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Coping with Social Stress: Implications for Psychopathology in Adolescent Girls

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PAGE 1

1 COPING WITH SOCIAL STRESS: IMPLICATIONS FOR PSYCHOPATHOLOGY IN ADOLESCENT GIRLS By LISA M. SONTAG 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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2 Copyright 2006 by Lisa M. Sontag

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3 To those who have always supported me and encouraged me to reach beyond my limits.

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4 ACKNOWLEDGMENTS I thank my supervisory committee chair (Dr. Ju lia A. Graber) and members of supervisory committee members (Dr. Eric Storch and Dr. Manfred Diehl) for th eir constructive and thoughtful input. I thank Dr. Elizabeth Hayes for assisting me with my analyses. I thank the participants of the st udy. I also thank the National Institute of Child Health and Human Development and the National Institute of Mental Health for providing support for this project.

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5 TABLE OF CONTENTS page ACKNOWLEDGMENTS...............................................................................................................4 LIST OF TABLES................................................................................................................. ..........7 LIST OF FIGURES................................................................................................................ .........8 ABSTRACT....................................................................................................................... ..............9 CHAPTER 1 INTRODUCTION..................................................................................................................11 Background..................................................................................................................... ........11 Stress......................................................................................................................... .......12 Peer stress.................................................................................................................13 Pubertal timing.........................................................................................................14 Biological correlates of stress..................................................................................16 Coping and Responses to Stress......................................................................................18 Proposed Study................................................................................................................. ......20 Research question 1.........................................................................................................21 Research question 2.........................................................................................................21 2 METHODS........................................................................................................................ .....23 Participants................................................................................................................... ..........23 Procedure...................................................................................................................... ..........23 Measures....................................................................................................................... ..........24 Demographic Data...........................................................................................................24 Biological Response to Stress.........................................................................................25 Pubertal Timing...............................................................................................................26 Experiences of Peer Stress...............................................................................................27 Appraisal...................................................................................................................... ....27 Coping......................................................................................................................... ....27 Internalizing Distress.......................................................................................................28 Aggression..................................................................................................................... ..29 Analysis Plan.................................................................................................................. ........29 3 RESULTS........................................................................................................................ .......32 Attrition Analyses............................................................................................................. ......32 Descriptive Analyses........................................................................................................... ...32 Tests of Main Effects.......................................................................................................... ....34 Biological Response to Stress.........................................................................................34 Pubertal Timing...............................................................................................................36

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6 Peer Stress.................................................................................................................... ...36 Tests of Mediation............................................................................................................. .....36 Pubertal Timing...............................................................................................................36 Peer Stress.................................................................................................................... ...38 4 DISCUSSION..................................................................................................................... ....51 APPENDIX A HOME DATA COLLECTION PROCEDURE AND SALIVA SAMPLE COLLECTION..................................................................................................................... ..57 B MIXED EFFECTS MODELS EXAMINING THE IMPACT OF TIME AND SYMPTOMS OF PSYCHOPATHOLOGY ON PATTERNS OF CORTISOL PRODUCTION..................................................................................................................... ..58 LIST OF REFERENCES............................................................................................................. ..60 BIOGRAPHICAL SKETCH.........................................................................................................65

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7 LIST OF TABLES Table page 3-1 Means and standard deviations of ad olescents demographic information, health, stress, coping, and psychological symptoms.....................................................................40 3-2 Intercorrelations among demographic information, health, stress, coping, and psychological symptoms....................................................................................................41 3-3 Mixed effects models examining the associ ation of internalizing distress and cortisol....42 3-4 Mixed effects models examining the a ssociation of aggression and cortisol....................43 3-5 Pubertal timing predicti ng internalizing distress...............................................................44 3-6 Pubertal timing pr edicting aggression...............................................................................45 3-7 Peer stress predicting internalizing distress.......................................................................46 3-8 Peer stress predicting aggression.......................................................................................47 B-1 Impact of time and internalizi ng distress on patterns of cortisol.......................................59 B-2 Impact of time and aggression on patterns of cortisol.......................................................59

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8 LIST OF FIGURES Figure page 1-1 Bio-psychosocial framework.............................................................................................22 3-1 Path model for pubertal timi ng to internalizing distress....................................................48 3-2 Path model for peer stress to internalizing distress............................................................49 3-3 Path model for peer stress to aggression............................................................................50

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9 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 COPING WITH SOCIAL STRESS: IMPLICATIONS FOR PSYCHOPATHOLOGY IN ADOLESCENT GIRLS By Lisa M. Sontag December 2006 Chair: Julia A. Graber Major Department: Psychology This study investigated the impact of social stress on girls psychosocial development during adolescence by integrating models of peer stress, pubertal timing, adrenocortical activity, and coping. Based on a sa mple of 111 girls ( Mage=11.84, SD = .77), we explored whether patterns of cortisol, pubertal timing, and peer stress were associated with symptoms of internalizing distress and aggres sion. Additionally, we examined whether coping strategies and involuntary responses to stress mediated these associations. Cortisol reactivity was not associated with adjustment; however, pubertal timing and peer stress were. Coping and involuntary responses mediated the association between pubertal timing and peer stress and adjustment. Findings indicate that learning to effectively adapt to stress may help girls transition more successfully into adolescence.

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11 CHAPTER 1 INTRODUCTION Background Adolescence is a period of rapid growth a nd change, both physically and psychologically. During the transition into adoles cence, individuals must learn to manage the physical changes their bodies endure due to the onset of puberty, changes in social context, and changes in school environment (Graber & Brooks-Gunn, 1996). Such experiences inherently place young adolescents at heightened risk for experi encing a great number of new daily stressors (Brooks-Gunn, 1991; Ge, Conger, & Elder, 2001). Because the chance of encountering some type of environmental or social stressor is in evitable, young adolescents must learn to adapt and to cope with these life experiences in order to successfully navigate the transition into adolescence and eventually into early adulthood. During the transition into adolescence, indi viduals experience more stressful events compared to older adolescents or children, which in turn is associated with an increase in such outcomes as depressive affect (Graber & Br ooks-Gunn, 1996; Rudolph, 2002). Of these stressful events, off-time pubertal maturation and interper sonal stress within the context of peers pose particular threats to adoles cents (Graber, Brooks-Gunn, & Ar chibald, 2005). According to Rudolphs model of interpersonal stress (2002), girls are at a pa rticular risk for experiencing higher levels of peer stress and consequently psychological maladjustment compared to boys, due to the fact that peer relati onships, specifically with close frie nds, are of greater importance to girls. In addition, some individuals exhibit disr egulations in the produc tion of cortisol in response to stressors which increases the risk for poor psychological outcomes. For example, variations in both basa l activity and stress reactivity have been linked to internalizing and externalizing problems among young adolescents (Klimes-Dougan, Hastings, Granger, Usher, &

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12 Zahn-Waxler, 2001). However, exposure to potentially stressful situa tions is not always linked to poor outcomes. The ability to cope with or res pond effectively to stress relies heavily upon the ability to interpret and react appropriately to the stressor itself or to the physiological, emotional, and behavioral responses to the stressor. By integrating models of social and biological indicators of stress and by using a more co mprehensive view of how adolescents respond to stressful experiences, this study explored what factors place some young adolescent girls at greater risk for maladjustment in th e face of stressful life experiences. Stress Stress may be best conceptualized as a mu ltidimensional concept that includes not only the stressor, but also the processing system, which includes the cognitive assessment of the stimuli, and the stress response (Compas, Orosan, & Grant 1993). Although conceptually stress may be a multilevel process, more often than not the experience of stress is quite automatic and usually occurs unconsciously. Moreover, not all e xperiences are equally st ressful to individuals, thus making appraisals of poten tially stressful experiences rele vant (Lazarus & Folkman, 1984). The transition into adolescence is marked not only by physical and sexual maturation, but also by increased exposure to new, many of th em challenging, events (Brooks-Gunn, 1991; Ge et al, 2001; Graber & Brooks-Gunn, 1996). Although ther e is evidence that st ress increases during early adolescence, the experience of particular ev ents as stressful is not necessarily pervasive among all adolescents (Brooks-Gunn, 1991). Rather, th e experience of an event as stressful is likely due to interactions among various changing life events (e.g., intera ctions among hormonal and physical changes, school transitions, peer gr oup changes, and altering family dynamics) that influence an adolescents interpretation of pa rticular events as stressful (Brooks-Gunn, 1991). One aspect of stress that seems to be particularly salient to adolescents is social stress. Social stress represents stimuli within the contex t of social interactions or relationships that

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13 evoke emotional, physical, and psychological ar ousal in individuals. Social stress may be broadly characterized as experien ces within a social context, in cluding interactions with others (e.g., peer stress), as well as how ones own de velopment (e.g., puberty) is experienced in a social context. Peer stress Peer stress may be best conceptualized as e xperiences within the peer context that exert significant pressure on an individu als ability to function adaptivel y. More concrete examples of peer stress include conflicts with close friends, being teased or hassled by other children, and being rejected by other childre n. Peer stress becomes increasi ngly salient as a threat to psychological well-being during adolescence due to the increasing amount of time spent with peers relative to other interpersonal relationships (La Greca, 2001). The relative salience of peer relationships and the impact of peer stress du ring the transition into adolescence are further supported by findings from Rudolph (2002) that demonstrated that levels of stress increase from preadolescence to adolescence independent of gender. Increased exposure to interpersonal stre ss during childhood and adolescence has been linked to disorders and sympto ms of psychopathology, namely anxiety, depression, behavior problems, and substance use (Coie, Dodge, & Kupersmidt, 1990; Hawker & Boulton, 2000). Specific aspects of peer stress, peer rejection a nd victimization, have been consistently linked to externalizing and inte rnalizing problems in adolescen ts (Deater-Deckard, 2001). A study examining aggression and peer victimization as predictors of behavioral and emotional adjustment found that greater experiences of pe er aggression predicted greater levels of both self-reported aggression and de linquency (Khatri, Kupersmi dt, & Patterson, 2000). Another study, conducted by Storch, Nock, Masia-Warner, and Barlas (2003), found that among Hispanic

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14 and African American children, overt peer vi ctimization was positively associated with depressive symptoms and aspect s of social anxiety. Additionall y, relational victimization was uniquely associated with depressive and a nxious symptoms for girls only. Recent work examining cross-national consiste ncy in the relationship between being bullied and psychosocial adjustment found that being the recipient of bullying behaviors was linked to poor emotional adjustment, poor school adjustment and poor relati onships with classmates (Nansel et al., 2004). As indicated, girls experien ce higher levels of peer stress compared to boys during adolescence (Rudolph, 2002). This differential tre nd is likely due to the fact that peer relationships, specifically with close friends, are of greater impor tance to girls. It is not to say that boys do not have experiences that could be in terpreted as stressful, bu t rather girls interpret comparable situations as more stressful and de trimental to their interpersonal relationships. Pubertal timing One aspect of social stress that is particularly salient to ad olescents is the experience of pubertal changes and whether those changes refl ect normative or off-time developmental trends within ones peer group. In or der to better understand the imp act of pubertal development on adolescents overall experiences of stre ss and the relationship between puberty and psychopathology, it is useful to distinguish between pubertal st atus and pubertal timing. According to Graber, Peterson, and Brooks-Gunn (1996) pubertal status re fers to the physical and physiological maturational levels of an indivi dual at a given point in time, relative to the overall pubertal process. Pube rtal timing, however, may be conceptualized as a social construction and best represents whether an indivi duals maturation is earlier, on-time, or later in comparison to same-age peers.

