of large glycoproteins found on B-cell membranes

or secreted by plasma cells. They are found most prevalently in blood serum but are also










present in mucosal tissues and external secretions such as milk. An antibody is an

immunoglobulin (Ig) that exhibits antigen-binding ability. Therefore, all antibodies are

Ig, but not all Ig are necessarily antibodies. The two terms, however, are often used

interchangeably. Antibodies have a wide range of functions, including targeting

infectious organisms, neutralization of toxins and removal of foreign antigens from body

circulation (Peakman and Vergani, 1997). Antibodies can serve as diagnostic tools for

clinical evaluations of immune diseases or disorders. For example, immunoglobulin G

(IgG) is measured in the serum of foals to determine if there has been a successful

transfer of maternal antibodies.

In horses, the maj or immunoglobulins are IgG, IgM, IgA and IgE (Nezlin, 1998).

Average concentrations of immunoglobulins in the serum of mature horses are presented

in Table 2-1.

Table 2-1. Immunoglobulin concentrations of serum and milk in mature horses
Sample IgG IgM IgA
Adult horse serum 1000-1500 100-200 60-350

Mare colostrum 1500-5000 100-3 50 500-1500

Mare milk 20-50 5-10 50-100
1From Tizard, 1996; presented as mg/dL.

IgG is synthesized and secreted from plasma cells found in the spleen, lymph nodes

and bone marrow (Tizard, 1996). IgG molecules have a long half-life (23-25 days) and

there is a continuous high-level stimulation for IgG production. As a result, the

concentration of IgG in blood and colostrum is higher than any other immunoglobulin

(Tizard, 1996). IgG is the smallest of the immunoglobulin classes, so it is therefore more

able to move through the body to travel to needed areas (Widmann and Itatani, 1998).

Four immunoglobulin subclasses have been described in horses: IgGa, IgGb, IgGc and









IgG(T) (Sheoran et al. 2000). IG(T) has also been divided into the subclasses IgG(Ta)

and IgG(Tb) (Tizard, 1996). These subclasses are distinguished from one another by

molecular structural differences and slight variations in biological function (Kuby, 1992).

Like IgG, IgM is also made and secreted from plasma cells in the spleen, lymph

nodes and bone marrow. It is found in the second highest concentration in serum,

following IgG (Tizard, 1996). IgM is the first immunoglobulin class produced by the

maturing B cell, and the first class synthesized by the neonate (Kuby, 1992). It is also the

first antibody produced in a primary response to an antigen (Widmann and Itatani, 1998;

Kuby, 1992). IgM is more efficient than other immunoglobulins in binding antigens

because of its larger molecular size (largest of the immunoglobulin classes) and its larger

number of binding sites. Because of its higher efficiency, IgM is also more able to

neutralize viral infectivity, cause agglutination and activate compliment than IgG

(Goldsby et al., 2003).

The immunoglobulin IgA is produced mainly by plasma cells in muscosa-

associated lymphoid tissues beneath surface epithelium (Widmann and Itatani, 1998).

While it is manufactured more than any other immunoglobulin class, serum concentration

of IgA is relatively low. This low concentration is due to the secretion of IgA in fluids

present on the epithelial surfaces of the alimentary, respiratory and reproductive tracts

and in such fluids as urine, saliva, tears and milk (Widmann and Itatani, 1998). Because

IgA is the maj or immunoglobulin in the external secretions of horses, it plays a vital role

in protecting the intestinal tract, respiratory tract, urogenital tract, mammary gland and

eyes against microbial invasion (Tizard, 1996).









Like IgM, IgE is produced predominantly by plasma cells located beneath body

surfaces. It is found in very low concentrations in the serum of healthy animals, partially

because the molecule is fairly unstable and has the shortest half-life of all the classes of

immunoglobulins (Tizard, 1996). IgE antibodies mediate immediate (type I)

hypersensitivity reactions that cause the symptoms of hay fever, asthma, hives and

anaphylactic shock (Kuby, 1992). IgE is also thought to be largely responsible for

immunity against parasitic worms (Tizard, 1996).

Passive Immunity in the Foal

Due to the mare's diffuse epitheliochorial placenta, there is no significant transfer

of immunoglobulins to the fetal circulation during pregnancy (Jeffcott, 1972, 1974a;

Erhard et al., 2001). Therefore, foals are born with a near absence of circulating

immunoglobulins and an easily compromised immune system. Although they are able to

produce their own antibodies soon after birth, foals will not produce levels approaching

those of the adult horse until 3-4 months of age (Jeffcott, 1974a). Foals receive the

needed antibodies via passive transfer from colostrum, or the mare's first milk. Prior to

birth, the mare's mammary gland is capable of selecting and concentrating a wide range

of serum Ig into the colostrum (Jeffcott, 1974a, 1975). When foals suckle this colostrmm

after birth, they take the antibody-rich fluid into their digestive tracts where the Ig can be

absorbed into the circulating blood.

For the transfer of passive immunity to be successful, the mare' s colostrum must

contain adequate amounts of the appropriate immunoglobulins, especially IgG (Rooke

and Bland, 2002). In addition, the immunoglobulins must be delivered intact to the site

of absorption and absorbed intact (Rooke and Bland, 2002). Because of the very low

level of proteolytic activity in the digestive tract of young foals, most immunoglobulins









are kept intact as they pass with the colostrum through the foal's stomach and small

intestine. Trypsin inhibitors found in colostrum further reduce the degradation of

immunoglobulins in the foals digestive tract (Krse, 1983; Tizard, 1996).

The immunoglobulins in colostrum are rapidly absorbed by non-specific

pinocytosis into the small intestine enterocytes. Maximum absorption occurs soon after

birth and declines thereafter, completely ceasing by 24 hours after birth (Raidal et al.,

2000). The foal's intestine shows selective permeability, with a greater affinity for IgG

and IgM (Tizard, 1996). Once inside the enterocyte, individual immunoglobulins merge

together to form one or more larger globules. These larger globules pass from the

enterocyte into the local lymphatics and later reach the systemic circulation (Jeffcott,

1974a).

The critical event in the transfer of intact immunoglobulin to the foal's circulation

is cessation of transfer across the enterocyte basolateral membrane. For this reason, "gut

closure" is the term used to define the cessation of transfer of IgG to the foal's

circulation. Gut closure, usually reached around 24 hours of age (Rooke and Bland,

2002), is characterized by a replacement of the immature epithelial cells with more

mature cells that no longer engage in pinocytosis (Kruse, 1983).

IgG displays a unique behavior in foal serum. At birth, before the foal has suckled,

foal serum IgG may be as low as 30 mg/dL (Erhard et al., 2001). However, foal IgG rises

rapidly after colostrum is ingested. Peak IgG values in foal serum occur between 18 and

24 hours after birth (Jeffcott, 1974a) and have been reported to be as high as 2, 160 mg/dL

(McGuire and Crawford, 1973). The IgG values in foal plasma appear to stay at near

peak levels for at least the first two days after foaling (Jeffcott, 1974b; Duvaux-Ponter et









al., 2004). After this peak, passively derived IgG molecules will gradually decline until

they are completely absent by around 5 months of age (Jeffcott, 1974a). Foals may begin

to process their own IgG molecules as early as 2 weeks of age, but levels reaching those

of the adult horse are not seen until around 4 months of age (Jeffcott, 1974a). Erhard et

al. (2001) reported that 7 day old foals had a mean IgG value of 1000 ml/dL. This value

then decreased, indicating the elimination of maternal IgG, and reached the lowest level

of 790 mg/dL at 35 days of age. However, foal serum IgG increased to around 1 100

mg/dL at 42 days after birth, indicating that endogenous IgG production was increasing

in the foal (Erhard et al., 2001). Therefore, behavior of IgG in the foal seems to begin

with a very low presuckle value, experience a dramatic rise after colostrum ingestion,

undergo a steady decline as maternal IgG is eliminated and shows an increase as the foal

begins to produce its own IgG.

Failure of Passive Transfer

Failure of passive transfer (FPT) is defined as the failure of absorption of maternal

immunoglobulins by the neonatal foal, a condition that predisposes the foal to life-

threatening infections (Kohn et al., 1989). Failure of passive transfer is the most

commonly recognized immune deficiency in horses and may predispose affected foals to

septicemia, infective arthritis and pneumonia (Raidal, 1996; Raidal et al., 2000). There

are conflicting views in the literature as to what antibody levels actually constitute failure

of passive transfer. Liu (1980) and McGuire et al. (1977) defined failure of passive

transfer as less than 200 mg IgG/dL serum and partial failure as between 200 and 400

mg/dL. LeBlanc et al. (1986) suggested failure of passive transfer as levels below 400

mg/dL, while Raidal (1996) and Tyler-McGowan et al. (1997) noticed an increased

susceptibility of foals to disease when IgG levels dropped below 800 mg/dL. Today, it is









common to define failure of passive transfer as IgG levels below 400 mg/dL serum

(Tizard, 1996; Erhard et al., 2001) and partial failure as levels between 400 and 800

mg/dL. IgG levels above 800 mg/dL are considered necessary to provide optimal

immune function (Erhard et al., 2001). In order to prevent failure of passive transfer, the

minimal concentration of colostral immunoglobulin required has been estimated to be

between 1,000 and 3,000 mg IgG/dL colostrum (LeBlanc et al., 1986). The possibility of

failure of passive transfer cannot be evaluated until the foal is about 18 hours of age, as

antibody absorption is essentially complete at this time (Tizard, 1996). Therefore, the

standard industry practice of testing foal IgG levels at 12 hours after foaling may give

misleading results, as complete antibody absorption has not happened yet. This practice

may still be needed, however, in order to be able to administer plasma or colostrum to the

foal before the foal's ability of absorption is completed.

Possible causes of failure of passive transfer fall into three categories: production

failure, ingestion failure and absorption failure (Tizard, 1996). A failure of the mammary

gland to concentrate immunoglobulins from the blood into colostrum can occur in maiden

mares foaling for the first time. Premature lactation, however, is the most common

production failure cause of failure of passive transfer. In this case, initial colostrum may

be of adequate amount with adequate IgG concentration, but the mare will commence

lactation prior to parturition. This steady leak of colostrum may occur for several hours

or several days before birth and significantly reduces the amount of IgG available to the

foal (Jeffcott, 1974a).

While less common, inabilities of ingestion and absorption are additional failure of

passive transfer causes. Ingestion failures can arise from a mare not allowing her foal to









nurse, weak or deformed foals that take longer than normal to stand, or a delayed or

defective suckling reflex (Jeffcott, 1974a; Tizard, 1996). Foals usually overcome these

factors, but it may take longer than the 24-hour period of intestinal permeability to IgG.

Absorption failures can be linked to stress at the time of parturition. The adrenal

hormones play important roles in the onset of parturition and can influence changes in the

permeability of small intestine cells after birth (Jeffcott, 1972). In conditions of stress at

parturition, the mare or foal could produce abnormal amounts of corticosteroids which

would therefore have a detrimental affect on the foal's antibody absorption (Jeffcott,

1974a).

Innate Immunity

Innate immunity is the first line of defense in Eighting an invading organism

(Goldsby et al., 2003). The skin, mucosal surfaces, macrophages and neutrophils all play

important roles in the innate immune system. The skin and mucosal surfaces act as

barriers against infection, and the macrophage and neutrophils act to phagocytize and kill

invading foreign cells. Inflammation is also an important part of innate immunity and

functions to draw immune cells to areas of injury or antigen attack. Because the innate

immune system is less specific than the acquired immune system, the innate system can

act quickly to begin an immune response (Goldsby et al., 2003).

Inflammation

By definition, inflammation is the response of tissue to the presence of

microorganisms or injury (Tizard, 1996). Inflammation is a vital protective mechanism

and the means by which defensive molecules and phagocytic cells gain access to the sites

of tissue microbial invasion or damage. Inflammation is classified according to its

severity and duration, with acute inflammation developing in less than an hour after









tissue damage and chronic inflammation occurring a much slower rate and being more

constant. There are five symptoms of acute inflammation: heat, redness, swelling, pain

and loss of function. These symptoms are a result of changes in the small blood vessels

in the damaged tissue (Tizard, 1996; Goldsby et al., 2003).

Immediately following microbial invasion or injury, blood flow to the effected area

greatly increases. This increase is due to a transient constriction of local arterioles and

dilation of all the small blood vessels in the area. The blood vessel permeability is also

increased, allowing fluid to move from the blood into the tissues where it causes edema

and swelling (Tizard, 1996). The changes in blood vessels allow an influx of

lymphocytes, neutrophils, monocytes and other immune cells into the area to participate

in clearance of the antigen (Kuby, 1992). Neutrophils are the first immune cells to arrive

in the inflamed tissues, followed by the slower moving monocytes. Once within the

inflamed tissues, these cells are attracted to sites of bacterial growth and tissue damage

and phagocytize and destroy any foreign material present. Monocytes will also remove

dead and dying tissue (Tizard, 1996).