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15 Research examining the relationship betw een pubertal maturation and changes in depressive or aggressi ve affect has found few links betw een pubertal status and negative outcomes (Brooks-Gunn, Graber, & Paikoff, 1994; Graber et al., 2005). In contrast, research focusing on the effects of pubertal timing has demons trated that the stress and conflict elicited by ones off-time maturation is more strongly linked to psychological and behavioral maladjustment (Graber et al., 2005 for a recent review). Additionall y, this research has also indicated that early maturing girls are particularly at risk for a variety of disorder s or symptoms of disorders, including anxiety, depression, a ggression, substance abuse, and eating disorders. A study by Graber, Seeley, Brooks-Gunn, and Lewinsohn (2 004) examining the association between pubertal timing and psychopathology in young ad ulthood found that women who were early maturers were at unique risk for persistent difficulty and development of psychopathology during adolescence and young adulthood. Other studies exam ining the role of pub ertal timing found that early maturing girls were at high risk for depr essive symptoms, body dissatisfaction, aggression, and delinquency problems (Caspi, Lynam, Moff itt, & Silva, 1993; Ge, Brody, Conger, Simons, & Murry, 2002; Ge et al., 2001; Ohring, Graber, & Brooks-Gunn, 2002). In order to explain the c onnection between hormonal and pubertal changes and negative affective and behavioral outcomes, Brooks-Gunn and colleagues (1994) proposed a model that included the possibility that social events or cont ext, as well as the adolescents perceptions of his or her pubertal processes, contribute to or function as mediators of hormonal effects on negative affect and behavior. In testing this model, Brooks-Gunn and Warren (1989) found that social events, not pubertal development, accounte d for a good deal of variance in affect and behaviors. In terms of social pr ocesses, adolescents who mature early or late in comparison to their peers are placed in socia lly deviant categories compared with on-time peers (Petersen &

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16 Crockett, 1985). Keeping in mind that girls as a group tend to mature a couple of years earlier than boys, early maturing girls are deviant in comparison to both other girls and boys, which places these girls at a heighten ed risk for maladjustment. This study explored the effects of pubertal timing within a social processes framework in order to expand on previous findings that have linked the social experience of being off-time and particular emotional or behavioral cha nges. As highlighted by Brooks-Gunn and colleagues (1994), social factors play a sign ificant role in conn ecting the pubertal timing and negative affect or behavior. The way an individual interprets his or her timing is likely to influen ce the types of social interactions he or she expe riences, and in turn is likely to influence potential affective or behavioral changes. Research has shown that ea rly maturing girls consiste ntly report poor quality of relationships at mid-adolescence and young a dulthood (Graber et al., 2004). By examining how early maturing girls cope with or adapt to po tentially stressful situations within the peer context, a better understanding of the mechanisms by which pubertal timing relates to maladjustment may emerge. Biological correlates of stress Under conditions interpreted as stressful, the limbic-hypothalamic-pituitary-adrenal (LHPA) axis in mammals (including humans) res ponds to this experience vi a a series of events that result in the secretion of glucocorticoids (cortisol in human and nonhuman primates, and corticosterone in rodents) from the adrena l cortex (Cicchetti & Walker, 2001). Prolonged exposure to environmental and intern al stress, and in turn disregul ations of cortisol levels, can affect psychological well-being. Pa st studies investigating the a ssociation between adrenocortical activity, stress, and psychosocial well-being found that variation in both the basal activity and in stress reactivity has been associated with psychopathology (Angold, 2003; Goodyer, Herbert,

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17 Tamplin, & Altham, 2000; Klimes-Dougan, Hasti ngs, Granger, Usher, & Zahn-Waxler, 2001; Southwick, Vythilingam, & Charney, 2005). However, much of this literature has focused primarily on diurnal patterns of ch ange and investigated cortisol re activity in clinical populations (Oosterlaan, Geurts, Knol, & Sergeant, 2005; Van Bokhoven et al., 2005; Van de Wiel, Van Goozen, Matthys, Snoek, & Van Engeland, 2004). Th erefore the question still remains as to how patterns of cortisol reactivity in normative sample s of adolescents reflect experiences of stress, particularly social stress, and how these patterns of reactivity are associated with changes in negative affect and behavior. For individuals who follow a typical day-ni ght schedule, cortisol production peaks during the last few hours of sleep (Gunnar & Vazquez, 2001 for a review). Cortisol levels then decline rapidly throughout the morning and decrease gra dually during the remainder of the day. When stress is induced, cortisol secretion initially incr eases. Following the onset of a stressor, cortisol usually takes about 10-15 min to produce a rise in circulating cortisol levels. About 20-30 min after the stressor, peak concentr ations of cortisol are found in saliva. Following this peak, the negative feedback loop of the LHPA axis begins to reestablish homeostatic functioning by reducing the level of circulating cortisol. Recent research examining the association betw een changes in daytime cortisol levels in response to social challenges (i.e ., public speaking task or mother -child conflict task) has shown that adolescents and children te nd to display increases in salivar y cortisol approximately 20 to 30 min following exposure to a social challenge tas k, and then display a decrease in levels of cortisol (Granger, Weisz, & Kauneckis, 1994; Klimes-Dougan et al., 2001; Schmidt et al., 1999). In addition, findings from these stud ies have indicated that maintain ing high levels of cortisol or

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18 displaying strong task-related decr eases are associated with highe r levels of internalizing and externalizing behavior. Findings such as those mentioned previously point to a link betw een stress response and psychopathology; however, activa tion of the L-HPA axis may not be directly linked to symptomatology. Additionally, there are few conclusive or consistent findings within the child and adolescent research about whether a true relationship between cortisol levels and psychopathology exists. Therefore, more research examining the association between cortisol and psychopathology is needed, especially w ithin the adolescent female population. Coping and Responses to Stress Because of the increase in stressful experi ences during the transition to adolescence (Brooks-Gunn, 1991), learning to adapt to the stressor and manage ones response to the stressful situation is crucial to leading a healthy and productive life. However, the effects of stress vary by individuals. Whereas most people fare quite we ll in the face of typical ly occurring stressful events, other individuals manife st symptoms of psychopathology, as mentioned previously. But the question therein lies, why do individuals demonstrate different ial outcomes to stress exposure and how do these differences emerge? Coping strategies offer one of the mechanisms through which stress differentially aff ects individuals. Understanding the process of coping and how adolescents effectively or ineff ectively react to stressful stimu li allows researchers to understand better why particular individua ls adapt well or adapt poorly. As suggested by Lazarus and Folkman (1984), c oping involves efforts to manage specific external and/or internal demands that are apprai sed as taxing or exceedin g the resources of the person. Coping differs from general responses to stre ss in that coping is viewed as volitional or under the persons control. In addition, Lazarus and Folkman emphasize the role of cognitive processes in determining what is experi enced as stressful and how one copes.

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19 Theoretical frameworks of coping, such as the one developed by Lazarus and Folkman (1984), adequately target volitional responses to stress; however, few models have included involuntary responses to stress. One compre hensive model, developed by Compas, Connor, Saltzman, Thomsen, and Wadsworth (1999), include s both volitional and involuntary responses to stressful stimuli. According to this model, stress response can be characterized as being either effortful or involuntary. Effortful responses ar e cognitive and behavioral reactions to stress experienced as volitional and purposeful such as acceptance, denial, and avoidance. Involuntary responses, as defined by Compas et al. (1999), include temperamentally based and conditioned cognitive, behavioral, and physiolo gical reactions to stress that may or may not be within conscious awareness and are not un der personal control, such as physiological ar ousal, intrusive thoughts, and rumination. In combination with the volitional responses to stress (i.e., coping), involuntary responses create a more representative model of how individuals re spond to external and internal stressors throughout their lifespan. Compas and colleagues (1999) further different iated effortful and involuntary responses to stress by distinguishing between engagement and disengagement responses. Engagement responses are directed toward a stressor or ones reac tions to the stressor and include approach responses. Disengagement responses are directed away from these target s and include avoidance responses. Given this model, an individual may respond to a stimulus in one or more of the following manners: effortful engagement (pri mary and secondary control), effortful disengagement, involuntary engagement, and i nvoluntary disengagement. Connor-Smith et al. (2000) tested this model using a sample of adoles cents and their parents. Findings indicated that not only was there adequate to excellent intern al consistency for each subtype of response to stress (i.e., primary control, secondary contro l, disengagement coping, involuntary engagement,

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20 and involuntary disengagement) but subscales of coping, specifically, mapped onto other standard measures of coping quite clearly. More important, however, was the finding that factors within this model of responses to stress correlated with interna lizing and externalizing behavior. Thus, these exploratory analyses suggest th at a model including both coping and involuntary responses adequately captured how adolescents adapt to stressor s. Additionally, how one copes with stress was associated with em otional or behavi oral outcomes. Other studies examining the association betw een responses to stress and emotional and behavioral outcomes have consistently demons trated that style of response mediates the relationship between stress, specifically fam ily conflict and chronic pain, and anxiety, depression, and aggression (Jas er et al., 2005; Wadsworth, Ra viv, Compas, & Connor-Smith, 2005). Extrapolating to other realms of stress, it is likely that an individuals type of response to social stress (e.g., peer stress) will mediate the relationship between social stress and psychopathology during adolescence. However, little empirical work has examined the effects of responses to stress on this relationship and even fewer studies have extended this research to examining how coping may serve as a mechanism through which biological indicators of stress (i.e., cortisol) and pubertal timing in fluence poor outcomes. Proposed Study This study investigated the impact of stress reactivity and social factors on negative outcomes from a bio-psychosocial perspective as a means to explain emotional and behavioral changes that occur during the tr ansition into adolescence. By in tegrating several theoretical models that focus on the contex t of peer stress, pubertal ti ming, adrenocortical activity, and coping (Figure 1), this study aimed to provide a more comprehensive appr oach to understanding the pathways to adjustment. Within this fr amework, this study examined physiological and environmental indicators of social stress and how these indicators were associated with

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21 symptoms of psychopathology, in particular inte rnalizing distress and aggression. Additionally, this study explored whether respon ses to stress mediated this rela tionship. Specifically, the study examined the following questions: Research question 1 Are physiological and environmen tal indicators of social stre ss associated with symptoms of internalizing dist ress and aggression? Specifically, is biological stress reactivity (i.e., patte rn of cortisol levels) associated with symptoms of psychopathology? Because of th e exploratory nature of the study with respect to the findings associated with cortis ol, it was predicted that pattern of reactivity was associated with symptoms of internal izing distress and aggression. However, specific predictions about the association be tween particular patterns of cortisol and behavioral outcomes were not made. Is pubertal timing associated with symptoms of internaliz ing distress and aggression? This study predicted that girls who reporte d early pubertal timi ng would demonstrate higher levels of internalizing distress a nd aggression compared to girls who reported being on-time or late. Are experiences of peer stress associated with symptoms of inte rnalizing distress and aggression? It was hypothesized that girls who reported a grea ter number of stressful peer experiences would display more symptoms of internalizing distress and aggression. Research question 2 Do coping strategies mediate the associat ion between biological and environmental indicators of stress and sy mptoms of psychopathology? Do coping strategies mediate the associati on between stress reactivity (i.e. cortisol patterns) and symptoms of internalizing distress and aggr ession? It was hypothesized that the 5 coping strategies or responses to stress (i.e., primary contro l, secondary control, effortful disengagement, involuntary engageme nt, and involuntary disengagement) would mediate the association betw een stress reactivity and symp toms of psychopathology. More specifically, it was predicted that effortful disengagement and involuntary disengagement would serve as mediators be tween stress reactivity and internalizing distress, whereas involuntary engagement would mediate th e association between stress reactivity and aggression. It was expected that primary and secondary control coping strategies would mediate the association be tween stress reactivity and internalizing distress and aggression.

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22 Coping Responses Psychopathology Internalizing Distress Aggression Social Stress Pubertal timing Peer Stress Biological Stress Response Cortisol Do coping strategies mediate the association between pubert al timing and symptoms of internalizing distress and aggression? It wa s expected that coping strategies would mediate the association between pubertal ti ming (i.e., early vs. on-time or late) and symptoms of psychopathology in the same wa y that was described for stress reactivity. Do coping strategies mediate the associat ion between peer stress and symptoms of internalizing distress and aggression? It wa s hypothesized that coping strategies would mediate the association between peer stress and symptoms of inte rnalizing distress and aggression in the same way that was descri bed for stress reactivity and pubertal timing. Figure 1-1. Bio-psychosocial framework

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23 CHAPTER 2 METHODS Participants Participants were 111 adolescent girls ( Mage = 11.84, SD = .77), who were drawn from a larger project, the Girls Health and Developmen t project, that examined biological correlates of girls social and emotional hea lth as they made the transition to puberty. Approximately 15% of the girls were in 5th grade, 47% in 6th grade, 31% in 7th grade, and 2% in 8th grade. Of the 111 girls, 48% were Caucasian, 36% African Americ an, and 16% Hispanic. Girls and their families were originally recruited in 1995-1996 from public schools in ethnically integrated, working-class and middle-class communities in the New York City area. The study included 138 girls at baseline; 111 of these gi rls participated in the final fo llow-up, approximately three years later. Analyses for the current st udy were completed using only girl s who participated in the final follow-up. Procedure Girls and their families were recruited via th eir schools. Each time families participated, parents signed informed consent forms at their homes, on their own behalf and for their childs participation. Girls gave assent for their participation. Mother s and children completed several tasks (Appendix A) during a home visit and comp leted surveys during the 3 consecutive days following the home visit. Girls completed survey s on their own affect and behaviors. Surveys were picked up from the families homes 3 days after the home visit. Girls received a gift (tote bag) for their participation and mothers were paid $75.