Cytokines play an important role in the acute-phase inflammatory response. These

low-molecular-weight proteins secreted by macrophages exert a variety of effects on

lymphocytes and other immune cells to regulate the intensity and duration of an immune

response. The three cytokines that play the largest role in acute inflammation are tumor

necrosis factor-a (TNF-u), interleukin 1 (IL-1) and interleukin 6 (IL-6). All three

cytokines act locally on endothelial cells to induce coagulation and increase vascular

permeability (Kuby, 1992). TNF-u, IL-1 and IL-6 also act on the brain to induce fever

and suppress appetite and on skeletal muscle to drive protein catabolism and mobilize









available amino acids. In addition, these cytokines operate on liver cells to increase

protein synthesis and secretion of clotting factors, complement components and protease

inhibitors, all of which aid in the host defense (Tizard, 1996). All three cytokines

activate B and T cells, while IL-6 can also increase immunoglobulin synthesis (Goldsby

et al, 2003).

Effects of Dietary PUFA Supplementation on Inflammation and Immune Function

Blood and Tissue Responses to Experimental Feeding of n-3 PUFA

Numerous studies have investigated the levels of different n-3 PUFA resulting in

the blood when feeding ALA and DHA, either alone or in combination. In humans,

many studies have looked at providing adults with dietary fish oil, a good source of EPA

and DHA. Helland et al. (1998) supplemented pregnant women with cod liver oil for 14

days, between three and eight weeks post partum. The women were divided into four

groups: Group 1 served as the control and received no supplementation, Group 2

received 2.5 mL of cod liver oil/day, Group 3 received 5 mL of cod liver oil/day, and

Group 4 received 10 mL of cod liver oil/day. Helland et al. (1998) found that the

pregnant women in Groups 3 and 4 (receiving 5 and 10 mL of cod liver oil/day,

respectively) showed a decreased plasma LA content and an increased ALA and DHA

plasma content. When EPA and DHA intake were computed on a bodyweight basis, the

women receiving 5 mL of cod liver oil were consuming the equivalent of 14 mg EPA and

DHA/kg of bodyweight and the women receiving 10 mL of cod liver oil were consuming

the equivalent of 28 mg of EPA and DHA/kg bodyweight.

Henderson et al. (1992) also supplemented pregnant women with EPA and DHA,

but not in the form of fish oil. Henderson and coworkers supplemented pregnant women

with six capsules of Bio-EFA for a total supplement weight of six grams of









supplementation. This supplement provided women with 1080 mg EPA and 720 mg

DHA per day. Assuming an average bodyweight of 70 kg, this dosage provided 15.43

mg EPA/kg BW and 10.29 mg DHA/kg BW. Similar to Helland et al. (1998), however,

Henderson et al. (1992) also started their supplementation period after lactation had

already commenced, supplementing women between two and five weeks post partum for

a total of 21 days. The results of Henderson et al. (1992) showed that daily

supplementation of lactating women with 6 g of an EPA and DHA source increased the

women's red blood cell content of EPA, DPA and total n-3 PUFA. Although it was not

significant, there was also a trend toward red blood cell DHA increase. Infant red blood

cells were also affected by supplementation of the mother, as EPA and DPA

concentrations of infant red blood cells significantly increased after the supplementation

period. However, similar to maternal results, there was no significant change in infant

red blood cell DHA. Unfortunately, this study only used five women and their infants, so

it may have been hampered by a small sample size.

Further evidence suggests that infants breast fed from omnivorous mothers have a

higher DHA concentration in their red blood cells than do infants of vegan mothers

(Sanders and Reddy, 1992). In fact, the difference in infant red blood cell DHA was

quite large in this study, with infants feeding from vegan mothers having 1.9% of the

total FA found in their red blood cells as DHA and infants feeding from omnivorous

mothers having 6.2% of their total red blood cell FA as DHA. The content of DHA in

breast milk reported by Sanders and Reddy (1992) was also significantly lower in vegan

women when compared to omnivorous women (0. 14 and 0.37% of fat, respectively). In

addition, infants fed conventional formula (low in DHA) have consistently lower plasma









and red blood cell levels of DHA than infants fed breast milk, which is higher in DHA

(Innis, 1991; Innis, 1992b).

The ability to increase blood concentrations of n-3 PUFA by feeding sources of

these FA has also been documented in animals. Bauer et al. (1998) fed adult dogs either

ground flax or sunflower seeds for 84 days and showed that plasma ALA, EPA and DPA

were elevated when dogs were fed flaxseed, compared to when dogs were fed sunflower

seeds. Plasma DHA, however, remained unchanged in the flax fed dogs, showing the

difficulty in converting ALA to DHA. The flax fed dogs also showed a plasma reduction

in AA and 22:5 n-6, providing evidence of competition between n-3 and n-6 PUFA for

the A6-desaturase in dogs (Bauer et al., 1998). However, the exact amount of supplement

Bauer and coworkers added to the diets of the dogs was not stated, so it is therefore

difficult to compare levels of supplementation to other studies.

In horses, Hansen et al. (2002) examined the effects of ALA supplementation on

equine fatty acid status by feeding adult horses a diet consisting of 8% flaxseed oil for 18

weeks. Hansen and coworkers found that the flaxseed oil supplemented horses showed

an increased plasma ALA and EPA compared to horses that did not receive any fat

supplementation. On the other hand, there were no increases in DHA noticed. A

weakness of this study, however, is the low sample size of only 12 horses (6 horses in the

control group, 6 horses in the supplemented group). Duvaux-Ponter et al. (2004) also

tested the effects of ALA on horses, but used pregnant mares and young foals as subj ects.

In this study, 26 pregnant mares were divided into two groups. The first group acted as

the control and was fed extruded rapeseed (high in n-6 FA), while the second group was

fed extruded linseed (high in n-3 FA). The mares were supplemented 1.5 months prior to









foaling until one month after foaling. While mare blood was not tested, supplementation

with extruded linseed caused an increase in the ALA content of foal plasma from foaling

until 4 weeks post parturition, and this increase was greater than the increase seen in foals

nursing the mares given rapeseed (Duvaux-Ponter et al., 2004). However, the exact

amount of linseed provided to the mares is unclear, as it was not stated in the paper.

The effects of feeding sources of EPA and DHA have also been documented in

horses. Hall et al. (2004a) fed ten adult mares either menhaden fish oil or corn oil for a

period of 14 weeks. Mares fed the menhaden fish oil consumed 22.93 g EPA per day and

19.58 g DHA per day. These amounts equated to a daily intake of 4.6 g EPA/100 kg

bodyweight and 3.9 g DHA/100 kg bodyweight. As a result of this supplementation, Hall

et al. (2004a) noticed higher plasma ALA, EPA and DHA and lower plasma LA in the

mares fed fish oil compared to the mares fed corn oil. Brinsko et al. (2005) examined the

effects of feeding a DHA source to stallions to determine the effects of FA

supplementation on semen. In this study, eight stallions were used in a 2 x 2 crossover

design. Stallions were fed a grain mix top-dressed daily with either 250 g of a

commercial nutriceutical containing 30% n-3 FA (resulting in 75 g of n-3 FA) or a grain

mix with no supplementation. Stallions were fed their respective diets for 14 weeks,

separated by a 14 week wash out period, before treatments were switched for another 14

weeks of supplementation. The authors found that when stallions were supplemented

with n-3 FA, their semen had almost three times the levels of DHA/billion sperm

compared to when stallions were not supplemented. Even though the relative percentage

of DHA in semen fatty acids was not significantly different between the two groups,

treated stallions showed a 1.5-fold increase in their semen DHA:DPA ratio when they









received n-3 supplementation (Brinsko et al., 2005). Therefore, it seems that

supplementation of DHA in horses may have the ability to affect the fatty acid

composition of body constituents other than just the plasma.

Effects of PUFA supplementation on the acquisition of passive immunity in the foal

In order for IgG to be maximally absorbed into the foal's intestinal cells, the cell

membranes must be fluid enough to allow the molecules to navigate through the

membrane. Membrane bilayers tend to exist at the transition point between a fluid and

solid-like (gel) state. The phospholipid fatty acyl chains present in membranes are one of

the key chemical determinants of this balance. PUFA of the cis configuration tend to

increase the fluidity of the membrane (Murphy, 1990; Mills et al., 2005). The fatty acid

composition of membrane phospholipids is also easily changed by manipulation of

dietary fat (Murphy, 1990), which, in tumn, can influence membrane fluidity.

Brasitus et al. (1985) showed that adjusting the fatty acid composition of the diet in

rats changed the composition of their enterocyte membranes. To do so, rats were fed

either unsaturated or saturated triglycerides provided by comn oil or butter fat,

respectively, for 6 weeks. The supplementation of comn oil, which is rich in LA, caused

an enhanced fluidity of the membranes of several intestinal cells (Brasitus et al., 1985).

When humans were supplemented with dietary n-3 PUFA, the fluidity of their

erythrocyte membranes was substantially increased (Lund et al., 1999). In this study, 17

adults were supplemented with three 1 g capsules of fish oil per day for 42 days. Fluidity

of the red blood cell membrane was determined by measuring the lateral diffusion

coefficient of the fluorophore ODAF by fluorescence recovery after photobleaching. The

results of Lund et al. (1999) suggest that supplementation with fish oil increased the

lateral diffusion coefficient of ODAF, therefore increasing the membrane fluidity. This









increase in fluidity was seen at 21 days after supplementation and continued to rise until

the termination of the study at 42 days (Lund et al., 1999).

A correlation between membrane fluidity and permeability was shown in young

rats by Meddings and Theisen (1989). These researchers examined the changes that

naturally occur in the membrane of jejunal microvilli in rats as they aged from 9 to 25

days. Study results showed a decreasing lipid fluidity as the rats aged, assessed by a

steady-state fluorescence polarization technique. This decrease in membrane fluidity

correlated to a decrease in membrane permeability (Meddings and Theisen, 1989). This

correlation may suggest that if it is possible to enhance membrane fluidity by feeding n-3

FA, it may therefore be possible to augment the amount of IgG that travels both into the

mare's mammary gland and across the foal's intestine.

To determine the effects of feeding PUFA on the IgG content of mare colostrum,

Kruglik et al. (2005) fed mares either corn oil (rich in LA) or encapsulated fish oil (rich

in EPA and DHA) from 60 days before foaling to 21 days after foaling. The mares fed

encapsulated fish oil consumed 8.6 g of EPA and 10.4 g of DHA per day. The results of

Kruglik et al. (2005) showed a higher presuckle colostrum IgG content in the fish oil fed

mares, suggesting that supplementation with Hish oil may have improved the fluidity and

permeability of mammary epithelial cells. However, Kruglik et al. (2005) did not specify

the amount of colostrum collected, and it has been reported that IgG amounts can vary

between the first 250 and 500 mL of colostrum (Lavoie et al., 1989). Therefore, if the

volume of colostrum gathered was different between mares, the differences seen in IgG

may have been attributed to colostrum volume and not to treatment. Studies have also

been performed that suggest that n-6 PUFA may increase mare colostrum IgG. Hoffman









et al. (1998) fed mares a high fat diet (10 % fat) through gestation and lactation. The fat

in this diet was provided primarily by corn oil, which is high in LA. Colostrum IgG

levels were higher in the mares fed the high fat diet, even though the dietary fat was rich

in n-6 and not n-3 FA (Hoffman et al., 2004). However, the volumes of harvested

colostrum were not stated in this study. In addition, colostrum was collected between 6

and 12 hours after foaling. Because the IgG of colostrum can vary dramatically in the

first 12 hours after foaling (Pearson et al., 1984), colostrum IgG values obtained from

mares in this study may have shown differences that were due to time and not treatment.

Studies have also been executed to determine the effect of feeding PUFA on foal IgG.

Kruglik et al. (2005) showed that mares supplemented with Hish oil produced foals that

showed no differences in IgG levels when compared to foals born to corn oil fed dams,

even though the same study showed a higher colostrum IgG in the mares fed fish oil.

Kruglik et al. (2005) sampled foal plasma at 24 hours, so peak IgG content should have

been reached. Therefore, it is unclear as to why the higher IgG levels in fish oil fed mare

colostrum did not cause an increase in the plasma of foals born to these mares. Duvaux-

Ponter et al. (2004) also failed to show a difference in foal serum IgG when mares were

supplemented with a source of n-3 FA. In this study, mares fed extruded linseed did not

produce foals with a higher serum IgG than mares fed extruded rapeseed (Duvaux-Ponter

et al., 2004). Foal blood was again sampled at 24 hours after foaling in this study, so

peak foal IgG should have been recorded. However, mare colostrum IgG was not tested,

so it is unclear if ALA could increase colostrum IgG. More research needs to be done to

determine the capability of dietary PUFA on modifying mare mammary and foal









enterocyte membrane composition and fluidity on the enhancement of passive transfer of

IgG.

Effects of PUFA supplementation on the inflammatory response

Numerous studies have shown anti-inflammatory effects of n-3 PUFA. Sadeghi et

al. (1999) fed groups of mice either a low fat diet (2.5% fat provided by corn oil) or diets

high fat diets providing 20% fat by coconut (rich in medium chain FA), olive (rich in

C18:1n-6), safflower (rich in LA) or fish oils. After 5 weeks on diet, mice were injected

with 1.0 mL of phosphate-buffered saline containing endotoxin from E. coli. In the mice

receiving the fish oil diet, lower plasma concentrations of the proinflammatory cytokines

TNF-u, IL-1 and IL-6 were seen after the inj section of endotoxin when compared to mice

fed olive or safflower oils. However, coconut oil fed rats also showed decreased amounts

of these cytokines (Sadeghi et al., 1999). Therefore, it is unclear if fish oil was

specifically responsible for the decreased proinflammatory cytokine production, or if this

difference was caused by a lack of n-6 PUFA. Unfortunately, the amount of feed offered

to the mice was not provided by the authors, so the amount of consumed FA could not be

calculated. Billiar et al. (1988) fed fish oil to rats for 6 weeks and observed a lower in

vitro production of IL-1 and TNF-a by macrophages. Unfortunately, the fish oil fed rats

in this study were compared to rats fed either corn or safflower oil, which are both high in

n-6 FA. Therefore, it is again unclear if fish oil reduces proinflammatory cytokine

production or if the feeding of n-6 FA increases cytokine production.

To test the inflammatory effects of PUFA in horses, Hall et al. (2004a) fed 10

adult mares 3.0% of their total diet (as-fed basis) with either corn oil or menhaden fish

oil. After 14 weeks of supplementation, the fish oil supplemented mares had neutrophils









with a 78-fold greater concentration of the lesser inflammatory LTBS when compared to

the neutrophils of mares fed corn oil (Hall et al., 2004a). In the same group of mares

during the same supplementation period, production of TNF-oc by bronchoalveolar lavage

fluid (BALF) cells was increased in both groups, but only the corn oil fed mares had an

increased production of inflammatory PGE2 their BALF cells (Hall et al., 2004b). When

mare BALF cells were stimulated with lipopolysaccharide, mares fed corn oil also

showed a higher production of inflammatory PGE2 (Hall et al., 2004b). Similar to the

studies discussed previously, however, Hall et al. (2004a, 2004b) compared horses fed

fish oil to horses fed corn oil and did not include a control group fed a diet without n-6 or

n-3 FA supplementation. Because the diets of both groups of horses were altered through

fat supplementation, it is unclear if the reported decreases in pro-inflammatory

eicosanoids seen in horses fed fish oil would have resulted if these horses had been

compared to a control group.

The delayed-type hypersensitivity (DTH) response has also been used to test the

anti-inflammatory effects of n-3 PUFA. Meydani et al. (1993) supplemental adult

humans with a low-fat, high-Hish diet (26% calories from fat, 1.23 g EPA and DHA

combined per day) or a low-fat, low-Hish diet (25% calories from fat, 0.27 g EPA and

DHA combined per day) for 24 weeks. This treatment period was compared to a

previous 6 week period where subj ects had been eating a current American diet of 3 5%

of calories from fat and 0.8% of calories from n-3 FA. A delayed-type hypersensitivity

(DTH) test was administered before and after the supplementation period using several

different antigens, including tetanus toxoid and Streptococcus (group C). Results of

Meydani et al. (1993) showed that the DTH response of adults consuming the low-fat,










high-fish diet was significantly less than the response of those consuming the low-fat,

low-fish diet, with diameter measurements of the DTH reactions of the low-fat, high-fish

diet participants being reduced by half.

Changing the n-6:n-3 ratio in dogs was also shown to effect the inflammatory

response (Wander et al., 1997). In this study, dogs were fed diets containing n-6:n-3

ratios of 31:1, 5.4: 1 or 1.4: 1 for 16 weeks, where the n-6 FA was provided by corn oil

and the n-3 FA was provided by fish oil. Dietary ratios were changed mostly by a

reduction in LA simultaneous to an increase in EPA and DHA. When the diameter of a

DTH response to keyhole limpet hemocyanin (KLH) was measured, dogs fed a n-6:n-3

ratio of 1.4 showed a much smaller reaction compared to the dogs fed ratios of 34: 1 and

5.4: 1 (Wander et al., 1997). Because the amount of n-6 FA in these diets decreased as

the n:6-n:3 ratios decreased (as opposed to holding the amount of n-6 FA stable and

increasing the amount of n-3), it is again unclear if differences seen in DTH response

were strictly caused by the increase in n-3 FA. It is quite plausible that these differences

may have been influenced by the decreasing n-6 FA. In contrast to dogs, the DTH

response of horses sensitized with KLH showed no differences between horses fed 3% of

the total diet (as-fed basis) either fish oil or corn oil (Hall et al., 2004b).

Effects of PUFA supplementation on disease resistance and survival

The maj ority of studies on inflammation and PUFA supplementation have shown

positive results with n-3 PUFA, particularly when n-3 supplementation reduces n-6 FA in

the diet. However, studies on the effect of PUFA on disease resistance show conflicting

results. When guinea pigs were fed diets high in either n-3 FA (1.4% and 0.9% fat

calories from EPA and DHA, respectively) or n-6 FA (15.4% fat calories from LA) for

13 weeks and infected with M~ tuberculosis, the guinea pigs fed a diet high in n-3 FA









showed a higher number of mycobacteria recovered from the spleen, the most

pronounced progression of the disease and a higher mean size of the tuberculin reaction

(Paul et al., 1997). The authors suggested that possible explanations for these results may

include the lower production of inflammatory mediators and the impairment in release of

lysosomal enzymes that kill mycobacteria (Paul et al., 1997). The study performed by

Paul et al. (1997) is possibly one of the best studies done to examine n-3 FA effects on

disease resistance, as animals consuming both fat supplemented diets were compared to a

no fat added control diet. In addition, the study utilized animals consuming the

experimental diets but that were not infected. These animals therefore acted as

uninfected controls within each diet. The benefits of a study design such as this is that a

direct comparison can be made between the n-3 FA supplemented group and the control

group, which in turn helps to determine disease effects are due strictly to the addition of

dietary n-3 FA.

Another well designed study compared disease responses of mice infected with

influenza (Byleveld et al., 1999). Challenging fish oil fed mice with influenza virus

produced a higher lung viral load, lower body weights and impaired production of IgG

and lung IgA when compared to mice fed beef tallow. Mice were fed fish oil or beef

tallow at 20% of dietary fat for 14 days, after which half of the mice from each treatment

were infected with influenza while the other half served as noninfected controls.

D'ambola et al. (1991) supplemented newborn rabbits with high (5 g/kg) or low (0.22

g/kg) doses of fish oil, safflower oil or saline for 7 days after birth. When the young

rabbits were supplemented with the higher levels of fat, both the fish and sunflower oil

supplemented rabbits had an impaired ability to clear Staphylococcus aureus when









compared to the saline control group (D'ambola et al., 1991). However, the low doses of

fish and safflower oil did not produce the same impaired ability to clear the bacteria. In

light of these results, the authors of this study concluded that high does of both n-3 and n-

6 FA can reduce the host's ability to kill S. aureus (D'ambola et al., 1991).

Positive results of supplementing with n-3 PUFA were shown when neonatal rat

pups were infected with group B streptococcus (Rayon et al., 1997). In this study,

researchers fed gestating rats a control diet (no fat added) or diets supplemented with

either comn or menhaden fish oil. Supplementation was begun on day 2 of gestation and

continued through lactation, but the amounts of diets and supplements fed were not

provided by the authors. Rat pups were then infected with the streptococcus bacteria at 7

days of age. The results of Rayon et al. (1997) showed that pups from mothers who had

been fed fish oil during gestation showed a significantly higher rate of survival (79%)

than those bomn to corn oil fed dams (49%), though this difference was not significant. In

this study, the lowered production of inflammatory mediators by fish fed rats when

compared to corn oil fed rats may have been responsible for the higher survival rates, as

group B streptococcal infections induce elevated levels of proinflammatory cytokines that

lead to septic shock (Rayon et al., 1997).

Feeding fish oil to weanling mice has been shown to prolong mice survival to a

murine retrovirus-induced immunodeficiency syndrome (MAIDS) that mimics human

AIDS (Femnandes, et al., 1992). Mice in this study were fed diets consisting of 5% corn

oil fed at an energy restriction of 40%, or diets fed ad libitum consisting of 5% comn oil,

20% corn oil or 20% menhaden fish oil. Mice were fed for 8 weeks before being inj ected

with the MAIDS plaque-forming units (Femnandes et al., 1992). Mice fed both the 5%









corn oil energy restricted and 20% fish oil diets showed significantly longer survival rates

than mice consuming the other diets. The authors explained the increase in survival rates

of these two groups as a result of a slowed the progression of the MAIDS disease

(Fernandes et al., 1992).

Thors et al. (2004) also showed positive immune effects on mice when feeding fish

oil. In this study, 120 female mice were fed a standardized, control diet for 6 weeks

before being divided into four groups and fed two different diets. The first two groups

were fed a diet enriched with fish oil at 10% of total diet weight, and the remaining two

groups were fed a diet enriched with corn oil at 10% of the total diet weight (Thors et al.,

2004). However, the amount of time these diets were fed was not clear. Mice were

intranasally inoculated with either Klebsiella or Streptococcus pneumoniae and the

inoculum was aspirated into the lungs. Survival rates of the mice fed a fish oil diet and

infected with Klebsiella pneumoniae were significantly higher than the rates seen in corn

oil fed mice infected with the same disease. However, survival rates of mice infected

with Streptococcus pneumoniae did not differ between the fish or corn oil fed mice

(Thors et al., 2004).

In general, the conflicting results of studies examining the effects of dietary PUFA

supplementation on disease resistance may be caused in part by study differences in the

type of animal used, type and amount of pathogen utilized, route of pathogen infection

and amount and duration of dietary PUFA supplementation. Because many of the above

studies did not clearly state this information, it is difficult to establish which differences

in disease response between studies could be attributed to PUFA treatment and which

could be attributed to differences in experimental design. However, Anderson and










Fritsche (2002) suggest that conflicting results may be rooted in the host' s ability to find

a proper balance between the necessary and excessive production of various

proinflammatory mediators.

Characteristics of Mare Milk

Mare Colostrum

Colostrum is the mare's first milk and is vital in transferring immunity to the

newborn foal. It has a much thicker, stickier consistency than milk and is often a pale to

deep yellow in color. Colostrum, produced in the mammary gland during the last

trimester of pregnancy, is only secreted for a very short time (Lavoie et al., 1989). By

24-96 hours after foaling, mammary secretions have completely transitioned from

colostrum to milk (Ullrey et al., 1966). Compositionally, colostrum is higher than milk in

fat content (Csap6, et al., 1995). The most important colostrum constituent, however, is

the immunoglobulins. Colostrum has high concentrations IgG but lower IgM and IgA

(Lavoie et al., 1989). Colostral IgG declines within the first 24 hours after birth. This

decline often corresponds to the change of a thick, pale yellow fluid to one of a thinner

consistency with a gray-white color (Pearson et al., 1984). Average colostral Ig

concentrations are shown in Table 2-1.

Factors Affecting Mare Colostrum IgG Content

Premature lactation, or "prelactation," is considered the most important cause of

failure of passive transfer in foals, as it is one of the main determinants of colostral IgG

levels (Jeffcott, 1974). Causes of premature lactation include placentitis and/or placental

separation, but the condition can occur without obvious placental pathology (Jeffcott,

1974b, 1975). Mares that experience prelactation for longer than 24 hours before foaling

tend to have lower colostral IgG concentrations than those who lactate normally (Koterba









et al., 1990). Morris et al. (1985) found that as the proportion of mares on a breeding

farm experiencing prelactation increased, so did the proportion of mares with low

colostral IgG concentrations. In addition, the proportion of foals with low serum IgG

concentration also increased.

Breed of mare may also affect colostral IgG concentration. Pearson et al. (1984)

found a significantly higher IgG concentration of more than 5,000 mg IgG/dL colostrmm

in Arabian mares when compared to Thoroughbred mares. Average time from birth until

colostrum IgG concentration declined to 1,000 mg/dL (the IgG concentration that cannot

prevent failure of passive transfer) was 19. 1 hours for the Arabians and only 8.9 hours for

the Thoroughbreds. LeBlanc et al. (1992) founder higher IgG colostral concentrations in

Thoroughbreds and Arabians when compared to Standardbreds. However, in another

study, LeBlanc et al. (1986) reported no differences between IgG colostral concentrations

in Thoroughbred, Quarter Horse, Arabian and Standardbred mares. The conflicting

results seen between these two studies should not have been due to different sampling

times or colostrum amounts taken, as both studies tested 10 mL of presuckle colostrum.

Therefore, the conflicting results may be explained by differences in body size and

weight between breeds. Larger breeds can sometimes produce larger volumes of

colostrum, and this large volume may lead to a dilution effect. However, the age of the

mare, number of lactations and herd management are factors that probably influence

colostral IgG concentration. Additionally, there is large individual variation in colostral

IgG content, making it difficult to attribute differences in colostral IgG as purely breed

oriented (Pearson et al., 1984). Further studies are needed to examine what, if any,

influence breed has on colostral IgG content.









Conflicting results exist in regard to the connection between a mare's age and her

colostrum quality. In a study involving Standardbred, Thoroughbred and Arabian mares,

mares between the ages of 3 and 10 years had the highest colostral IgG concentration and

FPT was most prevalent in foals born to dams of over 15 years (LeBlanc et al., 1992).

However, Morris et al. (1985) and Erhard et al. (2001) saw no significant effects of age

on IgG in mares of varying breeds. Both LeBlanc et al. (1992) and Erhard et al. (2001)

sampled colostrum before the foal had been allowed to suckle. However, Morris et al.

(1985) sampled colostrum during the first 2 hours after foaling. Since Morris et al.

(1985) sampled colostrum at a later time than the other two studies, any difference seen

in the colostrum of this study could have been attributed to time. However, time should

not have affected the values of LeBlanc et al. (1992) and Erhard et al. (2001). Therefore,

discrepancies in data reflecting the effect of mare age of colostrum IgG could be

explained by outside factors such as individual mare variation and management

differences.