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24 Measures Demographic Data Data concerning the characteristics of the part icipants were collected using standard items concerning age, household structur e, and race/ethnicity. Girls re ported their date of birth, and exact age was calculated from date of home visit. Mothers reported on family characteristics and child race/ethnicity. Race/ethnicity was colla psed into three categories: White, African American, and Hispanic. For regression analys es, two dummy coded variables were used: African American versus others and Hispanic versus other, with White as the omitted group. Family SES was assessed using the Hollings head Scale (Hollingshead, 1975), a scale based on survey data of social status tied to U.S. census categories. The standard scoring protocols were used for diffe rent household types. Mothers reported on the education and occupation of themselves and any other parent /caregiver in the house hold. For each head of household, education (coded on a 7point scale from 1 = less than 7th grade to 7 = graduate professional) was multiplied by a weight of 3 and occupation (coded on a 9-point scale from 1 = farm labor and menial service workers to 9 = higher executives and major professionals) was multiplied by a weight of 5. Thus the range of possible scores for family SES was 8 to 66 (Hollingshead, 1975). For one-parent households, th e education score and occupation score were summed to yield an SES score. In two-parent families, one parent in paid employment, the family SES was derived by adding the mean of th e parents education sc ores to the occupation score for the employed parent. If both parents were employed, the family SES score was the mean of the parents SES scores.

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25 Biological Response to Stress During the in-home visit, 5 saliva samples we re collected to assess cortisol levels throughout a battery of tasks. S ee the Appendix A for a complete list of tasks. Approximately 15-20 min occurred between collections. The un it of measurement for cortisol assayed was g/dl. Saliva was collected via Salivettes. Girls kept the cotton roll in their mouths for 2 min, resulting in sufficient amounts of saliva for repe at assays. Girls ingested a small amount of sweetened Kool-Aid to stimulate saliva flow. Stimulating saliva fl ow with orally administered substances such as powdered drink mix was reco mmended protocol at the time this protocol was implemented (Granger et al., 1994; Gunnar & V azquez, 2001; Hertsgaard, Gunnar, Larson, Brodersen, & Lehman, 1992; Nachmias, Gunna r, Mangelsdorf, Parritz, & Buss, 1996). Subsequent to the development of this proced ure, it was found that Kool-Aid may alter the results of the assay of cortisol from saliv a samples (Schwartz, McFadyen-Ketchum, Dodge, Pettit, & Bates, 1998). However, these effects were found to vary by assay kit used. The kit used in the present study was not highly susceptible to this problem. Sa liva samples were stored in a refrigerator before being transported to Columbia -Presbyterian Reproductive Endocrinology Department in New York City, where they were stored in a freezer at -20C until assayed for cortisol. Cortisol concentrat ions were determined using a radioimmunoassay adapted for measurements in saliva (Diagnosti c Products Company). The lower detection limit for this assay was 0.02 g/dl per 200 l of saliva. Saliva samp les were centrifuged at 3000 rpm for 10 min. A 200 l sample was used for duplicate analysis. All samples from a participant were analyzed in one assay run, with interand intra-assay coe fficients of variations less than 5 and 3%, respectively. Certain samples were excluded from analysis due to problems with the saliva sample. The lab processing the samples exclud ed participants samples if the samples were insufficient to

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26 process. Log transformations were applied to the cortisol data to reduce the large positive skew, which is consistent with standard procedures in cortisol research (Gunnar, 2000). However, original units were reported for ease of interpretation. Pubertal Timing Pubertal timing was based on self-reported age of menarche obtained during the home visit. A recent review of the use of self-reported menarche not ed that accuracy of recall is reduced as the time interval between menarche and recall is increased (Coleman & Coleman, 2002). However, if assessed within a period of 1 year from menarche, girls can typically recall menarche within 1 month of the exact date. Gi ven that the studys par ticipants have recently experienced menarche, the use of self-repor t can be considered a valid measure. Using self-reported age of menarc he, girls were classified as e ither early-maturers or other (on-time or late). Cut-off ages by race (White, African American, and Latina) were derived from a large, normative study of puberty (Herman-Gidde ns et al., 1997). Based on mean ages of menarche reported by race in the Herman-Giddens study, girls that reported age of menarche SD below the mean were categori zed as early. All other girls we re in the other group (on-time or late). According to an invest igation of age at menarche for gi rls in the United States, age of menarche for Hispanic girls tends to fall between ages fo r non-Hispanic white girls and non-Hispanic black girls (Chumlea et al., 2003 ). Because the Herman-Giddens study only examined White and African American girls, estim ates for early Latinas were calculated as SD below the mean menarcheal age of the sample. Cut off ages for early maturing girls were: 12.28 y for White, 11.55 y for African American, and 11.97 y for Latina. Late maturation could not be determined due to the mean age of assessmen t (just under 12 y) because the mean age of menarche for each race as determined by Herm an-Giddens et al. ( 1997) was greater than 12 years. Thirty five percent of the participants were classified as early maturers. Approximately

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27 28% of White participants, 33% of African American part icipants, and 40% of Latina participants were early maturers. Experiences of Peer Stress Participants experiences of peer stress were as sessed as part of the survey administered in the days after the home visit using a stressful ev ents checklist that was in cluded in a version of the Responses to Stress Questionnaire that wa s adapted for this study (RSQ; Connor-Smith, Compas, Wadsworth, Thomsen, & Saltzman, 2000). The RSQ was developed to assess experiences of stressful events and responses to stress in adolescent populations. The checklist provided information about how many stressful e xperiences the particip ants had encountered since the start of the school year. The RSQ can be tailored to specific stressors; this form of the RSQ was tailored to assess peer stress. For the st ressful events checklist, participants endorsed 9 items. Sum scores were calcula ted, with higher scores repres enting the experience of more stressful events. Peer stress, as discussed in the study, was operationalized as the number of stressful events a participant experienced. Appraisal Appraisal of stressful experiences was also a ssessed using the RSQ. Participants responded to a single item that assessed ove rall how stressful the problems e ndorsed in the stressful events checklist were for them on a likert scale (1 = not at all to 4 = very). Highe r scores indicated that the participant felt the experiences to be more stressful. Coping Coping was also assessed using the RSQ. Adap ted from the original RSQ for the purposes of this study, the measure consiste d of 38 items rated on a 4-point li kert scale (1 = not at all to 4 = a lot). The RSQ contains 5 subscales: primary effortful control, secondary effortful control, effortful disengagement, involuntary engagement and involuntary disengagement. In this study,

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28 the primary effortful control subscale contai ned 7 items that assessed responses to stress categorized as emotional expression, emo tional regulation, and problem solving ( = .80). The secondary effortful control subscale contained 4 items that measured responses to stress categorized as acceptance, positive th inking, and cognitive restructuring ( = .70). The effortful disengagement subscale containe d 9 items and assessed denial, a voidance, and wishful thinking ( = .75). The involuntary engagement subscale contained 9 items, wh ich assessed impulsive action, physiological arousal, and in trusive thoughts or rumination ( = .78). Finally, the involuntary disengagement subsca le contained 9 items that m easured inaction, emotional and cognitive numbing, and involunt ary avoidance or fleeing ( = .76). High scores on each subscale indicated that partic ipants were more likely to engage in these types of responses in the face of stress. Raw scores were reported as sum scores and used for reliability analyses. However, in order to control for overall responding bias, f actor scores reflecting the proportion of total responses (e.g., sum of scores on primary control it ems/sum of all items) we re used in analyzing the associations with internalizing distress and aggression as recommended by Connor-Smith and colleagues (2000). Internalizing Distress Internalizing distress was assessed during th e home visit using the anxiety/depression subscale of the Youth Self Report (YSR/11-18) created by Achenbach (1991). The YSR for ages 11-18 is a self-report measure designed to m easure competencies, adaptive functioning, and problems in youth and adolescents ages 11-18. It can be completed by those having a fifth grade reading level or administered ora lly. Participants were asked to report on behavior now or within the past 6 months and rated items on a likert scal e (0 = not true, 2 = very true or often true). Scores for the anxiety/depressi on subscale were reported as sum scores. The anxiety/depression subscale contained 16 items, with a reliability of = .83.

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29 Aggression Aggression was also assessed using the YSR/ 11-18 (Achenbach, 1991). Participants rated items on a likert scale (0 = not true, 2 = very true or often true ). Participants were asked to report on behavior now or within the pa st 6 months. Scores for the subs cale of aggression were reported as sum scores. The aggression subscale c ontained 19 items, with a reliability of = .86. Analysis Plan The goal of this study was to examine physiologi cal and environmental indicators of social stress and how these indicators were associated with symptoms of psychopathology, specifically internalizing distress and aggr ession. Additionally, this study explored whether responses to stress mediated this association. First, attrition analyses were performed to determine if the sample used in this study differed on key variab les from the original sample of participants recruited. Descriptive analyses we re performed on key variables. To address the first set of hypotheses, ma in effects were explored via ANCOVAs and hierarchical linear regression. As a means to explore the main effect of stress reactivity on internalizing distress and aggression, a combin ation of linear regression models and mixed models was used. Within the cortisol literature, researchers use multiple approaches to examine the association between stress reac tivity (i.e., change in cortisol levels) and outcomes of interest. The computation of the area under the curve (AUC) is a frequently used method in endocrinological research and th e neurosciences to explore info rmation that is contained in repeated measurements over time (Pruessner Kirschbaum, Meinlschmid, & Hellhammer, 2003). In the case of this study, AUC was employed to i nvestigate task-dependent changes in cortisol level over the period of the home visit. AUCcortisol was calculated from zero and log transformations were applied to the AUCcortisol value for each participant to reduce the large

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30 positive skew. To explore the main effects of stress reactivity, AUCcortisol was entered as the independent variable in a linear regression model. Although frequently used in endocrinological re search to capture pa tterns of change over time, the area under the curve as calculated from zero may neglect to capture idiosyncrasies of change that occur regardless of ones absolute leve ls of cortisol. Also, as indicated, calculating area under the curve requires data at each time poin t. Thus, in order to further explore potential associations between patterns of change in co rtisol production and symp toms of internalizing distress and aggression, mixed eff ects models were used. These models addressed the question of whether ones pattern of pr oduction of cortisol over the 5 ho me visit samples changed in association with ones symptoms of psychopath ology. In addition, mixed models do not require participants to have data at each time point. Thus, for this study, it was possible to estimate the desired associations with fewer th an 5 cortisol samples, allowing for a greater total sample size. Addressing the remaining components of the first set of research questions, the main effect of pubertal timing on internalizing distress and aggression was explored via a combination of ANCOVAs and a hierarchical linear regression model. The main effect of peer stress was explored using only a lin ear regression analysis. Mediation was tested using the guidelines delineated by Baron and Kenny (1986). The mediators were primary control coping, sec ondary control coping, disengagement coping, involuntary engagement responses, and involunt ary disengagement responses. Specifically, separate regression models tested the effects of the social stress predictors (peer stress, pubertal timing) or biological correlates of stress (cor tisol) on each mediator and both internalizing distress and aggression. A full model was then tested with the social stress predic tor and all the mediators entered on the same step. For mediation to occur, the predictor mu st have a significant

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31 association with the mediator and the outcome variable, and in the full model, the mediator must predict the outcome variable and the size and significance of the association between the predictor and the outcome variab le must be reduced. In all m odels, race and family SES was controlled for; in the models with peer stress as the predictor, appraisal was also controlled for. Researchers comparing methods to test medi ation have suggested that Baron and Kennys (1986) method neglects to provide a direct estimate of the size of the indirect effect of the independent variable on the dependent vari able (MacKinnon, Lockwood, Hoffman, West, & Sheets, 2002; Preacher & Hayes, 2004). In turn th ey suggest supporting research findings with a product of coefficients test, typically the Sobel Test, which states if ab (the indirect effect) is not significantly different from zero, there is no e ffect of mediation (Sobe l, 1982). However, according to Preacher and Hayes (2004) this method is also misleading because there is reason to be suspicious of the use of the normal distribution for computing the p value for the Sobel test because the sampling distribution of ab may not be normal. To address this issue, Preacher and Hayes (2006) recommend bootstrappi ng the sampling distribution of ab and deriving a confidence interval with the empirically derived bootstrappe d sampling distribution. This approach has been suggested as a way of circumventing the power problem introduced by asymmetries and other forms of non-normality in the sampling distribution of ab (Preacher & Hayes, 2004; Shrout & Bolger, 200 2). Given this recommendation, a test of the indirect effect was performed to support mediation effects consistent with Baron and Kennys (1986) guidelines.