Composition of Mare Milk

In mares kept without human influence, lactation lasts about one year, and drying

of the udder occurs several weeks to several days before the next foaling. There have

been, however, extreme cases noted of 2- or 3-year-old suckling foals (Feist and

McCullough, 1976). Today, the drying process is initiated by weaning foals at 4-6

months of age. Actual daily lactation yields of nursing mares are not well known, but are

estimated to be between 10 and 30 kg for light breed nursing mares (Doreau and Boulot,

1989). Peak lactation seems to occur at about two months postpartum (Bouwman and

van der Shee, 1978).










Compositionally, the fat content of mare milk is very low (Doreau and Boulot,

1989) but can be influenced by diet. Milk fat is also influenced by mare body condition

at foaling, with fat mares producing milk with a higher fat content than thin mares. The

increased lipid mobilization of fat mares may be explained this phenomenon (Doreau et

al., 1993). Crude protein in milk exists at between 1.7 and 3.0% (Doreau and Boulot,

1989) and decreases throughout lactation (Oftedal et al., 1983). Mare milk is different

from the milk of other species as it contains higher amounts of the amino acids cystine

and glycine (Doreau and Boulot, 1989). Milk carbohydrates are almost entirely made of

lactose, with very low levels of free glucose. Mare milk is also extremely low in ash,

with 0.7% as extreme (Doreau and Boulot, 1989). Milk is also different than colostrmm

in the amounts of immunoglobulins present. Levels of IgG, IgA and IgM all decrease as

colostrum transitions into milk and IgA becomes the predominant Ig present (Norcross,

1982). Average immunoglobulin concentrations in mare milk are shown in Table 2-1.

Peak colostrum IgG content is observed at foaling and rapidly declines during the

first 24 hours after foaling (Lavoie et al., 1989). In colostrum sampled within 2 hours

after foaling, mean IgG values were shown to be 16,583 mg/dL (Lavoie et al., 1989). At

4 hours post foaling, another study showed mean IgG values that were at lower levels of

5,450 mg/mL, and these values fell even further to 1,010 mg/dL by 9-12 hours after

foaling (Erhard et al., 2001). Colostrum IgG fell below 1,000 mg/dL by 13-16 hours post

foaling and continued to decrease until day 14 (Erhard et al., 2001). Duvaux-Ponter et al.

(2004) showed that these low milk IgG levels did not show any changes by 21 days after

foaling, suggesting that mare milk IgG levels stay at this low level for the duration of

lactation.









Effect of Diet on Fat and Fatty Acid Composition of Milk

Milk fatty acids are either synthesized de novo by acetyl-CoA carboxylase and fatty

acid synthase or are supplied exogenously. The mammary epithelial cells of lactating

animals are highly active in triglyceride biosynthesis (Clegg et al., 2001). If the FA are

not synthesized in the mammary epithelial cells, they can enter the cells either from

albumin in the plasma or from hydrolysis of chylomicron triglycerides by lipoprotein

lipase. Once inside the cell, FA are bound to fatty acid binding protein in the cytoplasm

or activated with acetyl-coenzyme A (CoA) and used for triglyceride synthesis. The

endoplasmic reticulum synthesizes microlipid droplets that fuse to form cytoplasmic

droplets which move to the apical membrane where they are enveloped to form the milk

fat globule. This globule is then secreted in a membrane-bound form into the milk

(Neville and Picciano, 1997).

Mare milk contains relatively little fat, with triglycerides as the predominate lipid

class (Dils, 1986). Mare milk naturally contains very small quantities of stearic (C18:0)

and palmitoleic (C16:0) acids and high quantities of linolenic (C18:3n-3) and linoleic

(C18:2n-6) acids (Csap6 et al., 1995). The higher amounts of unsaturated FA are

explained by the fact that horses consume large amounts of forages rich in unsaturated

FA (Csap6 et al., 1995). Milk composition, however, may be changed by manipulating

the diet, with the largest effects seen in the fat content (Sutton and Morant, 1989). Mare

milk long-chain FA composition is strongly related to the FA composition of the diet, as

no microbial FA hydrogenation occurs before intestinal absorption in horses (Doreau et

al., 1992; Hoffman et al., 1998).

The ratio of forage to grain in the mare' s diet can effect her milk composition.

Generally, fat content decreases as the percentage of grain increases (Doureau and









Boulot, 1989). Doreau et al. (1992) fed nursing mares diets containing either 95% hay

and 5% grain or 50% hay and 50% concentrate. Milk fat concentrations were higher for

the mares fed the 95:5 forage:grain diet compared to the 50:50 forage:grain diet. The

mares eating mostly forage also had higher linolenic and lower linoleic acid milk

contents than those eating mostly grain (Doreau et al., 1992). This effect is

understandable considering the fact that forage is high in linolenic acid. However,

because exact amounts of hay and grain fed and the fat composition of the diet

ingredients was not given, it is difficult to determine accurate values for percent fat of

each diet.

Studies in humans have also examined the effect of dietary fat on milk fat

composition. Henderson et al. (1992) found that supplementing pregnant women with 6

g of an EPA and DHA supplement for 21 days significantly increased EPA, DPA and

DHA and decreased total n-6 PUFA levels in breast milk when compared to pre-

supplementation levels. Helland et al. (1998) observed an increase in EPA and DHA in

breast milk when women were supplemented with 5 and 10 mL cod liver oil daily for 14

days compared to women receiving 5 mL of cod liver oil/day and those receiving no

supplementation. The changes in breast milk FA composition reported by Henderson et

al. (1992) and Helland et al. (1998) were noted as early as day two of supplementation.

Interestingly, daily supplementation of women with 20 g of flaxseed oil (approximately

10.7 g ALA/d) for 4 weeks increased the EPA and DPA breast milk content but failed to

produce an increase in DHA (Francois et al., 2003). The authors speculated that the

excess ALA supplied from flax oil may have competitively inhibited A6-desaturase from

converting DPA to DHA (Francois et al., 2003).









In dogs, feeding fat supplements with varying ratios between ALA and the sum of

EPA and DHA produced milk fat compositions highly correlated to the diet fed (Bauer et

al., 2004). Dogs were fed one of four diets containing 15% total fat as beef tallow and

varying amounts of linseed and menhaden fish oil to provide specific levels of ALA,

EPA and DHA. The diets were formulated as follows: the Lo/Lo diet contained 0.14%

ALA and 0.04% EPA and DHA, the Lo/Mod diet contained 0.29% ALA and 0.24% EPA

and DHA, the Lo/Hi diet contained 0.20% ALA and 0.66% EPA and DHA and the Hi/Lo

diet contained 6.82% ALA and 0.04% EPA and DHA (fatty acids are expressed as a

percentage of dry matter). Bitches fed the Hi/Lo diet had the highest milk ALA content,

while bitches fed the Lo/Hi diet had the highest EPA and DHA milk content. Milk

responses of EPA, DPA and DHA content were seen as a function of increasing dietary

n-3 PUFA content. There was no enrichment of DHA when the Hi/Lo diet was fed,

showing that ALA is inefficiently converted to DHA in the dog (Bauer et al., 2004).

Davidson et al. (1991) showed that mares fed a diet with 5% added fat produced

milk with a higher fat content than mares who were not supplemented with fat (2-3%

dietary fat). However, no differences in milk fat production were noted when mares were

fed a sugar and starch diet with 2.4% fat compared to a fat (corn oil) and fiber diet with

10.4% fat (Hoffman et al., 1998). Nonetheless, the FA composition of the milk mirrored

the FA supplied by the diet. The mares eating the high fat diet showed higher milk

concentrations of LA and lower concentrations of ALA, which can be explained, in part,

by the n-6 PUFA content of the corn oil (Hoffman et al., 1998). Spearman et al. (2005)

found that feeding gestating mares a mix of corn oil and linseed oil increased milk ALA

content when compared to mares fed corn oil. Duvaux-Ponter et al. (2004) observed









higher levels of ALA in mare milk when mares were supplemented with linseed oil.

Feeding mares 454 g of encapsulated fish oil per day increased EPA and DHA in the milk

but did not affect the ALA content when compared to mares fed corn oil (Kruglik et al.,

2005). Together, these studies show that the fat content and FA composition of the

mare's diet can influence milk composition.

Fatty Acid Transfer across the Placenta

The placenta is a pivotal organ in providing the developing fetus with essential

fatty acids. During the last trimester of pregnancy, fetal requirements for AA and DHA

are especially high due to rapid synthesis of brain tissue. To obtain these FA, the fetus

depends upon placental transfer, and thus on the FA status of the mother (Al et al., 2000).

Much of the research of placental FA transfer has been performed in humans, who

possess a discoid hemochorial placenta. In these studies, there has been considerable

evidence of transfer of ALA, EPA and DHA across the placenta (Innis, 2005). This

transfer is a multi-step process of FA uptake by fatty acid binding proteins and

intracellular translocation of the FA from the maternal to fetal environment. The fatty

acid binding proteins that facilitate this process favor the uptake of n-6 and n-3 PUFA

over non-essential FA (Innis, 2005).

Human placental preference for transfer of FA has been reported by one author to

be DHA>ALA>LA>AA (Haggarty et al., 1997), while others have speculated that DHA

and AA are preferred over all other FA (Campbell, 1996; Crawford, 2000).

Fetal plasma concentrations of AA and DHA are reported to be 300- to 400-fold higher

than maternal plasma levels while their LA and ALA levels are lower (Elias and Innis,

2001). However, human placenta does contain A6- and A'-desaturases (Innis, 2005), so









the higher concentration of AA and DHA in fetal circulation may be partially produced

by placental conversion of these FA from their 18 carbon precursors.

Human studies have shown that the maternal dietary intake of n-6 and n-3 PUFA

influences placental transfer of AA and DHA. Connor et al. (1996) supplemented

pregnant women with sardines and fish oil from the 26th to the 3 5th week of pregnancy in

amounts to provide 2.6 g of n-3 FA per day. When DHA blood levels of newborn infants

born to supplemented women were compared to those of newborn infants born to

unsupplemented women, newborn babies born to supplemented mothers had 35.2% more

DHA in red blood cells. Infants from supplemented women also showed a plasma DHA

content 45.5% higher than infants from unsupplemented mothers, concluding that

placental transfer of DHA in women is increased by maternal supplementation with DHA

(Connor et al., 1996). However, de Groot et al. (2004) reported that supplementing

pregnant women with ALA did not increase umbilical cord blood DHA, suggesting that

the placenta could not efficiently convert ALA to DHA. In this study, pregnant women

were supplemented daily with either 9.02 g LA and 2.82 g ALA (experimental group) or

10.94 g LA and 0.03 g ALA (control group) in the form of margarine. Supplementation

was provided from week 14 of pregnancy until delivery (de Groot et al., 2004). While

the umbilical venous plasma obtained from the subj ects at delivery showed no differences

in DHA content between groups, the experimental group did show an EPA concentration

twice that of the control group, suggesting that conversion of ALA to EPA in the human

placenta may be possible (de Groot et al., 2004).

In spite of its complex six-layered placenta, the transfer fatty acids from mare to

fetus is possible. Equine studies, while few in number, have shown a positive correlation









between maternal and umbilical vein plasma free FA levels (Stammers et al., 1991).

However, the same study also showed a difference in FA composition between maternal

and umbilical vein plasma. The phospholipids portion of the umbilical venous plasma

contained more longer chain derivatives of LA and ALA than was found in maternal

plasma, suggesting that these longer chain FA were of placenta origin, because maternal

plasma phospholipids in the horse contain very little longer chain PUFA (Stammers et al.,

1991).

The presence of A6 Of A5-desaturase, to the author' s knowledge, has not been

established in the equine placenta. However, many studies have produced results that

would imply these enzymes are present. In natural situations, long-chain PUFA

(particularly DHA) are virtually absent from maternal circulation and in very low

concentrations in other maternal lipid compartments. In spite of this occurrence, foal

plasma phospholipids are rich in long-chain PUFA which must therefore be provided to

the foal by placental formation and transfer (Stammers et al., 1987). Stammers et al.

(1988) showed that foals had higher plasma concentrations of AA, EPA and DHA than

did their dams. A 30 hour fast of the pregnant mares resulted in an even greater fetal

concentration of these fatty acids, resulting from the increased lipid mobilization in the

mares (Stammers et al., 1988). When Stammers et al. (1994) incubated equine placenta

in media enriched with LA, the lipid fractions released from the placenta consisted of

long-chain PUFA derivatives of LA such as C20:3n-6, C20:4n-6 and C22:6n-6. This

finding suggests that these PUFA would be seen in the umbilical plasma lipids rather than

the maternal plasma lipids. No studies exist in mares to test the ability of manipulation of










dietary fat to influence placental FA transfer, so much research needs to be done in this

area.

Conclusions

Because many of the studies investigating the effects of feeding n-3 FA to the horse

have not utilized a true control group that received no fat supplementation, research is

needed to compare the effects of n-3 supplementation with no n-3 supplementation (i.e.,

unaltered diet). This is especially important considering the fact that high forage diets

contain significant quantities of n-3 FA, but the addition of grain to the diet shift the

proportion of FA in favor of n-6. Studies comparing n-3 FA supplementation to baseline

diets are needed to validate that the biological effects observed when feeding n-3 FA are

truly due to the increase in these FA, and not to a decrease in n-6 FA.