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32 CHAPTER 3 RESULTS Attrition Analyses Due to the loss of 19.5% of the sample of gi rls from baseline (n = 138) to the final follow-up 3 years later (n = 111), univaria te analyses of non-response bias were conducted to determine if the remaining sa mple differed on key demographic factors, pubertal development variables, and outcomes (depression, peer prob lems, internalizing and externalizing behavior) assessed at base line. Results showed that families did not differ on variables used in this study. Some participants were ex cluded from particular anal yses because they did not have values for some variables. For analyses involving cortisol samples, some girls were excluded because their saliva samples were insu fficient to assay cortisol, whereas others participated via phone intervie w and survey if they moved, and thus did not have a cortisol sample. For the exact number of reports for each variable see Table 3-1. Descriptive Analyses Descriptive information (i.e., M and SD) are shown in Table 3-1 and correlations among the variables of interest are shown in Table 3-2. Contrary to the hypotheses, stress reactivity (AUCcortisol) was not associated with internalizing distress or aggr ession (r = .02, ns, and r = .12, ns, respectively). In fact, only two variables demonstrated significant correla tions with stress re activity: pubertal timing (r = .23, p < .05), and involuntary engagement (r = .27, p < .05). Pubertal timing also demonstrated signifi cant associations with the outcomes. For the dichotomous pubertal timing variable (e arly vs. other), ANCO VAs (controlling for SES and race) were conducted, as the F-values means, and standard deviations for the

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33 effects may be more illuminating than correlations. As expected, girls who were early maturers reported more internalizing distre ss, F (1, 104) = 4.83, p < .05, with an average score of 6.63 (SD = 4.76) compared to other girls (M = 4.57, SD = 4.44), and more aggressive symptoms, F ( 1, 104) = 4.54, p < .05, with an average score of 8.77 (SD = 6.39) compared to other girls (M = 6.29, SD = 4.96). Peer stress was positively associated w ith both internalizing distress (r = .40, p < .01) and aggression (r = .23, p < .05). A ppraisal of the stressful experiences was positively associated with both peer stress (r = .41, p < .01) and in ternalizing distress (r = .28, p < .05). As anticipated, the potential mediators of the association betw een biological and environmental indicators of social stress and adjustment demonstrated consistent associations with the outcomes of interest. Internalizing distress was positively associated with voluntary disengagement, involuntary en gagement, and involunt ary disengagement responses (Table 3-2). Additionally as pred icted, internalizing distress was negatively associated with primary control strategies (r = -.48, p < .01), meaning that girls who used problem solving and emotional expression and re gulation tactics to c ope with peer stress reported fewer symptoms of anxiety and depression. The use of secondary control strategies, such as acceptance or cognitive re structuring, was also negatively associated (r = -.45, p < .01) with internalizing distress. This suggested that adolescent girls who attempted to manage stressful peer experien ces by using positive self-talk or accepting these stressors as something from which to learn experienced fewer anxious and depressive symptoms than girls were less likely to use these strategies.

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34 Similar to the findings for internalizing distress, aggression was positively correlated with involuntary engagement responses, and involuntary disengagement responses (Table 3-2). As hypothesized, primary control engagement coping and secondary control engagement coping were negatively correlated with aggression. The use of disengagement coping strategies, such as denial, avoidance, and wishful thinking, was not correlated with aggression. Tests of Main Effects As indicated, in order to test whethe r or not physiological and environmental indicators of social stress were associated with symptoms of in ternalizing distress and aggression, a series of hierar chical regression analyses we re performed. All analyses controlled for race/ethnicity (African Ameri can versus other, Hispanic versus other, White as omitted group) and family SES. Biological Response to Stress Controlling for race and family SES, AUCcortisol was not significantly associated with internalizing distress, F (4, 65) = .59, p = .67, or aggression, F (4, 65) = .33, p = .86, meaning amount of total stress reactivity over the 5 points of cortisol assessment were not associated with symptoms of internalizing di stress or aggression. Sample sizes for these analyses were much lower than the main gr oup of participants (N=111). This occurred because in order to calculate an AUCcortisol score, participants need ed to have 4 out of the 5 samples and were not missing sample 1 or sa mple 5, in addition to needing race, SES, internalizing distress, and aggression scores. An unrestricted covariance structure was used for each model and all continuous between-person variables were centered on th e grand mean. Because race and family SES were shown not to be significant predictors of AUCcortisol, they were not included in the

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35 mixed effect models. Researchers claim that including covariates that do not exhibit associations with the dependent variable can ge nerate spurious significant associations in models, and thus it is recomme nded to exclude covariates from the analyses that would otherwise be included in t ypical regression and ANCOVA an alyses (Rovine, von Eye, & Wood, 1988; Weisberg, 1979). One set of anal yses was performed for each set of symptoms (i.e., internalizing distress and a ggression), resulting in 2 sets of analyses. However, because internalizing distress a nd aggression showed not to be significant predictors of participants pa tterns of change in cortisol results from the 2 sets of analyses will be discussed in combination. In Model 1 (see Tables 3-3 and 3-4), the va riance in cortisol was partitioned into withinand between-person va riance; 41.18% of the variance was due to within-person variability and 58.82% was due to between-per son variability. In Models 2 and 3, fixed effects were added in a systematic fashion and pseudo R2 statistics were calculated to determine the amount of variance these mode ls accounted for relative to the baseline model. In Model 2, time was included as a leve l-1 predictor of cortisol. Results demonstrated that time was a significant pred ictor of cortisol levels and accounted for 43% of the within-person vari ance. In Model 3, the effect s of internalizing distress (Table 3-3) or aggression (Table 3-4) were added. Bo th internalizing distress and aggression were not significan t predictors and did not acc ount for any between-person variance. In addition, the inte ractions between time and in ternalizing distress and time and aggression were not signifi cantly associated with cor tisol levels. Thus, although results showed that cortisol levels change d over the 5 in-home coll ections, symptoms of

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36 psychopathology were not associated with how co rtisol levels changed over time. These results corroborate the findings from the area under the curve analyses. Pubertal Timing To test whether or not pubertal timi ng was associated with symptoms of internalizing distress and aggression, a series of hierarchical regression models was performed (Table 3-5). Controlling for r ace/ethnicity and SES, pubertal timing was significantly associated with internalizing distress, such that girls who were early maturers demonstrated higher levels of intern alizing distress compared to other girls. Controlling for race/ethnicity and SES, pubertal timing was also significantly associated with aggression, such that girls who reported early maturation demons trated higher levels of aggression compared to other girls. Th ese findings were consistent with bivariate correlations reported in Table 3-2. Peer Stress As expected, results indicated that peer stress was significantly associated with both internalizing distress and aggression (T ables 3-7 and 3-8). Controlling for race, SES, and appraisal, higher levels of peer st ress were associated with greater symptoms of internalizing distress and aggression. Tests of Mediation As indicated, a series of regression models were perf ormed to test effects of mediation as specified by Baron and Kenny ( 1986), with subsequent examination of tests of mediation as proposed by Preacher and Hayes (2006). Pubertal Timing Figure 3-2-1 shows the model testing mediat ed pathways of pubertal timing (early vs. other) to internalizing distress. The standardized coefficients are shown in the

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37 figures. In all, 5 tests of mediation (o ne for each mediator) were performed for internalizing distress. As can be seen in Figure 3-2-1, there was evidence for full mediation of the effect of timing on inte rnalizing distress via primary control and involuntary engagement responses. As per sp ecifications of Bar on and Kenny (1986), the coefficient of pubertal timing predicting inte rnalizing distress was reduced and was no longer significant when the mediators were included in the model (i.e., for pubertal timing to internalizing distress, when mediated by primary control, was reduced from .20, p < .10, to .08, ns, and was reduced from .20, p < .10, to .11, ns, when mediated by involuntary engagement). Results from Preacher and Hayes (2006) test of the indirect effect found that the indirect effect (ab = .11) of pubertal timing on internalizing distress through primary control was estimated to lie between .03 and .27 with 95% confidence. Also, the indirect effect (ab = .10) of pube rtal timing on internalizing distress through involuntary engagement was estimated to li e between .03 and .20 with 95% confidence. For both indirect effects, mediation was said to occur because the i ndirect effects (ab) were significantly different from zero. The tests of mediation demonstrated that early pubertal timing predicted less use of primary control strategies which subsequently predicted fewer symptoms of internalizing distress. Conversely, early timing predicte d greater use of involuntary engagement responses, which subsequently predicted great er symptoms of internalizing distress. Pubertal timing was not associated with secondary control strategies, voluntary disengagement strategies, and i nvoluntary disengagement responses. Potential mediation effects on the as sociation between pubertal timing and aggression were not examined. Although init ial analyses demonstrated that pubertal

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38 timing was significantly associated with aggression (Table 3-6), analyses for tests of mediation demonstrated that pubertal timing di d not demonstrate a si gnificant association with aggression ( = .15, p = .14). In the tests of mediation, listwise deletion was utilized, thus excluding part icipants who did not have sc ores for all the necessary variables needed to illustra te mediation (i.e., pubertal ti ming, internalizing distress, coping scores, and all covariates). This difference in analysis between the general regression and the te sts of mediation accounts for th e emergence of a significant association between pubertal ti ming and aggression in the or iginal regression analysis and the non-significant associ ation that emerged in the test of mediation. Peer Stress Figure 3-2 shows the model testing medi ated pathways of peer stress to internalizing distress; and Fi gure 3-3 shows the model examin ing the association between peer stress and aggression. As shown in Figure 3-2 and 4, peer stress was positively associated with voluntary disengagement; however, because voluntary engagement strategies were not associated with either internalizing di stress or aggression, mediation effects did not emerge. Peer stress was not a ssociated with invol untary engagement and disengagement responses. Two mediation effects emerged for both in ternalizing distress and aggression. As can be seen in Figure 3-2, there was evidence fo r partial mediation of the effect of peer stress on internalizing distress via primary control and secondary control strategies. The coefficient of peer stress pr edicting internalizi ng distress was reduced and was no longer significant when the mediators we re included in the model (i.e., for peer stress to internalizing distress, when mediated by pr imary control, was reduced from .35, p < .01, to .26, p < .05, and was reduced from .35, p < .01, to .25, p < .05, when mediated by

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39 secondary control). Noteworthy was the fact that the association be tween peer stress and primary control was only a trend. However, us ing Preacher and Hayes (2006) test of the indirect effect supported the finding of partial mediation, demonstrating that ab was significantly different from zer o with 95% confidence for primary control, ab = .10, CI (.02, .21), and for secondary control strategies, ab = .10, CI (.01, .23). Figure 3-3 shows evidence for fu ll and partial mediation of the effect of peer stress on aggression via primary control and sec ondary control strategies, respectively. The coefficient of peer stress predicting aggre ssion was reduced and wa s no longer significant when the mediators were included in the model (i.e., for peer stress to aggression, when mediated by primary control, was reduced from .25, p < .05, to .20, p < .10, and was reduced from .25, p < .05, to .17, p = .13, when mediated by secondary control). Supporting these findings, ab was significantl y different from zero with 95% confidence for primary control, ab = .06, CI (.01, .16), and for secondary control strategies, ab = .08, CI (.01, .24). For tests of the indirect effect ab was significantly different from zero, which demonstrated mediation. This means that greater peer stress predicted less use of primary and secondary control strategies wh ich subsequently predicted fewer symptoms of internalizing di stress and aggression.

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40 Table 3-1 Means and standard deviations of adolescents demographic information, health, stress, coping, and psychological symptoms Variable NMSD Age 11111.84.78 SES 11033.0716.72 Cortisol sample 1 89.17.16 Cortisol sample 2 84.14.16 Cortisol sample 3 80.12.17 Cortisol sample 4 71.09.12 Cortisol sample 5 73.10.14 Cortisol AUC 729.7210.20 Age of menarche 4611.26.87 Peer stress 982.601.96 Degree of hassle 962.161.00 Primary control 101.23.05 Secondary control 100.13.03 Effortful disengagement 101.24.05 Involuntary engagement 100.20.04 Involuntary disengagement 100.19.04 Internalizing distress 1095.214.62 Aggression 1097.075.54 Note. Coping and stress responses ar e reported as proportional scores.