In addition, little research has addressed responses yielded by different n-3 FA

(e.g., ALA, EPA, DHA) to determine if differences in dietary FA source can influence

biological responses in the horse. In particular, little data exists that compares the effects

of different n-3 FA sources fed to the mare and the subsequent response of her nursing

foal. It is unclear if supplementing the mare during gestation with n-3 FA can affect the

IgG composition of her colostrum and milk and subsequently the IgG concentration in

her foal. Furthermore, it is unknown if increasing the gestating mare' s n-3 FA intake can

result in greater placental transfer of n-3 FA, therefore allowing the foal to be born with

an already elevated level of these FA.

Lastly, clear effects of supplementation with ALA or an EPA/DHA combination on

the inflammatory response in horses have yet to be elucidated. Therefore, in an attempt

to answer some of these questions, the obj ectives of this study were:






50


1. Examine the effect of dietary n-3 supplementation of mares on the FA composition
of mare milk and mare and foal plasma and red blood cells;
2. Examine the difference of efficiencies of ground flaxseed (ALA) and encapsulated
fish oil (EPA and DHA) in augmenting EPA and DHA in the mare and foal;
3. Determine if n-3 FA supplementation of the mare can increase the IgG content of
colostrum, milk and foal plasma.
4. Determine in supplementation with flaxseed or fish oil can alter the inflammatory
response in mares and foals.















CHAPTER 3
MATERIALS AND METHODS

Animals

This trial used 36 pregnant Thoroughbred (n=24) and Quarter Horse (n=8) mares

and their subsequent foals. Mare age ranged from 4 to 20 years with a mean of 10.5 & 4.1

years (mean & SE). Mares were paired according to breed and stratified according to

expected foaling date before being assigned to three treatment groups. The order of

treatment assignment was determined by numbering three pennies, each penny

corresponding to a separate treatment, and placing them into a hat. Pennies were then

drawn at random to determine the order of treatment assignment. Treatment groups were

then balanced for mare age and parity.

For the duration of this trial, mares and foals were housed at the University of

Florida's Horse Research Center in Ocala, Florida. Pregnant mares were housed on

pasture until signs of foaling were evident. At this time, mares were moved into small

paddocks until foaling. All mares, with the exception of one, foaled outside. After

foaling, mares and foals were kept in a box stall for 24 hours and then turned out in a

small paddock for one week before being returned to pasture. A routine vaccination and

anthelmintic schedule was followed for all animals. This experiment was performed in

accordance with the regulations and approval of the Institutional Animal Care and Use

Committee of the University of Florida.









Diets and Treatments

The basal diet for all treatment groups consisted of a commercial grain-based

concentrate (Gest-O-Lac; Ocala Breeders Sales, Ocala, Florida) and pasture or hay. The

grain-based concentrate was offered at 1.0% BW in late gestation and 1.0-2.0% BW

during lactation in order to maintain bodyweight and a minimum body condition score of

5. The concentrate was formulated to meet or slightly exceed nutrient requirements for

late gestation and lactation based on NRC recommendations (NRC, 1989). From

December to March, mares were fed Coastal bermudagrass hay ad-libitum and had access

to dormant bahiagrass pasture. From April to June, mares only had access to bahiagrass

pasture. Trace mineralized salt blocks were available at all times. Foals were provided

with access to the same grain-based concentrate that was fed to mares via creep feeders

that were placed in the pasture.

Mares received one of three treatments: 1) basal diet with no supplementation

(CON, n = 12); 2) basal diet supplemented with milled flaxseed (Pizzey's Milling,

Manitoba, Canada; FLAX, n=12); or 3) basal diet supplemented with encapsulated fish

oil (United Feeds, Inc., Indiana; FISH, n = 12). Both FLAX and FISH were fed to mares

in amounts to provide 6 g total n-3 FA/100 kg BW per day. This level of

supplementation was chosen based on the studies of O'Connor et al. (2004) and Siciliano

et al. (2003) which demonstrated changes in plasma fatty acid composition when horses

were supplemented with similar levels of fish oil. Mares and foals were brought in from

pasture at 0700 and 1500 h each day, placed into box stalls and individually fed the grain

mix concentrate. Half of the daily allotment of flaxseed or fish oil supplement was hand

mixed into the grain provided in the morning feeding and the remaining half of the

supplements were mixed into the grain provided in the afternoon feeding. Foals had the









opportunity to share the mares' feed, but this depended upon the individual temperament

of each mare. Supplementation began 28 days before the expected foaling date and

continued until 84 days post-partum.

The nutrient composition of the grain-based concentrate and the flaxseed and

encapsulated fish oil supplements is presented in Table 3-1. The nutrient content of the

Coastal bermudagrass hay and bahiagrass pasture is presented in Table 3-2.



Table 3-1. Nutrient composition of the grain mix concentrate and the milled flaxseed and
encapsulated fish oil supplements
Nutrients Concentrate Flaxseed Fish Oil

DM, %2 92.7 91.5 91.2

DE, Mcal/kg3 3.41 3.0 3.7
CP, % 15.5 22.9 11.8
ADF, % 11.9 19.0 5.9
NDF, % 26.3 40.0 9.9
Fat, % 4.2 37.7 21.5
Ca, % 1.06 0.24 0.33

P, % 0.70 0.74 0.15

Zn, mg/kg 248 41 33
Cu, mg/kg 64 11 4
SValues are presented on a 100% DM basis (except DM).
2 DM, dry matter; DE, digestible energy; CP, crude protein; ADF, acid detergent fiber;
NDF, neutral detergent fiber.
3 Calculated using the equation: DE (Mcal/kg) = 4.07 0.055(%ADF) (NRC, 1989).










Table 3 -2. Nutrient composition of the bahiagrass pasture (by month) and Coastal
bermudagrass hay


Pasture

Jan. Feb. March April

64.1 65.0 44.1 30.5

1.9 2.0 1.9 2.2

10.7 11.7 11.8 16.0

41.4 40.2 43.5 35.4

68.5 64.5 67.7 54.7

2.1 2.5 2.4 3.1

0.61 0.68 0.64 0.72

0.24 0.25 0.25 0.36

38 36 40 32

6 6 8 8


Nutrient

DM, %2

DE,Mcal/kg3

CP, %

ADF, %

NDF, %

Fat, %

Ca, %

P, %

Zn,mg/kg

Cu,mg/kg


Dec.

45.2

1.9

11.2

42.6

69.3

1.9

0.53

0.29

27

6


May
23.0

2.4

19.2

34.4

59.4

3.1

.50

0.39

33

8


June

17.5

2.3

19.4

36.6

63.0

3.0

0.40

0.40

30

9


Hay
90.8

1.9

8.9

38.1

71.4

1.5

0.35

0.21

46

5


Presented on a 100% DM basis (except DM).
2 DM, dry matter; DE, digestible energy; CP, crude protein; ADF, acid detergent fiber;
NDF, neutral detergent fiber.
3 Calculated using the equation: DE (Mcal/kg) = 4.22 0. 11(%ADF) + 0.0332(%CP) +
0.00112(%ADF)2 (NRC, 1989).


Bodyweights

Mares were weighed at 28 and 14 d prior to expected foaling date (d-28, d-14), at

foaling (dO) and every 14 days thereafter. Foals were weighed at birth (dO) and every 14

days thereafter. A digital livestock scale with an accuracy of a 0.5 kg was used to obtain

body weights.

Blood Sample Collection and Processing

Blood samples were collected from mares by jugular venipuncture at 28 and 14 d

prior to expected foaling, at foaling (dO), and at 28, 56 and 84 d after foaling for

acquisition of plasma, serum and/or red blood cells. Blood samples were collected from









foals via jugular venipuncture at birth before the foal was allowed to nurse (dO), 36 h

post-parturition, and 7, 28, 56 and 84 d post-foaling for acquisition of plasma, serum

and/or red blood cells. A square patch of hair was shaved over the foal's jugular vein to

allow for easier blood sampling. Precision Glide Vacutainer brand blood collection

needles (20G, 1 V/2 in. for mares; 20G, 1 in. for foals) were used to collect blood into

Beckton Dickinson Vacutainers containing sodium heparin, to facilitate harvesting of

plasma and red blood cells, or tubes containing no anticoagulant for harvesting of serum.

With the exception of samples obtained at birth or 36 h post-parturition, all blood

samples were collected between 0700 and 0900 h and prior to the mare's morning grain

feeding. After collection, blood samples were immediately placed on ice and transported

to the Animal Nutrition Laboratory for further processing.

In the laboratory, blood samples for obtaining serum were allowed to clot for 30

min to 1 h and then centrifuged at 5590 x g for 7 min to allow for separation of serum.

Serum was collected with plastic disposable pipets and aliquoted into polypropylene

cryogenic vials (2-3 vials, 0.5-1.0 mL each). Samples were frozen at -800C until further

analysis for IgG using a commercially available single radial immunodiffusion kit (SRID

Kit, VMRD, Inc., Pullman, WA). See Appendix B for a description of the IgG analysis.

Blood samples for obtaining plasma and red blood cells were first used to

determine the hematocrit (packed cell volume). Hematocrit values were determined in

duplicate using whole blood drawn into a microcapillary tube, centrifuged and read on a

microcapillary reader. After determination of hematocrit, each vacutainer was gently

rotated and 5.0 mL of whole blood was pipetted into a separate glass tube, labeled, and

centrifuged at 5590 x g for 15 minutes to separate the plasma and red blood cells. A










pipet was used to transfer 1.0 mL of plasma to each of four polypropylene cryogenic

vials. Samples were frozen on a slant at -200C to increase the surface area and ensure

more efficient freeze drying before being stored at -800C until further analysis of fatty

acids.

Once plasma had been removed, an aspirator was used to remove any additional

plasma and the thin layer of while blood cells lining the top of the red blood cells in each

tube. Two mL of cold saline was then added to each tube and the tubes were gently

mixed and centrifuged at 5590 x g for 7 min. After centrifuging, the supernatant was

aspirated off and an additional 2.0 mL of cold saline was added. The tubes were again

mixed and centrifuged at 5590 x g for 7 min. This procedure was repeated once more for

a total of three saline washes. After the supernatant of the final wash had been aspirated

off, exactly 2.0 mL of cold saline was added to the remaining red blood cells in each

tube. The tubes were mixed well before 2.0 mL of the red blood cell suspension was

transferred into labeled polypropylene cryogenic vials. These tubes were frozen at an

angle at -200C before being placed into storage at -800C until analyzed for fatty acid

content.

Colostrum and Milk Collection and Processing

Colostrum was obtained from the mare within 1 h of birth and before the foal had

suckled (dO). Approximately 120 mL of colostrum was recovered into a pre-labeled, pre-

weighed plastic cup. The cup was covered with a lid and stored at 40C until transfer to

the Animal Nutrition Laboratory for processing.

Milk samples were obtained 36 h post-partum and between 0700 and 0900 h on 7,

14, 28, 56 and 84 d post-foaling for determination of fatty acid and IgG content. To

facilitate milk collection, foals were muzzled for approximately 30 min to allow the









mare's udder to fill. The entire udder was then milked out into a pre-labeled, pre-

weighed plastic cup. If the udder contained more milk than one cup could hold, the udder

was milked out into multiple cups whose content was then mixed in a larger container

and approximately 120 mL was transferred to the pre-labeled, pre-weighed sample cup.

The excess milk was discarded. After collection, milk samples were immediately placed

on ice and transported to the Animal Nutrition Laboratory for further processing.

In the laboratory, colostrum and milk samples were gently swirled to mix and

strained through four layers of cheesecloth to remove any dirt and debris in the sample.

The samples were then returned back to the original pre-weighed sample cups. After

straining, the sample was mixed again and approximately 1.0 mL was aliquoted into each

of three pre-labeled polypropylene cryogenic vials. These vials were then stored at -800C

until further analysis for IgG content. The remaining colostrum or milk sample was

weighed to determine a wet sample weight and then freeze dried. Freeze dried milk

samples were stored at -200C until used for the determination of fatty acid composition.

Fatty Acid Analysis

Fatty acids in plasma and red blood cells were extracted and methylated using the

procedure of Folch et al. (1957). Fatty acids were analyzed by gas chromatography (CP-

3800 Gas Chromatograph, Varian, Inc., Palo Alto, CA) using a WCOT fused silica

column (CP-SEL 88, lengthl00 m, internal diameter 0.25 mm, flow rate 5.0 mL/min,

Varian, Inc., Palo Alto, CA). The carrier gas was helium with a pressure of 29.5 psi (1

min), 35.4 psi (0.42 psi/min, total of 45 min) and 37.9 psi (0.17 psi/min, held for 50 min,

total of 110 min). The temperature program was 1200C for 1 min, increased to 1900C at

50C/min and held at 1900C for 30 min (total of 45 min), increased to 2200C at 20C/min

and held at 2200C for 50 min, giving a total run time of 110 min. Fatty acids were









identified by comparison of peak retention times for samples and reference standards

(Nu-Chek Prep, Inc., Elysian, MN). The FA identified included C8:0, C10:0, C12:0,

C14:0, C14:1, C16:0, C16:1, C17:0, C17:1, C18:0, C18:1n-9, C18:2n-6 (LA), C18:3n-3

(ALA), C20:0, C20:1, C20:2, C20:3, C20:4n-6 (AA), C20:5n-3 (EPA), C22:0, C22:5n-3,

C22:6n-3 (DHA) and C24:1. Nonadecanoic acid (C19:0) was added to the samples and

used as an internal standard to assess FA recovery. Total n-6 FA were defined as the sum

of C18:2 n-6 and C20:4n-6 while total n-3 FA were defined as the sum of C18:3n-3,

C20:5n-3, C22:5n-3 and C22:6n-3.