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41Table 3-2 Intercorrelations among demographic informa tion, health, stress, coping, an d psychological symptoms 1 2 3 4 5 6 7 8 9 10 11 12 1. SES --2. Cortisol AUC -.02 --3. Pubertal Timing -.06 .23* --4. Peer Stress .05 -.05 .02 --5. Degree of Hassle .16 .06 -.09 .41** --6. Primary Control .11 -.13 -.22* -.23* -.18 --7. Secondary Control -.03 .20 -.05 -.27** -.20 .48** --8. Vol. Disengagement -.05 -.09 .07 .19 .04 -.59** -.26** --9. Inv. Engagement .03 .27* .21* .17 .26* -.44** -.57** -.19 --10. Inv. Disengagement -.08 -.11 .06 .13 .10 -.62** -.64** .01 .35** --11. Internalizing Distress .10 .02 .21* .40** .28** -.48** -.45** .19 .40** .42** --12. Aggression -.04 .12 .21* .23* .13 -.34** -.41** -.05 .46** .43** .56**--Note. p < .10; p < .05; ** p < .01

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42 Table 3-3 Mixed effects models examining the a ssociation of internalizi ng distress and cortisol Parameter Model 1 Model 2 Model 3 Fixed Effects Initial status Intercept 00 -1.12*** (0.04) -0.96*** (0.04) -0.96*** (0.04) Internalizing Distress 01 -.002 (0.01) Rate of change Intercept 10 -0.09*** (0.01) -0.09*** (0.01) Time X Internalizing Distress 11 -0.003 (0.002) Variance Components Level 1 Within-person residual eij 0.07*** (0.02) 0.04*** (0.004) 0.04*** (0.004) Level 2 In initial status 0 j 0.10*** (0.65) 0.11*** (0.02) 0.12*** (0.02) In rate of change 1 j 0.006*** (0.002) 0.005*** (0.002) Pseudo R2 and Goodness of Fit R2 (within person variance) 0.43 0.00 R2 (variance in initial status) 0.00 0.00 R2 (variance in rate of change) 0.00 0.17 Deviance (-2LL) 260.4 135.1 153.4 Deviance (-2LL) 125.3*** -18.3 Note. *** p < .001

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43 Table 3-4 Mixed effects models examining th e association of aggression and cortisol Parameter Model 1 Model 2 Model 3 Fixed Effects Initial status Intercept 00 -1.12*** (0.04) -0.96*** (0.04) -0.96*** (0.04) Aggression 01 -.002 (0.01) Rate of change Intercept 10 -0.09*** (0.01) -0.09*** (0.01) Time X Aggression 11 -0.003 (0.002) Variance Components Level 1 Within-person residual eij 0.07*** (0.02) 0.04*** (0.004) 0.04*** (0.004) Level 2 In initial status 0 j 0.10*** (0.65) 0.11*** (0.02) 0.12*** (0.02) In rate of change 1 j 0.006*** (0.002) 0.005*** (0.002) Pseudo R2 and Goodness of Fit R2 (within person variance) 0.43 0.00 R2 (variance in initial status) 0.00 0.00 R2 (variance in rate of change) 0.00 0.17 Deviance (-2LL) 260.4 135.1 155.3 Deviance (-2LL) 125.3*** -20.2 Note. *** p < .001

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44 Table 3-5 Pubertal timing pr edicting internalizing distress Variable R2 R2 BSE B Step 1 .006 African American -.10.99-.01 Latina -.071.30-.01 Family SES .02.03.08 Step 2 .051* .045*African American -.19.97-.02 Latina -.211.28-.02 Family SES .03.03.09 Pubertal Timing 2.12.95.21* Note. p < .05

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45 Table 3-6 Pubertal timing predicting aggression Variable R2 R2 BSE B Step 1 .028 African American 1.061.17.09 Latina -.841.55-.06 Family SES -.04.04-.11 Step 2 .068* .04*African American .951.15.08 Latina -1.001.52-.07 Family SES -.04.04-.10 Pubertal Timing 2.401.13.20* Note. p < .05

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46 Table 3-7 Peer stress predicting internalizing distress Variable R2 R2 BSE B Step 1 .08 African American .071.08.01 Latina .481.41.04 Family SES .01.03.03 Degree of Hassle 1.29.47.28**Step 2 .173** .094**African American .081.02.01 Latina .501.35.04 Family SES .01.03.03 Degree of Hassle .64.51.14 Peer Stress .81.26.38** Note. ** p < .01

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47 Table 3-8 Peer stress predicting aggression Variable R2 R2 BSE B Step 1 .031 African American .721.26.06 Latina -.151.66-.01 Family SES -.03.04-.09 Degree of Hassle .75.57.14 Step 2 .082* .051* African American .731.23.06 Latina -.131.62-.01 Family SES -.03.03-.09 Degree of Hassle .20.61.04 Peer Stress .68.31.25* Note. p < .05

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48 a) .20 / .08 for primary control b) .20 / .11 for involuntary engagement Figure 3-1. Path model for pubertal timing to inte rnalizing distress. Each pathway controls for race and family SES. At the top of the model, the value was calculated for the pathway between pubertal timing and internaliz ing distress. On the left side of the model, the values were calculated separately for each pathway for pubertal timing to each potential mediator. The values on the right side of the model were calculated with all variables (covariate s, predictors, and mediators) entered simultaneously into the model. (a) On the right side, change in values for pathway between pubertal timing and internalizi ng distress when primary control is simultaneously entered; (a) On the right side, change in values for pathway between pubertal timing and internalizing dist ress when involuntary engagement is simultaneously entered. p < .10, p < .05, ** p < .01, *** p < .001

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49 a) .35** / .26* for primary control b) .35** / .26* for secondary control Figure 3-2. Path model for peer stress to internal izing distress. Each pathway controls for race, family SES, and degree of hassle. At the top of the model, the value was calculated for the pathway between peer st ress and internalizing distress. On the left side of the model, the values were calculated separately for each pathway for peer stress to each potential mediator. The values on the right side of the model were calculated with all variables (covariates, predictors, and mediators) entered simultaneously into the model. (a) On the right side, change in values for pathway between peer stress and internalizing distress when primary cont rol is simultaneously entered; (b) On the right side, change in values for pathway between peer stress and internalizing distress when secondary control is s imultaneously entered. p < .10, p < .05, ** p < .01, *** p < .001

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50 a) .25* / .19 for primary control b) .25* / .17 for secondary control Figure 3-3. Path model for peer stress to aggressi on. Each pathway controls for race, family SES, and degree of hassle. At the top of the model, the value was calculated for the pathway between peer stress and aggression. On the left side of the model, the values were calculated separately for each pathway for peer stress to each potential mediator. The values on the right side of th e model were calculated with all variables (covariates, predic tors, and mediators) entere d simultaneously into the model. (a) On the right side, change in values for pathway between peer stress and aggression when primary control is simulta neously entered; (b) On the right side, change in values for pathway between peer stress and aggression when secondary control is simultaneously entered. p < .10, p < .05, ** p < .01, *** p < .001

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51 CHAPTER 4 DISCUSSION Although much is known about stress and copi ng during adolescence, few studies have examined the influence of coping strategies on the relationship between social stress and adjustment. More specifically, relatively little is known as to how adolescents cope with being off-time with respect to puberty, and how respons es to being off-time influence psychosocial outcomes (Compas et al., 1999; Connor-Smith et al., 2000; Ge et al., 2001; Jaser et al., 2005; Klimes-Dougan et al., 2001). The goal of this st udy was to examine the association of biological and psychosocial indicators of stress and psychopathology from an integrated bio-psychosocial perspective and to expand upon the current under standing of how biological and social factors work in combination to influence negative outcomes during adolescence. This study examined the effect of peer stre ss on adjustment and why the impact of peer stress on adjustment varies among young adolescent girls. Consistent with prior research, girls who experienced more peer stress reported higher levels of internalizi ng distress and aggression (Deater-Deckard, 2001; Nansel et al., 2004; Rudolph, 2002). More over, as expected, coping strategies, specifically primary and secondary control strategies, mediated both of these associations. Specifically, girl s who experienced more peer stress used fewer primary and secondary control strategies, whic h are typically considered to be adaptive and effective means of coping, such as problem solving, positive thinki ng, emotional regulation, etc. This association, in turn, accounted for greater le vels of internalizi ng distress and aggression. Recently studies examining the impact of social stress on adju stment during adolescence have begun to explore how stress responses influence this relationship; however most of these studies have focused on the direct association between stress responses and adjust ment or examined how coping and stress responses moderated the association be tween stressful life events and adjustment

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52 (Connor-Smith, et al., Hampel & Petermann, 200 6). Building upon prior research, the present study focused specifically on peer stress and demons trated that how an ad olescent responds to peer stress mediates the association between stressful experiences and adjustment during adolescence. These findings are important because they provide a more thorough understanding of how stressful experiences with peers im pact adolescents psyc hosocial well-being. This study also examined the effect of pubert al timing on adjustment. As anticipated, girls who were early maturers, compared to those w ho were on-time or late demonstrated higher levels of internalizing distress and aggression. This finding is consistent w ith prior research that has demonstrated that experiencing puberty ea rlier than ones peers may place girls at a heightened risk for a variety of behavioral and emotional problems (Graber, 2003; Weichold, Silbereisen, & Schmitt-Rodermund, 2003). However, based on findings from this study, this association may be partially accounted for by the way girls deal with being early maturers. The use of primary control strategies (i.e., emo tional expression, emotional regulation, and problem solving) has been shown to attenuate the effect s of stressful experiences, whereas, the use of involuntary engagement (i.e., im pulsive action, physiological ar ousal, and intrusive thoughts or rumination) has been shown to intensify the effect s of stress on the individual (Compas, et al., 1999; Wadsworth, Raviv, Compas, & Connor-Smith, 2005) In this study, thes e two responses to stress mediated the association between early pubertal timing and in ternalizing distress. Meaning, early maturers used fewer primary cont rol strategies and more involuntary engagement strategies, which in turn accounted for gr eater levels of inte rnalizing distress. Although main effects of pubertal timing were de monstrated for both internalizing distress and aggression, these effects were reduced in the full regression (i.e., when stress response factors were included). The main effect of pube rtal timing on internaliz ing distress was reduced,

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53 but remained statistically significant, thus allowi ng for mediation effects of stress responses to be examined, as recommended by Baron and Kenny (1986) However, the main effect of pubertal timing on aggression was reduced to the point that it was no longer si gnificant, hind ering tests of mediation. According to Baron and Kenny (1986) mediation effects can not be tested if a significant effect between the inde pendent variable (pubertal timi ng) and the dependent variable (aggression) does not exist. The drop in signi ficance was likely due to the exclusion of participants that did not have re sponses to stress scores. Five of these participants were early maturers and 5 of them were on-time or late. Proportionally, there was a greater drop in the number of early maturers included in the an alyses. For this reas on, it likely became more difficult to demonstrate significance. Because the inability to test mediating effects of coping and stress responses on the association between pubertal timing and aggression was likely due to an attrition effect, future research should revisit this issue in order to demonstrate whether or not using particular coping strategi es benefits early maturers. Although an abundance of resear ch exploring the relationshi p between pubertal timing and maladjustment exists, few studies ha ve attempted to explore exactly how pubertal timing relates to adjustment and how girls cope with the soci al and emotional ramifications of being earlier than their peers (Brooks-Gunn et al., 1994; Caspi et al., 1993; Ge et al., 2002; Graber et al., 2005). The findings from this study are important because they demonstrate that some of the association between early timing and adjustment may be accounted for by how adolescents cope with or react to the stre ss of being off-time. Although examining the influence of individual coping strategies and stress responses is useful and informative, future research expl oring coping and peer st ress should also examine coping styles and how they impact adjustment. Recent research exploring coping has suggested

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54 that individuals have a tendency to respond to stress using a partic ular set of coping strategies and involuntary responses rath er than responding with one strategy (Reinhard, Wolff, & Wadsworth, 2006). Research that fo cuses on one type of stress re sponse may be missing the big picture of how individuals deal with stress. Thus, it may be informative to understand how these different combinations of strategi es (i.e., coping styles) either atte nuate or exaggerate the effects of peer stress. Contrary to expectation, this study failed to demonstrate an association between stress reactivity and symptoms of internalizing distress and aggression; as a result, potential mediating effects of coping strategies could not be explored. This study found no connection between how cortisol levels changed over th e course of a home visit (that included a variety of tasks) and symptoms of psychopathology. Much of the curren t literature has found associations between cortisol reactivity and psychopat hology, but mostly in samples re porting borderline or clinical levels of internalizing and externalizing be haviors (Angold, 2003; K limes-Dougan, et al., 2001; Oosterlaan, et al., 2005). In a study similar in design to the current study (i.e., normative adolescent samples exposed to social challe nge tasks), Klimes-Dougan and colleagues (2001) demonstrated links between stress reactivity and internalizing symptoms, but were unable to find clear associations between st ress reactivity and aggression. It was only until adolescents displayed clinical levels of a ggression that a significant association with stress reactivity emerged. Thus, because most of the girls in this study displayed low or at most marginally high levels of internalizing distress and aggressi on, associations between stress reactivity and symptoms of psychopathology may not have emer ged. In turn, further research examining adrenocortical activity in normative adolescent sa mples should be conducted in order to provide

PAGE 55

55 a more thorough understanding of whether or not a reliable connection between stress reactivity and symptoms of psychopathology exists. Some of the inconsistency in findings may be due to analytic differences. Most studies examining stress reactivity in child and adolescent samples utilize reactivity categories (i.e., increased dramatically, remained stable, decreased slightly, etc.) to expl ore stress reactivity and adjustment (Granger, et al., 1994; Klimes-Dougan, et al., 2001; Schmidt et al., 1999). This study utilized area under the curve and mixed modeling to explore patterns of change. There exists a debate as to what method is most appropriate to utilize when explori ng adrenocortical activity and adjustment. Thus further research explor ing the method of AUC and mixed modeling in different age groups of both boys and girls is necessary to under stand the implications of using these methods of analysis. This study has taken informative steps in unders tanding better how soci al stress influences psychosocial development; however, some limitati ons of the study exist. The examination of stress and coping was based solely on adolescent girls, rather than both boys and girls. Although researchers have suggested that social stress may be more detr imental to adolescent girls psychosocial well-being (Rudolph, 2002), it would be beneficial to examine further if gender differences during early adolescen ce emerge with respect to how gi rls and boys cope with social stress, and whether particular c oping strategies are more problem atic for one gender versus the other. In addition, the study focused on early adolescence, particularly 12 year olds, which prevented exploration of developmental changes in coping and stress responses over the course of adolescence and the impact of late pubertal timi ng. Additionally, due to the fact that data were only collected at a single time point, the direction of associations between social stress, coping, and psychopathology were inferred from theoreti cal perspectives and previous research

PAGE 56

56 exploring stress, coping and adjust ment. Thus, results should be interpreted with some caution. For example, it is unclear if girl s who utilize particular types of coping strategies such as primary and secondary control are more socially skilled a nd experience less peer st ress. A final limitation was the fact that participants were drawn from a large metropolitan area, limiting generalization to adolescents in suburban and rural areas. Despite the limitations, results of this st udy provide useful information regarding the identification of specific coping strategies and stress responses that me diate the relationship between stress and internalizing distress, and aggression. These findings speak to skills that could be taught in programs that emphasize how to effectively adapt to the social and psychological demands of transitioning into a dolescence. Although the present study focuses on negative outcomes, potential also exists to understand better what factors promote positive development (i.e., prosocial behavior, academic success, positive self-esteem) in the face of stressful social situations. U nderstanding these factors and how they affect psychosocial development may ultimately expand our current unders tanding of resilience in the face of stress.

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57 APPENDIX A HOME DATA COLLECTION PROCEDURE AND SALIVA SAMPLE COLLECTION 1. Consents 2. Specimen and questionnaire delivery details 3. Saliva #1 4. Maze task 5. Neighborhood/peer questions 6. Saliva #2 7. Cold pressor task #1 8. Cold pressor questions 9. Cold pressor task #2 10. Cold pressor questions 11. Disagreement Questions 12. Saliva #3 13. Daily routines/ nutri tion/ sleep questions 14. Physical exam 15. Menstruation & social activities questions 16. Saliva #4 17. Peer issues interaction task 18. Disagreement interaction task 19. Saliva #5

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58 APPENDIX B MIXED EFFECTS MODELS EXAMINING THE IMPACT OF TIME AND SYMPTOMS OF PSYCHOPATHOLOGY ON PATTERNS OF CORTISOL PRODUCTION

PAGE 59

59 Table B1. Impact of time and internaliz ing distress on patterns of cortisol Model Level-1 Model Level-2 Model Composite Model A ij oi ije Cortisol j i 0 00 0 ) (0 00 j ij ite Cortisol B ij ij i oi ije Time Cortisol 1 j i 0 00 0 j i 1 10 1 ij itTime Cortisol10 00 )1 0 ij j j ijTime e C ij ij i oi ije Time Cortisol 1 j iDep Anx Dep Anx0 01 00 0) / / ( j iDep Anx Dep Anx0 11 10 1) / / ( ij itTime Cortisol10 00 ) )( / / [(01ijTime Dep Anx Dep Anx ij j j ijTime e1 0( ) Note. (A) unconditional means mode l (partitions variance in to between and within variance); (B) unconditional growth model (do cortisol levels vary over time); (C) examines effect of internalizing distress on initia l status and rate of change of cortisol Table B2. Impact of time and aggr ession on patterns of cortisol Model Level-1 Model Level-2 Model Composite Model A ij oi ije Cortisol j i0 00 0 ) (0 00j ij ite Cortisol B ij ij i oi ije Time Cortisol 1 j i 0 00 0 j i1 10 1 ij itTime Cortisol10 00 ij j j ijTime e1 0( C ij ij i oi ije Time Cortisol 1 j iAgg Agg0 01 00 0) ( j i iAgg Agg1 11 10 1) ( ij itTime Cortisol10 00 ) )( [(01 ijTime Agg Agg )1 0 ij j j ijTime e Note. (A) unconditional means m odel (partitions variance into between and within variance); (B) unconditional growth model (do cortisol levels vary over time); (C) exam ines effect of aggression on initial st atus and rate of change of cortisol

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60 LIST OF REFERENCES Achenbach, T. M. (1991). Manual for the Youth Se lf-Report and 1991 Profile Department of Psychiatry, University of Vermont, Burlington, VT. Aldenderfer, M. S., & Blashfield, R. K. (1984). Cluster Analysis Beverely Hills, CA: Sage Publications. Angold, A. (2003). Adolescent depression, cortisol, and DHEA. Psychological Medicine, 33 573-581. Brooks-Gunn, J. (1991). How stressful is the tran sition to adolescence for girls? In M. E. Colten & S. Gore (Eds.), Adolescent stress: Causes and consequences (pp. 131-149). New York: Aldine de Gruyter. Brooks-Gunn, J., Graber, J. A., & Paikoff, R. L. (1994). Studying links between hormones and negative affect: Models and measures. Journal of Research on Adolescence, 4 469-486. Caspi, A., Lynam, D., Moffitt, T. E., & Silva, P. A. (1993). Unraveling girls' delinquency: Biological, dispositional, and contextual contributions to adolescent misbehavior. Developmental Psychology, 29 19-30. Chumlea, W. C., Schubert, C. M., Roche, A. F., Kulin, H. E., Lee, P. A., Himes, J. H., et al. (2003). Age at menarche and raci al comparisons in US girls. Pediatrics, 111 110-113. Cicchetti, D., & Walker, E. F. (2001). Stress and development: Biological and psychological consequences. Development & Psychopathology, 13 413-418. Coie, J. D., Dodge, K. A., & Kupersmidt, J. B. ( 1990). The role of poor peer relationships in the development of disorder. In S. R. Asher & J. D. Coie (Eds.), Peer rejection in childhood (pp. 274-305). New York: Cambridge University Press. Coleman, L. and Coleman, J. (2002). The measurement of puberty: A review. Journal of Adolescence, 25 535-550. Compas, B. E., Connor, J. K., Saltzman, H., Harding Thomsen, A., & Wadsworth, M. (1999). Getting specific about coping: Effortful and involuntary responses to stress in development. In M. Lewis & D. Ramsay (Eds.), Soothing and stress (pp. 229-256). Mahwah, NJ: Lawrence Erlbaum Associates. Connor-Smith, J. K., Compas, B. E., Wadswort h, M. E., Thomsen, A. H., & Saltzman, H. (2000). Responses to stress in adolescence: Measurement of coping and involuntary stress responses. Journal of Consulting and Clinical Psychology, 68 976-992. Deater-Deckard, K. (2001). Annotation: Recent res earch examining the role of peer relationships in the development of psychopathology. Journal of Child Psychology and Psychiatry, 42 565-579.

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61 Ge, X., Brody, G. H., Conger, R. D., Simons R. L., & Murry, V. M. (2002). Contextual amplification of pubertal transition effects on deviant peer affiliation and externalizing behavior among African American children. Developmental Psychology, 38 42-54. Ge, X., Conger, R. D., & Elder, G. H. (2001). P ubertal transition, stressful life events, and the emergence of gender differences in adolescent depressive symptoms. Developmental Psychology, 37 404-417. Goodyer, I. M., Herbert, J., Tamplin, A., & A ltham, P. M. E. (2000). First-episode major depression in adolescents. British Journal of Psychiatry, 176 142-149. Graber, J. A. (2003). Puberty in context. In C. Hayward (Ed.), Gender differences at puberty (pp. 307-321). New York: Cambridge University Press. Graber, J. A., & Brooks-Gunn, J. (1996). Transi tions and turning points: Navigating the passage from childhood through adolescence. Developmental Psychology, 32 768-776. Graber, J. A., Brooks-Gunn, J., & Archibald, A. B. (2005). Links between girls' puberty and externalizing and internalizing behaviors: Moving from demonstrating effects to identifying pathways. In D. M. Stoff & E. J. Susman (Eds.), Developmental psychobiology of aggression New York: Cambridge University Press. Graber, J. A., Seeley, J. R., Brooks-Gunn, J., & Lewinsohn, P. M. (2004). Is pubertal timing associated with psychopathology in young adulthood? Journal of the American Academy of Child and Adolescent Psychiatry, 43 718-726. Granger, D. A., Weisz, J. R., & Kauneckis, D. (1994). Neuroendocrine reactivity, internalizing behavior problems, and control-related co gnitions in clinic-referred children and adolescents. Journal of Abnormal Psychology, 103 267-276. Gunnar, M. R. (2000). Early adversity and the deve lopment of stress reactivity and regulation. In C. A. Nelson (Ed.), The effects of adversity on ne urobehavioral development: The Minnesota Symposia on Child Psychology (Vol. 31, pp. 163-200). Mahwah, NJ: Erlbaum. Gunnar, M. R., & Vazquez, D. M. (2001). Low co rtisol and a flattening of expected daytime rhythm: Potential indices of risk in human development. Development & Psychopathology, 13 515-538. Hampel, P., & Petermann, F. (2006). Perceived st ress, coping, and adjustment in adolescents Journal of Adolescent Health, 38 409-415. Hawker, D. S., & Boulton, M. J. (2000). Twen ty years' research on peer victimization and psychosocial adjustment: A meta-analytic review of cross-sectional studies. Journal of Child Psychology and Psychiatry, 41 441-455. Hertsgaard, L., Gunnar, M. R., Larson, M., Brodersen, L., & Lehman, H. (1992). First time experiences in infancy: When they app ear to be pleasant, do they activate the adrenocortical stress response? Developmental Psychobiology, 25 319-333.

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62 Hollingshead, A. B. (1975). Four factor index of social status. Unpublished manuscript, Yale University. Jaser, S. S., Langrock, A. M., Keller, G., Merc hant, M. J., Benson, M., Reeslund, K., et al. (2005). Coping with the stress of parental depression II: Adolescent and parent reports of coping and adjustment. Journal of Clinical Child a nd Adolescent Psychology, 34 193-205. Khatri, P., Kupersmidt, J. B., & Patterson, C. (2000). Aggression and peer victimization as predictors of self-reported beha vioral and emotional adjustment. Aggressive Behavior, 26 345-358. Klimes-Dougan, B., Hastings, P. D., Granger, D. A., Usher, B. A., & Zahn-Waxler, C. (2001). Adrenocortical activity in at-risk and nor mally developing adol escents: Individual differences in salivary cortisol basal levels, diurnal variation, and responses to social challenges. Development & Psychopathology, 13 695-719. La Greca, A. M. (2001). Friends or foes? P eer influences on anxiety among children and adolescents. In W. K. a. T. Silverman, P.D.A. (Ed.), Anxiety disorders in children and adolescents: Research, assessment and intervention (pp. 159-186): Cambridge University Press. MacKinnon, D. P., Lockwood, C. M., Hoffman, J. M., West, S. G., & Sheets, V. (2002). A comparison of methods to test mediation and other intervening variable effects. Psychological Methods, 7, 83-104. Meinlschmid, G., & Hellhammer, D. H. (2003). Tw o formulas for computation of the area under the curve represent measures of total horm one concentration versus time-dependent change. Psychoneuroendocrinology, 28 916-931. Nachmias, M., Gunnar, M. R., Mangelsdorf, S., Parritz, R. H., & Buss, K. (1996). Behavioral inhibition and stress reactivity: The m oderating role of attachment security. Child Development, 67 508-522. Nansel, T. R., Craig, W., Overpeck, M., Saluja, G., Ruan, J., & Health Be haviour in School-aged Children Bullying Analyses Working Group. ( 2004). Cross-national consistency in the relationship between bullying behavi ors and psychosocial adjustment. Archives of Pediatrics and Adoles cent Medicine, 158, 730-736. Ohring, R., Graber, J. A., & Brooks-Gunn, J. (2002). Girls' recurrent and concurrent body dissatisfaction: Correlates and consequences over 8 years. International Journal of Eating Disorders, 31 404-415. Oosterlaan, J., Geurts, H. M., Knol, D. L., & Se rgeant, J. A. (2005). Low basal salivary cortisol is associated with teacher-reported symptoms of conduct disorder. Psychiatry Research, 134 1-10. Petersen, A., & Crockett, L. (1985). Pubert al timing and grade effects on adjustment. Journal of Youth and Adolescence, 14 191-206.