Intradermal Skin Test

To examine the effect of n-3 FA supplementation on the inflammatory response,

mares and foals were sensitized with phytohemagglutinin (PHA; Lectin from Pha~seobts

vulgaris, Sigma-Aldrich, Inc., St. Louis, Missouri) at 84 d post-partum. Twenty-Hyve

milligrams of PHA was reconstituted in 16.7 mL of phosphate buffered saline (PB S) to

give a Einal concentration of 150 Cpg/100 CLL. A 4 x 4 cm patch of hair was surgically

clipped on the midsection of both sides of the neck on mares and foals and inj ected

intradermally with 100 pIL of the PHA suspension. Precision Glide brand intradermal

inj section needles (26 G, 3/8 in.) were used to deliver the PHA. Needles were changed

between each inj section site on the right and left side of the neck. Skin thickness

measurements were obtained by pinching the skin between the thumb and forefinger and

measuring the skin fold thickness in mm with an electronic digital micrometer (Marathon

Watch Company, Ltd., Ontario, Canada). Measurements of each injection site were

obtained after clipping but before inj ecting (h 0) and at 2, 4, 6, 8, 12, 24 and 48 h after

inj section. Skin thickness measurements from the right and left sides of the neck were

averaged to give a single thickness measurement for each time point.










Supplement and Feed Sample Analysis

The same batch of milled flaxseed, encapsulated fish oil and Coastal bermudagrass

hay were available for the duration of the trial. However, the source of commercial grain

mix was replenished approximately every 2 wk due to storage limitations and the volume

of feed needed. Samples of the flaxseed, encapsulated fish oil and grain mix were

obtained at 4 wk intervals. These samples were then dried at 600C and stored at 200C for

later analysis. Samples of bahiagrass pasture were obtained at 4 wk intervals from four,

16 ha pastures. Pasture grass clippings were only obtained from areas where grazing was

evident. At each 4-wk collection, clippings from the four pastures were composite,

dried at 600C and stored at 200C for later analysis. Throughout the trial, each round bale

of Coastal bermudagrass hay that was offered to the mares was core sampled (5 cores per

bale), dried at 600C and stored at 200C. After the completion of the trial, all samples of

Coastal bermudagrass hay were composite into one sample for analysis. All feeds and

supplements were analyzed for fatty acid content using the method described above. In

addition, feeds were analyzed for DM, DE, CP, NDF, ADF, total fat, Ca, P, Mg, Zn and

Cu by wet chemistry (Dairy One Forage Analysis Lab, Ithaca, NY).

Statistical Analysis

Four mares either delivered dead foals or their foals died shortly after birth. Only

pre-foaling data was used from these mares. One mare experienced a red bag during

foaling and her foal was subsequently given plasma, so IgG data from this mare and foal

were not included in the statistical analysis. One foal was euthanized at 30 d of age, so

only data taken up to that time point were used. The final number of mare and foal pairs

successfully completing this study was 11 CON, 11 FLAX and 9 FISH.










The MIXED procedure of SAS (V. 9.1, SAS Inst., Inc., Cary, NC) was used to

analyze fatty acid composition of colostrum, milk, plasma and all feeds, IgG content of

colostrum, milk, mare serum and foal serum, and mare and foal bodyweights. The

sources of variation included treatment, time and treatment x time interaction. Breed

effects were also tested for mare and foal bodyweights, mare serum IgG, mare colostrmm

and milk IgG and foal serum IgG. Sex effects were tested for foal serum IgG. In

addition, principle forage source (hay or pasture) was examined as a main effect for mare

plasma and red blood cell fatty acids. Fatty acids analyzed included linoleic (LA), co-

linolenic (ALA), arachidonic (AA), eicosapentaenoic (EPA) and docosahexaenoic (DHA)

acids as well as total n-3 and total n-6 fatty acids and the ratio of n-6:n-3 fatty acids. For

IgG and fatty acid analysis, horse nested within treatment was considered as a random

variable and used as an error term to test the effects of all sources of variation. Dunnett' s

test was used to separate means. The homogeneity of regression for skin thickness values

was evaluated using the GLM and MIXED procedures in SAS. Horse nested within

treatment was used as an error term.

Due to missing values and unbalanced treatment groups after foaling, all data are

expressed as least square means + SE unless otherwise stated. Values were considered

significant at p < 0.05 and trends were considered at p < 0.10.















CHAPTER 4
RESULTS

Feed and Supplement Analysis

The fatty acid composition of the grain mix concentrate and the flaxseed and

encapsulated fish oil supplements is presented in Table 4-1. The fatty acid composition

of pasture forage was similar from December through March (Appendix A). Therefore,

the fatty acid composition of pasture samples collected in December, January, February

and March was averaged and presented as "winter" pasture (Table 4-2). Similarly, the

fatty acid composition of pasture forage was not different between the months of April,

May and June (Appendix A). Thus, the fatty acid composition of pasture samples from

these months was also averaged and presented as "spring" pasture (Table 4-2).

Spring pasture contained lower quantities of C18:0 (P = 0.01) and C18:1 (P =

0.004) and higher quantities of ALA (P = 0.03) and total n-3 FA (P = 0.03) than winter

pasture (Table 4-2). Hay contained higher concentrations of C16:0 (P = 0.0001), C18:0

(P = 0.003) and C18:1 (P = 0.0001) compared to winter and spring pasture forage (Table

4-2). In addition, hay contained lower concentrations of ALA (P = 0.0001) resulting in a

lower total n-3 FA content (P = 0.0001) and a higher n-6:n-3 FA ratio (P = 0.0001) in hay

compared to winter and spring pasture (Table 4-2). No differences were observed in LA,

AA, EPA, DHA or total n-6 FA content between hay and pasture forage. When principle

forage source (hay or pasture) was included in the model as a main effect, forage source

did not influence FA levels in any of the milk or blood samples examined in this study (P

= 0. 11).









Mare Fatty Acid Intake

Horses were housed on bahiagrass pastures throughout the trial. Because of winter

dormancy and reduced quantity of pasture forage, mares were offered unlimited access to

Coastal bermudagrass hay during the months of December, January, February and March.

During this four month period, hay was assumed to be the primary forage source.

Limited evidence of grazing in pastures and reasonable consumption of hay (based on the

number of round bales fed and expected DM intake) during this period support this

assumption. All hay was removed from pastures in the first week of April. Therefore,

pasture served as the primary forage source from April until the conclusion of the trial in

late June.

Average daily intake of long chain FA by mares on each treatment from December

to March (when Coastal bermudagrass hay was the primary forage source) and from

April to June (when bahiagrass pasture was the primary forage source) is shown in Tables

4-3 and Table 4-4, respectively.

From December to March (when hay was the primary forage source), FLAX mares

consumed 255% more n-3 FA and FISH mares consumed 257% more n-3 FA than CON

mares. From April to June (when pasture was the primary forage source), FLAX and

FISH mares consumed 138% and 137% more n-3 FA than CON mares, respectively.

This change in percentages reflects the higher n-3 FA content of spring bahiagrass

pasture compared to Coastal bermudagrass hay. From December to March, the total

diet provided a total n-3 FA intake of 4.3 g n-3 FA/100 kg BW in CON mares, 11.3 g n-3

FA/100 kg BW in FLAX mares and 11.3 g n-3 FA/100 kg BW in FISH mares. From

April to June, the total diet provided a total n-3 FA intake of 17.4 g n-3 FA/100 kg BW in

CON mares, 24.8 g n-3 FA/100 kg BW in FLAX mares and 24.3 g n-3 FA/100 kg BW in









FISH mares. Within the supplemented groups, the milled flaxseed and encapsulated fish

oil supplied 6.5 to 7.0 g total n-3 FA/100 kg BW, or approximately 65% of the total n-3

FA intake in the winter and 30% of the total n-3 FA intake in the spring.

For the duration of the trial, FLAX mares consumed higher ALA (P = 0.0001) than

FISH and CON mares while FISH mares consumed higher EPA (P = 0.0001) and DHA

(P = 0.0001) than FLAX and CON mares. There were no differences between the

consumption of total n-3 FA between FISH and FLAX mares (P = 0.94), but both

treatments consumed more total n-3 FA than CON mares (P = 0.0001). No treatment

effect was observed for total n-6 FA intake (P = 0.12).

Mare and Foal Bodyweight

Treatment had no effect on mare BW at any time during the trial (Table 4-5). CON

mares foaled 3 colts and 9 fillies, FLAX mares foaled 7 colts and 5 fillies and FISH

mares foaled 4 colts and 8 fillies. There were no differences in foal BW due to sex (P =

0.58), breed (P = 0.62) or treatment (P = 0.75). At birth, CON foals weighed 51.0 & 4.1

kg and gained 107.3 & 4.1 kg over the trial period. FLAX foals weighed 54.4 & 3.5 kg at

birth and gained 103.9 & 3.5 kg, and FISH foals weighed 56.3 & 3.8 kg at birth and

gained 107.6 & 3.9 kg over the trial period (Table 4-6). There was a significant effect of

time (P = 0.0001) on foal BW, which reflected an increase in BW as foals grew from

birth to 84 d of age.

Mare Plasma Fatty Acid Composition

Omega-6 Fatty Acids

The FA found in the highest concentration in mare plasma was LA, which made up

almost half of the total FA found in plasma (Table 4-7). An overall treatment effect was

noted for mare plasma LA, AA and total n-6 FA (Table 4-7). Before supplementation









began (d-28), plasma n-6 FA concentrations were similar between treatments (Table 4-8).

In response to supplementation, mares fed FISH had lower plasma LA (P = 0.05), greater

plasma AA (P = 0.03) and tended to have lower plasma total n-6 FA (P = 0. 10) than

FLAX or CON mares (Tables 4-7 and 4-8).

An overall effect of time was detected for plasma LA (P = 0.07), AA (P = 0.01) and

total n-6 FA (P = 0.08) and may have reflected the effects of both parturition and dietary

treatment (Table 4-8). Plasma LA declined from baseline (d-28) to foaling (dO) in CON

(P = 0.05) and FISH mares (P = 0.02). After foaling, plasma LA returned to pre-

treatment levels in CON mares but remained lower in FISH mares. Plasma AA increased

(P = 0.01) from baseline to foaling in FISH mares but did not change in CON mares.

Total plasma n-6 FA decreased from d-28 to dO in CON (P = 0.05) and FISH mares (P =

0.04, Figure 4-1). In contrast to the responses seen in FISH and CON mares, plasma LA,

AA and total n-6 FA did not change over the course of the trial in FLAX mares.

Omega-3 Fatty Acids

The n-3 FA found in the highest concentration in mare plasma was ALA, with

concentrations ranging from 2.99 to 3.65 g ALA/100 g fat (Table 4-7). Overall treatment

effects were detected for plasma ALA, EPA, DHA and total n-3 FA (Table 4-9). Before

supplementation, no differences in plasma n-3 concentrations were observed between

treatment (Table 4-9). In response to dietary treatment, FISH mares had higher plasma

EPA (P = 0.0001), higher plasma DHA (P = 0.0001) and higher plasma total n-3 FA (P =

0.01) than CON mares (Table 4-7). When mares were fed FLAX, plasma ALA tended to

be higher (P = 0.09) than that observed in the plasma of CON or FISH and total n-3 FA

plasma content was similar to both FISH and CON mares (Table 4-7).









Overall effects of time were detected in plasma ALA (P = 0.02), EPA (P = 0.0001),

DHA (P = 0.001) and total n-3 FA (P = 0.0005; Table 4-9). From d-28 to dO, plasma

ALA increased in FLAX mares (P = 0.05) but decreased in FISH mares (P = 0.02). After

foaling, the plasma ALA of FISH mares returned to baseline levels while the plasma

ALA of FLAX mares remained at an elevated level. Plasma ALA did not change over

time in CON mares. Plasma EPA increased (P = 0.002) through d+28 in mares fed FISH,

after which this FA stabilized at levels above CON and FLAX mares. Plasma DHA and

total n-3 increased (P = 0.001) in response to FISH, but remained unchanged in the

plasma of CON or FLAX mares for the duration of the trial (Table 4-9; Figure 4-2). In

contrast to the effects observed in FISH mares, plasma EPA, DHA and total n-3 FA did

not change in response to dietary treatment in FLAX or CON mares (Table 4-9; Figure 4-

2).

Treatment did not affect the ratio of n-6:n-3 FA in mare plasma (P = 0.24; Table 4-

10). However, an overall effect of time was detected, as the ratio of plasma n-6:n-3 FA

decreased over the course of the trial in all treatments (P = 0.02; Table 4-10).

Mare Colostrum and Milk Fatty Acid Composition

Treatment had no effect on the total fat content of mare colostrum (P = 0.95) or

milk (P = 0.12, Table 4-11). As colostrum transitioned into milk, the total fat content

increased (P = 0.0003) for all treatments (Table 4-11). The FA found in the highest

concentrations in mare colostrum and milk were C16:0, C18:1 and LA (Table 4-12).

An overall effect of time was detected for all FA examined in mare milk (Tables 4-

13 and 4-14). All treatments experienced a decrease in total milk n-6 FA (P = 0.0001)

and an increase in total milk n-3 FA (P = 0.0001) as lactation progressed (Tables 4-13

and 4-14). As a result, the ratio of n-6:n-3 FA decreased in mare milk from foaling









through 84 d post-foaling (P = 0.0001; Table 4-10). From 36h to through 14 d post-

foaling, milk LA and total n-6 FA decreased in FLAX (P = 0.0005) and FISH mares (P =

0.0003), and then remained constant for the duration of the trial (Table 4-13). Milk from

mares fed FISH showed an increase in EPA (P = 0.0001) and DHA (P = 0.0001) content

from 36h to through 14 d post-foaling, and these levels remained steady until 84 d post-

foaling (Table 4-14).

Overall effects of treatment were not noted for any of the n-6 FA examined in

mare milk (Table 4-12, Figure 4-3). However, overall effects of treatment were observed

for milk ALA (P = 0.0001), EPA (P = 0.0001), DHA (P = 0.0001) and n-6:n-3 FA ratio

(P = 0.01; Tables 4-10 and 4-12). At foaling, the colostrum of FLAX mares contained

higher levels of ALA (P = 0.05) than CON and FISH mares (Table 4-14, Figure 4-4). As

lactation progressed, FLAX mares continued to have a higher ALA content in their milk

compared to FISH or CON mares (P = 0.01). FISH mares had a higher colostrum DHA

content than CON and FLAX mares (P = 0.03) and had higher EPA (P = 0.0001) and

DHA (P = 0.0001) concentrations in milk than CON or FLAX mares as lactation

progressed (Table 4-14, Figure 4-4). The colostrum of FLAX mares contained greater

total n-3 FA than the colostrum of CON mares (P = 0.05), but total n-3 FA was not

different than FISH mares. Over the course of lactation, the n-6:n-3 FA ratio tended to be

lower in the milk of FLAX mares (P = 0.09) when compared to the milk of CON and

FISH mares (Table 4-10).

Foal Plasma Fatty Acid Composition

Omega-6 Fatty Acids

Similar to the mare, the FA found in the highest concentration in foal plasma was

LA, making up roughly one third of the total FA found in plasma (Table 4-15). An









overall treatment effect was not observed for any of the n-6 FA examined in foal plasma

(Table 4-16, Figure 4-5). However, at foaling (dO), plasma AA concentrations were

highest in foals born to FLAX mares (P = 0.04, Table 4-16). At 14 d post-foaling, foals

suckling FISH mares showed a higher plasma AA concentration than foals suckling CON

mares (P = 0.04), but were similar to foals suckling FLAX mares (P = 0.30). No other

effects of treatment on n-6 FA were detected at any time point over the course of the trial.

An overall effect of time was detected in plasma LA (P = 0.0001), AA (P = 0.0001)

and total n-6 FA (P = 0.0001; Table 4-16, Figure 4-4). Plasma LA and total n-6 FA

increased (P = 0.0001) and plasma AA decreased (P = 0.0001) from foaling to 14 d post-

foaling in all treatments (Table 4-16). Plasma LA and total n-6 FA increased from 14 to

84 d of age in foals suckling CON (P = 0.005) and FISH mares (P = 0.008), but remained

stable in foals nursing FLAX mares. Plasma AA increased from 14 to 84 d of age in

Omega-3 Fatty Acids

The n-3 FA found in the highest concentration in foal plasma was ALA, with levels

ranging from 2.48 to 3.33 g ALA/100 g fat (Table 4-15). An overall effect of treatment

was observed in foal plasma ALA, EPA, DHA and total n-3 FA (Table 4-15, Figure 4-6).

At foaling, foals born to FISH mares tended to have a higher total n-3 FA plasma content

than foals born to CON or FLAX mares (P = 0.09; Table 4-17, Figure 4-6). Foals

suckling FLAX mares had higher plasma ALA (P = 0.04) than foals suckling CON mares

and foals nursing FISH mares had higher plasma EPA (P = 0.0001), DHA (P = 0.0001)

and total n-3 FA (P = 0.002) than foals nursing both CON and FLAX mares (Table 4-15

and 4-17).

An overall effect of time was detected in all n-3 FA in foal plasma (P = 0.0001;

Table 4-17, Figure 4-6). From foaling to 84 d of age, the plasma ALA and total n-3 FA









content increased in foals, regardless of mare treatment (P = 0.0001). Plasma EPA

increased in FLAX foals from foaling to 28 d of age (P = 0.0001), but returned to foaling

levels by 56 d of age (Table 4-17). Plasma EPA increased from birth to 14 d of age in

FISH foals (P = 0.0001), but decreased from 28 to 56 d of age. However, the plasma

EPA concentration in FISH foals was still higher at 84 d of age than the concentrations at

foaling (P = 0.0005). From birth to 14 d of age, plasma DHA decreased in CON (P =

0.0001) and FLAX (P = 0.0001) foals and then remained steady until the end of the trial.

However, the DHA concentration in the plasma of FISH foals remained elevated through

56 d of age, declining slightly by 84 d (Table 4-17).

Omega-6:Omega-3 Fatty Acid Ratios

An overall effect of treatment on the n-6:n-3 ratio was observed in foal plasma

(Table 4-10). At birth, no difference in n-6: n-3 FA ratio was detected between

treatments. After suckling treated mares, FISH foals had a lower n-6:n-3 FA ratio (P =

0.002) than FLAX or CON foals (Table 4-10). An overall effect of time on the n-6:n-3

FA ratio was also detected in foal plasma (P = 0.001, Table 4-10). From birth to 14 d of

age, the plasma n-6:n-3 ratio increased in CON (P = 0.001) and FLAX (P = 0.01) foals.

The plasma n-6:n-3 FA ratio returned to levels seen at foaling by 28 d of age in FLAX

foals, while the plasma n-6:n-3 FA ratio of CON foals did not return to baseline levels

until 56 d of age. The plasma n-6:n-3 ratio in FISH foals remained steady over the course

of the trial (Table 4-10).

Fatty Acid Correlations

Positive correlations (P = 0.0001) between mare plasma and milk FA were found

for ALA, EPA, DHA and total n-3 FA, while a negative, but weak correlation between

mare plasma and mare milk was found for total n-6 FA (P = 0.003; Table 4-18). No









correlation was found between mare plasma LA and mare milk LA, while mare plasma

AA and mare milk AA tended to be negatively correlated (P = 0.10).

Mare milk ALA, EPA, DHA and total n-3 FA were positively correlated (P =

0.0001) with foal plasma ALA, EPA, DHA and total n-3 FA (Table 4-18). Mare milk

AA and total n-6 FA were negatively correlated to foal plasma AA (P = 0.0001) and total

n-6 FA (P = 0.03). No correlation between milk LA and foals plasma LA was detected.

Fatty Acid Composition of Red Blood Cells

Mare Red Blood Cell Fatty Acids

Fatty acids with chain lengths longer than 18 carbons were not detected in mare red

blood cells, and LA was the only n-6 FA observed (Table 4-19). An overall effect of

treatment was noted for LA (Table 4-19, Figure 4-7). While no differences in LA

concentration were found in mare red blood cells before supplementation, there was a

tendency (P = 0.10) for FISH mares to have a higher red blood cell LA content than both

CON and FLAX mares (P = 0.10, Table 4-19). An overall effect of time was not detected

for mare red blood cell n-6 FA content (Table 4-20, Figure 4-7). However, the red blood

cell LA content of FISH mares increased from pre-supplementation to foaling (P = 0.02;

Table 4-20). The LA content of CON and FLAX red blood cells did not fluctuate during

the study (Table 4-20).

Foal Red Blood Cell Fatty Acids

Linoleic acid was the only n-6 FA and ALA was the only n-3 FA found in foal red

blood cells; fatty acids with chain lengths longer than 18 carbons were not detected

(Table 4-21). An overall effect of treatment was detected for red blood cell LA, but not

ALA (Table 4-21). At foaling, no differences were observed in red blood cell LA content

(Table 4-22, Figure 4-8). In response to suckling supplemented mares, FISH foals had a









higher red blood cell LA content than both CON and FLAX foals (P = 0.04, Table 4-21,

Figure 4-8). Foals belonging to FLAX mares had higher (P = 0.03) ALA in red blood

cells at birth than foals belonging to CON mares, but had similar red blood cell ALA as

foals born to FISH mares. Treatment of the mare did not affect ALA content of foal red

blood cells at any other time point during the study (Table 4-22, Figure 4-9).

An overall effect of time was found in foal red blood cell LA (P = 0.03) but not

ALA (Table 4-22). The LA content of red blood cells increased in FISH foals from

foaling to 14 d of age (P = 0.01) and stayed elevated for the duration of the study. In

contrast, the LA in red blood cells of CON and FLAX foals did not change during the

trial (Table 4-22).

Mare Serum, Colostrum and Milk IgG

An overall effect of treatment was not detected in mare serum or colostrum IgG

concentrations (Table 4-23). Mare breed (P = 0.78) or age (P = 0.56) did not affect

serum IgG content. Similarly, colostrum IgG was not affected by mare breed (P = 0.67)

or age (P = 0.58).

Milk IgG was not affected by treatment (P = 0.65) or breed (P = 0.67, Table 4-24).

However, an overall effect of time on milk IgG was detected (P = 0.0001, Table 4-24).

Milk from all mares showed a decline in IgG from 36 h through 84 d post-foaling (Table

4-24). The overall decline in milk IgG concentration from 36 h to 84 d post-partum was

139.4 & 630.7 mg/dL for CON mares, 157.0 & 677.5 mg/dL for FLAX mares and 132.5 &

659.2 mg/dL for FISH mares.

Mare serum IgG at foaling was not correlated with mare age (Table 4-25).

Similarly, colostrum IgG was not correlated with mare age, although FLAX mares tended

to show an inverse relationship (r = -0.58, P = 0.06) between mare age and colostrum IgG










(Table 4-25). Mare serum IgG at foaling was not correlated to colostrum IgG, and

colostrum IgG was not correlated to foal serum IgG at 36 h post-foaling. However, a

weak correlation between mare serum IgG at foaling and foal serum IgG at 36 h post-

foaling was detected across treatments (r = 0.42, P = 0.02; Figure 4-10). Within

treatments, dO serum IgG from CON and FLAX mares showed no correlation with foal

36h serum IgG content, but serum IgG from FISH mares at dO was correlated to FISH

foals serum IgG at 36 h post-foaling (r = 0.63, P = 0.05, Table 4-25).

Foal Serum IgG

All foals had serum IgG concentrations that were very low at birth and reflected the

pre-suckle status of the foal (Figure 4-1 1). The IgG content of foal serum increased to,

and peaked at, 36 h post-foaling, indicating that passive transfer of IgG had taken place.

An overall effect of time was noted for foal serum IgG (P = 0.0001), as the IgG of all

foals steadily declined from 36 h to 84 d post-foaling (Table 4-25, Figure 4-12).

No overall effect of treatment was observed for foal serum IgG (Table 4-25).

However, foals suckling FISH mares tended to have lower serum IgG than foals nursing

FLAX mares at 36h (P = 0.09) and 7 d post-foaling (P = 0.10). In addition, FISH foals

tended to have lower IgG than CON foals at 28 d post-foaling (P = 0.10).

Mare and Foal Responses to the Intradermal Skin Test

Mare Response to PHA

An overall effect of treatment was not detected in the skin thickness of mares in

response to a paired intradermal skin test using PHA as the stimulant (P = 0.89; Table 4-

26). However, an overall effect of time was observed (P = 0.0001; Table 4-26). Before

inj section, no differences were observed in mare skin thickness (P = 0.56; Figure 4-13).

All mares experienced a significant increase in skin thickness from 0 to 2 h (P = 0.0001)









and from 2 to 4 h post-inj section (P = 0.0001; Table 4-26, Figure 4-13). Skin thickness

was greatest between 4 and 8 h post-injection and then decreased. At 48 h, skin thickness

was still elevated above that measured before PHA inj section at 0 h (P = 0.0001).

Foal Response to PHA

An overall effect of time (P = 0.0001) on skin thickness in foals in response to PHA

injection was detected, reflecting an inflammatory response (Figure 4-14). Foal skin

thickness increased (P = 0.0001) from 0 to 4 h, remained elevated through 8 h post-

injection and then declined through 48 h post-injection (P = 0.0001, Figure 4-14). At 48

h post-inj section, skin thickness had not yet declined to baseline thickness measured

before PHA inj section (P = 0.0001).

An overall effect of treatment on foal skin thickness was not detected (P = 0.58;

Table 4-27). However, CON foals peaked at 4 h (P = 0.0001), whereas skin thickness

remained elevated in FLAX and FISH foals through 6 h (P = 0.0001; Figure 4-14, Table

4-27). At 6 h post-inj section, FLAX foals had greater skin thickness than CON foals (P =

0.02), while the skin thickness of FISH foals was intermediate between FLAX and CON

foals.

Comparing Mare and Foal Responses to PHA

Across treatments, skin thickness in response to PHA inj section was different

between mares and foals (P = 0.0001; Table 4-28, Figure 4-15). Although thickness was

not different before inj section of PHA (Oh), mares exhibited a greater (P = 0.0001)

inflammatory response to intradermal PHA compared to foals (Table 4-28, Figure 4-15).