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63 Preacher, K. J., & Hayes, A. F. (2004). SPSS and SAS procedures for estimating indirect effects in simple mediation models. Behavior Research Methods, In struments, and Computers, 36, 717-731. Preacher, K. J., & Hayes, A. F. (2006). Asymptotic and resampling strategies for assessing and comparing indirect effects in simple and multiple mediator models Manuscript submitted for publication. Pruessner, J. C., Kirschbaum, C., Reinhard, C., Wolff, B., & Wadsworth, M. (2006, March). Coping and involuntary stress response clusters predicting symptoms of psychopathology for ado lescents living in poverty. Paper presented at the Biennial Mee ting of the Society for Research on Adolescence, San Francisco. Rovine, M. J., von Eye, A., & Wood, P. (1988). Th e effect of low covariat e criterion correlations on the analysis-of-covariance. In E. Wegmen (Ed.), Computer science and statistics: Proceedings of the 20th symposium of the interface (pp. 500-504). Alexandria, VA: American Statistical Association. Schmidt, L. A., Fox, N. A., Sternberg, E. M., Gold, P. W., Smith, C. C., & Schulkin, J. (1999). Adrenocortical reactivity and social competence in seven year-olds. Personality and Individual Differences, 26 977-985. Schwartz, D., McFadyen-Ketchum, S. A., Dodge, K. A., Pettit, G. S., & Bates, J. E. (1998). Peer group victimization as a predictor of children' s behavior problems at home and in school. Development & Psychopathology, 10 87-99. Shrout, P. E., & Bolger, N. (2002). Mediation in experimental and none xperimental studies: New procedures and recommendations. Psychological Methods, 7, 422-445. Sobel, M. E. (1982). Asymptotic intervals for indi rect effects in structural equation models. In S. Leinhart (Ed.), Sociological methodology 1982 (pp.290-312). San Francisco: Jossey-Bass. Southwick, S. M., Vythilingam, M., & Charney, D. S. (2005). The psychobiology of depression and resilience to stress: Implicat ions for prevention and treatment. Annual Review of Clinical Psychology, 1 255-291. Storch, E. A., Nock, M. K., Masia-Warner, C., & Barlas, M. E. (2003). Peer victimization and social-psychological adjustment in Hispanic and African-American children. Journal of Child and Family Studies, 12 439-452. Van Bokhoven, I., Van Goozen, S. H. M., Van E ngeland, H., Schaal, B., Arseneault, L., Seguin, J. R., et al. (2005). Salivary cortisol and aggression in a population-based longitudinal study of adolescent males. Journal of Neural Transmission, 112 1083-1096. Van de Wiel, N., Van Goozen, S. H. M., Matth ys, W., Snoek, H., & Van Engeland, H. (2004). Cortisol and treatment effects in children with disruptive behavior di sorders: A preliminary study. Journal of American Academy of Child and Adolescent Psychiatry, 43 1011-1018.

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64 Wadsworth, M. E., Raviv, T., Compas, B. E ., & Connor-Smith, J. K. (2005). Parent and adolescent responses to poverty-related stre ss: Tests of mediated and moderated coping models. Journal of Child and Family Studies, 14 283-298. Weichold, K., Silbereisen, R. K., & Schmitt-Rode rmund, E. (2003). Short-term and long-term consequences of early versus late physical ma turation in adolescents. In C. Hayward (Ed.), Gender differences at puberty (pp. 241-276). New York, NY: Cambridge University Press. Weisberg, H. I. (1979). Statistical adjustments and uncontrolled studies. Psychological Bulletin, 86 1149-116.

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65 BIOGRAPHICAL SKETCH Lisa M. Sontag is a third-year developmental psychology graduate student at the University of Florida. She received a Bachelor of Science in Psychology at Tulane University. Her research focuses on adolescent developmen t from a bio-psychosocial orientation. In particular, her research explores how peer relatio ns, stress reactivity, pubertal timing, and coping contribute to both healthy adjustment and emoti onal and behavioral problems. Currently she is the co-investigator of the APEX (Adolescent Peer Experiences) St udy that investigates how peer relationships influence psychosocial deve lopment during the middle school years.


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Title: Coping with Social Stress: Implications for Psychopathology in Adolescent Girls
Physical Description: Mixed Material
Copyright Date: 2008

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Source Institution: University of Florida
Holding Location: University of Florida
Rights Management: All rights reserved by the source institution and holding location.
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COPING WITH SOCIAL STRESS: IMPLICATIONS FOR PSYCHOPATHOLOGY IN
ADOLESCENT GIRLS




















By

LISA M. SONTAG


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

Lisa M. Sontag


































To those who have always supported me and encouraged me to reach beyond my limits.









ACKNOWLEDGMENTS

I thank my supervisory committee chair (Dr. Julia A. Graber) and members of supervisory

committee members (Dr. Eric Storch and Dr. Manfred Diehl) for their constructive and

thoughtful input. I thank Dr. Elizabeth Hayes for assisting me with my analyses. I thank the

participants of the study. I also thank the National Institute of Child Health and Human

Development and the National Institute of Mental Health for providing support for this proj ect.












TABLE OF CONTENTS


page

ACKNOWLEDGMENTS .............. ...............4.....


LIST OF TABLES ................ ...............7............ ....


LIST OF FIGURES .............. ...............8.....


AB S TRAC T ......_ ................. ............_........9


CHAPTER


1 INTRODUCTION ................. ...............11.......... ......


Background ................. ...............11.......... ......
Stress............... ...............12.
Peer stress ................. ...............13.................

Pubertal timing .................. ...............14.......... .....
Biological correlates of stress .............. ...............16....

Coping and Responses to Stress ................. ...............18........... ...
Proposed Study .............. ...............20....
Research question 1............... ...............21...
Research question 2............... ...............21...


2 METHODS .............. ...............23....


Participants .............. ...............23....
Procedure .............. ...............23....
M measures ................... .......... ...............24.......

Demographic Data............... ...............24..
Biological Response to Stress .............. ...............25....
Pubertal Timing ................. ...............26.......... .....
Experiences of Peer Stress............... ...............27.
Apprai sal ................. ...............27.................
Coping ................ ...............27...
Internal izing Distress............... ...............28
Ag gre ssi on ................ ...............29................
Analysis Plan .............. ...............29....

3 RE SULT S .............. ...............32....


Attrition Analy ses............... ...............32
Descriptive Analyses .............. ...............32....
Tests of Main Effects ................. ...............34................
Biological Response to Stress .............. ...............34....
Pubertal Timing ................. ...............36.......... .....












Peer Stress .............. ...............36....
Tests of M edition ................ ...............36........... ....
Pubertal Timing ........._.___..... .__ ...............36....
Peer Stress .............. ...............38....


4 DI SCUS SSION ........._.___..... .___ ...............5 1....


APPENDIX


A HOME DATA COLLECTION PROCEDURE AND SALIVA SAMPLE
COLLECTION .............. ...............57....


B MIXED EFFECTS MODELS EXAMINING THE IMPACT OF TIME AND
SYMPTOMS OF PSYCHOPATHOLOGY ON PATTERNS OF CORTISOL
PRODUC TION ................. ...............58.................


LIST OF REFERENCES ................. ...............60................


BIOGRAPHICAL SKETCH .............. ...............65....










LIST OF TABLES


Table page

3-1 Means and standard deviations of adolescents' demographic information, health,
stress, coping, and psychological symptoms .............. ...............40....

3-2 Intercorrelations among demographic information, health, stress, coping, and
psychological symptoms ........... ......._._ ...............41....

3-3 Mixed effects models examining the association of internalizing distress and cortisol....42

3-4 Mixed effects models examining the association of aggression and cortisol ....................43

3-5 Pubertal timing predicting internalizing distress .............. ...............44....

3-6 Pubertal timing predicting aggression .............. ...............45....

3-7 Peer stress predicting internalizing distress ................ ...............46...............

3-8 Peer stress predicting aggression .............. ...............47....

B-1 Impact of time and internalizing distress on patterns of cortisol ................ ................. .59

B-2 Impact of time and aggression on patterns of cortisol ................ ......... ................59










LIST OF FIGURES

Figure page

1-1 Bio-psychosocial framework ................. ...............22................

3-1 Path model for pubertal timing to internalizing distress ................. ................. ......48

3-2 Path model for peer stress to internalizing distress. ......_................. ................ ..49

3-3 Path model for peer stress to aggression. ....__ ......_____ .......__ ..........5









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

COPING WITH SOCIAL STRESS: IMPLICATIONS FOR PSYCHOPATHOLOGY IN
ADOLESCENT GIRLS

By

Lisa M. Sontag

December 2006

Chair: Julia A. Graber
Major Department: Psychology

This study investigated the impact of social stress on girls' psychosocial development

during adolescence by integrating models of peer stress, pubertal timing, adrenocortical activity,

and coping. Based on a sample of 111 girls (Mage=11.84, SD = .77), we explored whether

patterns of cortisol, pubertal timing, and peer stress were associated with symptoms of

internalizing distress and aggression. Additionally, we examined whether coping strategies and

involuntary responses to stress mediated these associations. Cortisol reactivity was not

associated with adjustment; however, pubertal timing and peer stress were. Coping and

involuntary responses mediated the association between pubertal timing and peer stress and

adjustment. Findings indicate that learning to effectively adapt to stress may help girls transition

more successfully into adolescence.
































































10









CHAPTER 1
INTTRODUCTION

Background

Adolescence is a period of rapid growth and change, both physically and psychologically.

During the transition into adolescence, individuals must learn to manage the physical changes

their bodies endure due to the onset of puberty, changes in social context, and changes in school

environment (Graber & Brooks-Gunn, 1996). Such experiences inherently place young

adolescents at heightened risk for experiencing a great number of new daily stressors

(Brooks-Gunn, 1991; Ge, Conger, & Elder, 2001). Because the chance of encountering some

type of environmental or social stressor is inevitable, young adolescents must learn to adapt and

to cope with these life experiences in order to successfully navigate the transition into

adolescence and eventually into early adulthood.

During the transition into adolescence, individuals experience more stressful events

compared to older adolescents or children, which in turn is associated with an increase in such

outcomes as depressive affect (Graber & Brooks-Gunn, 1996; Rudolph, 2002). Of these stressful

events, off-time pubertal maturation and interpersonal stress within the context of peers pose

particular threats to adolescents (Graber, Brooks-Gunn, & Archibald, 2005). According to

Rudolph' s model of interpersonal stress (2002), girls are at a particular risk for experiencing

higher levels of peer stress and consequently psychological maladjustment compared to boys,

due to the fact that peer relationships, specifically with close friends, are of greater importance to

girls. In addition, some individuals exhibit disregulations in the production of cortisol in

response to stressors which increases the risk for poor psychological outcomes. For example,

variations in both basal activity and stress reactivity have been linked to internalizing and

externalizing problems among young adolescents (Klimes-Dougan, Hastings, Granger, Usher, &









Zahn-Waxler, 2001). However, exposure to potentially stressful situations is not always linked to

poor outcomes. The ability to cope with or respond effectively to stress relies heavily upon the

ability to interpret and react appropriately to the stressor itself or to the physiological, emotional,

and behavioral responses to the stressor. By integrating models of social and biological

indicators of stress and by using a more comprehensive view of how adolescents respond to

stressful experiences, this study explored what factors place some young adolescent girls at

greater risk for maladjustment in the face of stressful life experiences.