The skin thickness of neither the mares or the foals returned to pre-inj section values by 48

h post-inj section (P = 0.0001).









Table 4-1. Fatty acid composition of the grain mix concentrate and the milled flaxseed
and encapsulated fish oil supplements
Fatty acid Grain mix Flaxseed Fish Oil
C8:0 ND ND ND

C10:0 ND ND ND

C12:0 ND ND ND

C14:0 ND ND 8.62

C16:0 17.18 5.60 21.14

C16:1 0.21 ND 13.77

C17:0 ND ND ND

C17:1 ND ND ND

C18:0 2.20 2.77 3.79

C18:1 26.28 13.90 7.87

C18:2n-6 (LA) 49.63 16.31 7.23

C18:3n-3 (ALA) 3.72 61.20 2.35

C20:4n-6 (AA) ND ND 0.69

C20:5n-3 (EPA) ND ND 15.03

C22:5 n-3 (DPA) ND ND 2.11

C22:6n-3 (DHA) ND ND 12.54
Total n-62 49.63 16.31 7.92

Total n-33 3.72 61.20 32.03

n-6:n-3 13.34 0.27 0.25
SPresented as g fatty acid per 100 g fat; ND = not detected in the feed stuff
2 Calculated as C18:2 + C20:4.
3 Calculated as C18:3 + C20:5 + C22:5 + C22:6.









Table 4-2. Fatty acid composition of winter and spring bahiagrass pasture and Coastal
bermudagrass hay'
Pasture

Fatty acid Winter2 Spring3 Hay
C8:0 ND ND ND
C10:0 ND ND ND
C12:0 ND ND ND
C14:0 ND ND ND
C16:0 22.07 & 0.69a 23.22 & 0.67a 39.30b
C16:1 ND ND ND
C17:0 0.93 & 0.05a 0.531 0.28a 0.00b
C17:1 ND ND ND
C18:0 4.97 & 0.38a 3.36 & 0.22b 6.65"
C18:1 4.21 & 0.60a 1.39 & 0.02b 7.080

C18:2n-6 (LA) 23.71 + 1.96 18.13 A 1.55 23.48
C18:3n-3 (ALA) 41.52 & 3.28a 52.47 & 1.76b 15.900
C20:4n-6 (AA) ND ND ND
C20:5n-3 (EPA) ND ND ND
C22:5 n-3 (DPA) ND ND ND
C22:6n-3 (DHA) ND ND ND
Total n-64 23.71 + 1.90 18.13 A 1.55 23.48
Total n-35 41.52 & 3.28a 52.47 & 1.76b 15.900
n-6:n-3 0.59 & 0.08a 0.35 & 0.04a 1.45b
SPresented as g fatty acid per 100 g fat; ND not detected in the forage.
2 Winter Mean of December, January, February and March.
3 Spring = Mean of April, May and June.
4 Calculated as C18:2 + C20:4.
SCalculated as C18:3 + C20:5 + C22:5 + C22:6.
a,b,c Values in the same row having different superscripts differ at P < 0.05.










Table 4-3. Mare average daily fatty acid intake from December-Marchl
Mare diet


Treatment
CON
FLAX
FISH


Fatty acid
C18:2n-6 (LA)


Grain
135.49
129.24
137.57
10.16
9.69
10.31
ND
ND
ND

ND
ND
ND
ND
ND
ND

135.49
129.24
137.57
10.16
9.69
10.31

13.34:1
13.34:1
13.34:1


Hay
21.37
20.66
21.37
14.58
14.10
14.58
ND
ND
ND

ND
ND
ND
ND
ND
ND

21.37
20.66
21.37
14.58
14.10
14.58

1.47:1
1.47:1
1.47:1


Supplement
ND
10.45
8.7


Total diet
156.86
160.35
167.64


C18:3n-3 (ALA)



C20:4n-6 (AA)



C20:5n-3 (EPA)



C22:6n-3 (DHA)



Total n-64



Total n-3


CON
FLAX
FISH
CON
FLAX
FISH

CON
FLAX
FISH
CON
FLAX
FISH

CON
FLAX
FISH
CON
FLAX
FISH

CON
FLAX
FISH


ND
39.22
2.83
ND
ND
0.83

ND
ND
18.10
ND
ND
15.10

ND
10.45
9.54
ND
39.22
38.56

ND
0.27:1
0.25:1


24.73
63.01
27.72
ND
ND
0.83

ND
ND
18.10
ND
ND
15.10

156.86
160.35
168.48
24.73
63.01
63.45

6.34:1
2.54:1
2.66:1


n-6:n-3


SPresented as g fatty acid/d; ND
2 CON no supplement, FLAX =


=not detected in any of the feedstuffs.
supplemented with milled flaxseed, FISH:


supplemented with encapsulated fish oil.
3Hay intake estimated at 1.0% BW (DM basis).
4 Calculated as C18:2 + C20:4.
SCalculated as C18:3 + C20:5 + C22:5 + C22:6.










Table 4-4. Mare average daily fatty acid intake from April-Junel
Mare diet

Faty aidTretmet2 Grain Spig Supplement Total diet
pasture


30.91
31.47
30.91


ND
9.84
8.24


C18:2n-6 (LA)


CON
FLAX
FISH

CON
FLAX
FISH

CON
FLAX
FISH

CON
FLAX
FISH

CON
FLAX
FISH

CON
FLAX
FISH

CON
FLAX
FISH

CON
FLAX
FISH


135.49
129.24
137.57

10.16
9.69
10.31

ND
ND
ND

ND
ND
ND

ND
ND
ND

135.49
129.24
137.57

10.16
9.69
10.31

13.34:1
13.34:1
13.34:1


166.40
170.55
176.72

99.62
137.69
102.45

ND
ND
0.82

ND
ND
17.16

ND
ND
14.34

166.40
170.55
177.51

99.62
137.69
136.27

1.67:1
1.24:1
1.30:1


C18:3n-3 (ALA)



C20:4n-6 (AA)



C20:5n-3 (EPA)



C22:6n-3 (DHA)



Total n-64



Total n-3


89.46
91.09
89.46

ND
ND
ND

ND
ND
ND

ND
ND
ND

30.91
31.47
30.91

89.46
91.09
89.46

0.35:1
0.35:1
0.35:1


ND
36.91
2.68

ND
ND
0.82

ND
ND
17.06

ND
ND
14.34

ND
9.84
9.03

ND
36.91
36.50

ND
0.27:1
0.25:1


n-6:n-3


SPresented as g fatty acid/d; ND
2 CON no supplement, FLAX =


=not detected in any of the feedstuffs.
supplemented with milled flaxseed, FISH:


supplemented with encapsulated fish oil.
3Pasture intake estimated at 1.0% BW (DM basis).
4 Calculated as C18:2 + C20:4.
SCalculated as C18:3 + C20:5 + C22:5 + C22:6.










Table 4-5. Mare bodyweightsl


SPresented in kg.
2 CON no supplement, FLAX = supplemented with milled flaxseed, FISH =
supplemented with encapsulated fish oil.
3 d-28 to d-14 d before expected foaling; dO = foaling; d+14 to d+84 = d post-foaling.

Table 4-6. Foal bodyweights1,2
Treatment

Time4 CON FLAX FISH SEM

dO 51.0a 54.4a 56.3a 2.21

d+14 74.1b 75.5b 75.4b 2.20

d+28 91.90 95.40 95.0" 2.20

d+42 109.4d 116.0d 115.0d 2.25

d+56 125.1e 127.6e 131.5e 2.23

d+70 144.8f 142.4f 144.4f 2.34

d+84 158.3g 158.5g 163.9g 2.25
Presented in kg.
2 Effect of time (P = 0.0001), effect of treatment (P = 0.75), effect of treatment x time
(P 0.31).
3 CON no supplement, FLAX = supplemented with milled flaxseed, FISH =
supplemented with encapsulated fish oil.
4 dO foaling; d+14 to d+84 d post-foaling.
a~b~c~d~e~f~g Values in the same column having different sub scripts are different at P < 0.05.


Treatment

Time3 CON FLAX

d-28 629.2 619.0

d-14 631.3 626.3

dO 554.9 544.2

d+14 553.0 551.7

d+28 556.0 550.7

d+42 560.9 552.9

d+56 561.7 548.2

d+70 556.6 542.8

d+84 556.6 552.4


FISH

635.9

639.7

559.2

559.3

562.5

567.5

567.4

557.7

565.0


SEM

13.66

13.51

8.83

8.81

8.81

8.87

8.84

9.00

8.90











Table 4-7. Overall effect of treatment on the fatty acid composition of mare plasma
Treatment

Fatty Acid CON FLAX FISH SEM P-value
C8:0 ND ND ND NA NA

C10:0 ND ND ND NA NA

C12:0 ND ND ND NA NA

C14:0 ND ND ND NA NA

C16:0 16.15 16.01 16.48 0.25 0.42

C16:1 0.88 0.88 1.10 0.09 0.17

C17:0 0.70 0.73 0.73 0.04 0.78

C17:1 ND ND ND NA NA

C18:0 20.08 20.18 20.45 0.32 0.72

C18:1 10.28 9.78 9.70 0.28 0.29

C18:2n-6 (LA) 46.43 46.87 44.37 0.71 0.05

C18:3n-3 (ALA) 2.99 3.65 3.06 0.23 0.09

C20:4n-6 (AA) 1.50 1.33 1.82 0.13 0.03

C20:5n-3 (EPA) 0.02 0.02 0.56 0.06 0.0001

C22:6n-3 (DHA) 0.05 0.03 0.61 0.05 0.0001
Total n-63 48.64 48.92 47.04 0.64 0.10

Total n-34 3.03 3.69 4.22 0.26 0.01

n-6:n-3 16.33 16.21 13.32 1.35 0.24
SPresented as g fatty acid per 100 g fat, ND = not detected in plasma, NA = not
applicable.
2 CON no supplement, FLAX = supplemented with milled flaxseed, FISH =
supplemented with encapsulated fish oil.
3 Calculated as C18:2 + C20:4.
4 CRIC111ated as C18:3 + C20:5 + C22:5 + C22:6.













Table 4-8. Omega-6 fatty acid content of mare plasma


Time2

dO d+28 d+56 d+84 SEM Treatment


P-values


Treatment x
Time
0.79


Fatty acid

C18:2 (LA)
CON
FLAX
FISH
C20:4 (AA)
CON
FLAX
FISH


d-28


47.0'
45.8
46.7'

1.7Y'z
1.8
1.7'


Time

0.07


0.05


43.1z
45.5
42.3z

2.2a,b,y
1.5a
2.7b'z


47.5'
47.2
44.6z


46.97
47.7
44.9z


47.6a"y
48.1a
43.4b~z


0.70
0.73
0.73

0.12
0.13
0.13


0.03


0.01


0.60


1.3z
1.2
1.4'


Total n-63
CON 49.2Y 45.8z 49.5Y 48.9Y 49.7'
FLAX 48.4 47.6 49.1 49.5 50.0
FISH 49.2Y 45.7z 46.8Y~z 47.6Y~z 45.9z
Presented as g fatty acid per 100 g fat.
2 d-28 d before expected foaling; dO foaling; d+28 to d+84
3 Calculated as C18:2 + C20:4.


0.10


0.08


0.79


0.63
0.65
0.65


d post-foaling.


a~b Values in the same column for each fatty acid not sharing a common superscript are different at P < 0.05.
y~z Values in the same row not sharing a common superscript are different at P < 0.05.












Table 4-9. Omega-3 fatty acid content of mare plasma
Time2


P-values


Treatment
x Time
0.12


Fatty acid

C18:3 (ALA)
CON
FLAX
FISH
C20:5 (EPA)
CON
FLAX
FISH
C22:6 (DHA)
CON
FLAX
FISH
Sum n-33
CON
FLAX
FISH


d-28


3.0
2.5x
3.2x

0.0
0.0
0.0x

0.0
0.0
0.0x

2.9
2.6
2.9x


dO d+28 d+56 d+84 SEM Treatment


Time

0.02


0.09


2.3a
3.3b,y
2.2a"y

0.01
0.0
0.3'

0.17a
0.0a
0.64b'y


2.8
3.6'
3.3x

0.0a
0.1a
1.1b~z

0.0a
0.1a
0.95b,y


3.4
4.2'
2.9x

0.02a
0.0a
1.0Ob,z

0.04a
0.0a
0.89b,y


3.4
4.5'
3.8x

0.03a
0.0a
0.5b,y

0.04a
0.03a
0.71b,y

3.5a
4.5a"b
5.1b,y


0.23
0.23
0.24

0.06
0.06
0.06

0.05
0.05
0.05

0.25
0.26
0.26


<0.0001


<0.0001


<0.0001


<0.0001


0.001


0.0004


0.01


0.0005


0.01


2.9a
3.8a
5.3b,y


3.4a
4.2a~b
4.8b~y


2.5
3.3
3.0x


SPresented as g fatty acid per 100 g fat.
2 d-28 d before expected foaling; dO foaling; d+28 to d+84 = d post-foaling.
3 Calculated as C18:3 + C20:5 + C22:5 + C22:6.
a~b Values in the same column for each fatty acid not sharing a common superscript are different at P < 0.05.
y~z Values in the same row not sharing a common superscript are different at P < 0.05.