Stress

Stress may be best conceptualized as a multidimensional concept that includes not only

the stressor, but also the processing system, which includes the cognitive assessment of the

stimuli, and the stress response (Compas, Orosan, & Grant 1993). Although conceptually stress

may be a multilevel process, more often than not the experience of stress is quite automatic and

usually occurs unconsciously. Moreover, not all experiences are equally stressful to individuals,

thus making appraisals of potentially stressful experiences relevant (Lazarus & Folkman, 1984).

The transition into adolescence is marked not only by physical and sexual maturation, but

also by increased exposure to new, many of them challenging, events (Brooks-Gunn, 1991; Ge et

al, 2001; Graber & Brooks-Gunn, 1996). Although there is evidence that stress increases during

early adolescence, the experience of particular events as stressful is not necessarily pervasive

among all adolescents (Brooks-Gunn, 1991). Rather, the experience of an event as stressful is

likely due to interactions among various changing life events (e.g., interactions among hormonal

and physical changes, school transitions, peer group changes, and altering family dynamics) that

influence an adolescent' s interpretation of particular events as stressful (Brooks-Gunn, 1991).

One aspect of stress that seems to be particularly salient to adolescents is social stress.

Social stress represents stimuli within the context of social interactions or relationships that










evoke emotional, physical, and psychological arousal in individuals. Social stress may be

broadly characterized as experiences within a social context, including interactions with others

(e.g., peer stress), as well as how one's own development (e.g., puberty) is experienced in a

social context.

Peer stress

Peer stress may be best conceptualized as experiences within the peer context that exert

significant pressure on an individual's ability to function adaptively. More concrete examples of

peer stress include conflicts with close friends, being teased or hassled by other children, and

being rejected by other children. Peer stress becomes increasingly salient as a threat to

psychological well-being during adolescence due to the increasing amount of time spent with

peers relative to other interpersonal relationships (La Greca, 2001). The relative salience of peer

relationships and the impact of peer stress during the transition into adolescence are further

supported by findings from Rudolph (2002) that demonstrated that levels of stress increase from

preadolescence to adolescence independent of gender.

Increased exposure to interpersonal stress during childhood and adolescence has been

linked to disorders and symptoms of psychopathology, namely anxiety, depression, behavior

problems, and substance use (Coie, Dodge, & Kupersmidt, 1990; Hawker & Boulton, 2000).

Specific aspects of peer stress, peer rej section and victimization, have been consistently linked to

externalizing and internalizing problems in adolescents (Deater-Deckard, 2001). A study

examining aggression and peer victimization as predictors of behavioral and emotional

adjustment found that greater experiences of peer aggression predicted greater levels of both

self-reported aggression and delinquency (Khatri, Kupersmidt, & Patterson, 2000). Another

study, conducted by Storch, Nock, Masia-Warner, and Barlas (2003), found that among Hispanic









and African American children, overt peer victimization was positively associated with

depressive symptoms and aspects of social anxiety. Additionally, relational victimization was

uniquely associated with depressive and anxious symptoms for girls only. Recent work

examining cross-national consistency in the relationship between being bullied and psychosocial

adjustment found that being the recipient of bullying behaviors was linked to poor emotional

adjustment, poor school adjustment and poor relationships with classmates (Nansel et al., 2004).

As indicated, girls experience higher levels of peer stress compared to boys during

adolescence (Rudolph, 2002). This differential trend is likely due to the fact that peer

relationships, specifically with close friends, are of greater importance to girls. It is not to say

that boys do not have experiences that could be interpreted as stressful, but rather girls interpret

comparable situations as more stressful and detrimental to their interpersonal relationships.

Pubertal timing

One aspect of social stress that is particularly salient to adolescents is the experience of

pubertal changes and whether those changes reflect normative or off-time developmental trends

within one's peer group. In order to better understand the impact of pubertal development on

adolescents' overall experiences of stress and the relationship between puberty and

psychopathology, it is useful to distinguish between pubertal status and pubertal timing.

According to Graber, Peterson, and Brooks-Gunn (1996), pubertal status refers to the physical

and physiological maturational levels of an individual at a given point in time, relative to the

overall pubertal process. Pubertal timing, however, may be conceptualized as a social

construction and best represents whether an individual's maturation is earlier, on-time, or later in

comparison to same-age peers.









Research examining the relationship between pubertal maturation and changes in

depressive or aggressive affect has found few links between pubertal status and negative

outcomes (Brooks-Gunn, Graber, & Paikoff, 1994; Graber et al., 2005). In contrast, research

focusing on the effects of pubertal timing has demonstrated that the stress and conflict elicited by

one's off-time maturation is more strongly linked to psychological and behavioral maladjustment

(Graber et al., 2005 for a recent review). Additionally, this research has also indicated that early

maturing girls are particularly at risk for a variety of disorders or symptoms of disorders,

including anxiety, depression, aggression, substance abuse, and eating disorders. A study by

Graber, Seeley, Brooks-Gunn, and Lewinsohn (2004) examining the association between

pubertal timing and psychopathology in young adulthood found that women who were early

maturers were at unique risk for persistent difficulty and development of psychopathology during

adolescence and young adulthood. Other studies examining the role of pubertal timing found that

early maturing girls were at high risk for depressive symptoms, body dissatisfaction, aggression,

and delinquency problems (Caspi, Lynam, Moffitt, & Silva, 1993; Ge, Brody, Conger, Simons,

& Murry, 2002; Ge et al., 2001; Ohring, Graber, & Brooks-Gunn, 2002).

In order to explain the connection between hormonal and pubertal changes and negative

affective and behavioral outcomes, Brooks-Gunn and colleagues (1994) proposed a model that

included the possibility that social events or context, as well as the adolescent's perceptions of

his or her pubertal processes, contribute to or function as mediators of hormonal effects on

negative affect and behavior. In testing this model, Brooks-Gunn and Warren (1989) found that

social events, not pubertal development, accounted for a good deal of variance in affect and

behaviors. In terms of social processes, adolescents who mature early or late in comparison to

their peers are placed in socially "deviant" categories compared with on-time peers (Petersen &









Crockett, 1985). Keeping in mind that girls as a group tend to mature a couple of years earlier

than boys, early maturing girls are deviant in comparison to both other girls and boys, which

places these girls at a heightened risk for maladjustment.

This study explored the effects of pubertal timing within a social processes framework in

order to expand on previous findings that have linked the social experience of being "off-time"

and particular emotional or behavioral changes. As highlighted by Brooks-Gunn and colleagues

(1994), social factors play a significant role in connecting the pubertal timing and negative affect

or behavior. The way an individual interprets his or her timing is likely to influence the types of

social interactions he or she experiences, and in turn is likely to influence potential affective or

behavioral changes. Research has shown that early maturing girls consistently report poor quality

of relationships at mid-adolescence and young adulthood (Graber et al., 2004). By examining

how early maturing girls cope with or adapt to potentially stressful situations within the peer

context, a better understanding of the mechanisms by which pubertal timing relates to

maladjustment may emerge.

Biological correlates of stress

Under conditions interpreted as stressful, the limbic-hypothalami c-pituitary-adrenal

(LHPA) axis in mammals (including humans) responds to this experience via a series of events

that result in the secretion of glucocorticoids (cortisol in human and nonhuman primates, and

corticosterone in rodents) from the adrenal cortex (Cicchetti & Walker, 2001). Prolonged

exposure to environmental and internal stress, and in turn disregulations of cortisol levels, can

affect psychological well-being. Past studies investigating the association between adrenocortical

activity, stress, and psychosocial well-being found that variation in both the basal activity and in

stress reactivity has been associated with psychopathology (Angold, 2003; Goodyer, Herbert,










Tamplin, & Altham, 2000; Klimes-Dougan, Hastings, Granger, Usher, & Zahn-Waxler, 2001;

Southwick, Vythilingam, & Chamney, 2005). However, much of this literature has focused

primarily on diurnal patterns of change and investigated cortisol reactivity in clinical populations

(Oosterlaan, Geurts, Knol, & Sergeant, 2005; Van Bokhoven et al., 2005; Van de Wiel, Van

Goozen, Matthys, Snoek, & Van Engeland, 2004). Therefore the question still remains as to how

patterns of cortisol reactivity in normative samples of adolescents reflect experiences of stress,

particularly social stress, and how these patterns of reactivity are associated with changes in

negative affect and behavior.

For individuals who follow a typical day-night schedule, cortisol production peaks during

the last few hours of sleep (Gunnar & Vazquez, 2001 for a review). Cortisol levels then decline

rapidly throughout the morning and decrease gradually during the remainder of the day. When

stress is induced, cortisol secretion initially increases. Following the onset of a stressor, cortisol

usually takes about 10-15 min to produce a rise in circulating cortisol levels. About 20-30 min

after the stressor, peak concentrations of cortisol are found in saliva. Following this peak, the

negative feedback loop of the LHPA axis begins to reestablish homeostatic functioning by

reducing the level of circulating cortisol.

Recent research examining the association between changes in daytime cortisol levels in

response to social challenges (i.e., public speaking task or mother-child conflict task) has shown

that adolescents and children tend to display increases in salivary cortisol approximately 20 to 30

min following exposure to a social challenge task, and then display a decrease in levels of

cortisol (Granger, Weisz, & Kauneckis, 1994; Klimes-Dougan et al., 2001; Schmidt et al., 1999).

In addition, findings from these studies have indicated that maintaining high levels of cortisol or










displaying strong task-related decreases are associated with higher levels of internalizing and

externalizing behavior.

Findings such as those mentioned previously point to a link between stress response and

psychopathology; however, activation of the L-HPA axis may not be directly linked to

symptomatology. Additionally, there are few conclusive or consistent findings within the child

and adolescent research about whether a true relationship between cortisol levels and

psychopathology exists. Therefore, more research examining the association between cortisol

and psychopathology is needed, especially within the adolescent female population.

Coping and Responses to Stress

Because of the increase in stressful experiences during the transition to adolescence

(Brooks-Gunn, 1991), learning to adapt to the stressor and manage one's response to the stressful

situation is crucial to leading a healthy and productive life. However, the effects of stress vary by

individuals. Whereas most people fare quite well in the face of typically occurring stressful

events, other individuals manifest symptoms of psychopathology, as mentioned previously. But

the question therein lies, why do individuals demonstrate differential outcomes to stress exposure

and how do these differences emerge? Coping strategies offer one of the mechanisms through

which stress differentially affects individuals. Understanding the process of coping and how

adolescents effectively or ineffectively react to stressful stimuli allows researchers to understand

better why particular individuals adapt well or adapt poorly.

As suggested by Lazarus and Folkman (1984), coping involves efforts to manage specific

external and/or internal demands that are appraised as taxing or exceeding the resources of the

person. Coping differs from general responses to stress in that coping is viewed as volitional or

under the person's control. In addition, Lazarus and Folkman emphasize the role of cognitive

processes in determining what is experienced as stressful and how one copes.









Theoretical frameworks of coping, such as the one developed by Lazarus and Folkman

(1984), adequately target volitional responses to stress; however, few models have included

involuntary responses to stress. One comprehensive model, developed by Compas, Connor,

Saltzman, Thomsen, and Wadsworth (1999), includes both volitional and involuntary responses

to stressful stimuli. According to this model, stress response can be characterized as being either

effortful or involuntary. Effortful responses are cognitive and behavioral reactions to stress

experienced as volitional and purposeful such as acceptance, denial, and avoidance. Involuntary

responses, as defined by Compas et al. (1999), include temperamentally based and conditioned

cognitive, behavioral, and physiological reactions to stress that may or may not be within

conscious awareness and are not under personal control, such as physiological arousal, intrusive

thoughts, and rumination. In combination with the volitional responses to stress (i.e., coping),

involuntary responses create a more representative model of how individuals respond to external

and internal stressors throughout their lifespan.

Compas and colleagues (1999) further differentiated effortful and involuntary responses

to stress by distinguishing between engagement and disengagement responses. Engagement

responses are directed toward a stressor or one's reactions to the stressor and include approach

responses. Disengagement responses are directed away from these targets and include avoidance

responses. Given this model, an individual may respond to a stimulus in one or more of the

following manners: effortful engagement (primary and secondary control), effortful

disengagement, involuntary engagement, and involuntary disengagement. Connor-Smith et al.

(2000) tested this model using a sample of adolescents and their parents. Findings indicated that

not only was there adequate to excellent internal consistency for each subtype of response to

stress (i.e., primary control, secondary control, disengagement coping, involuntary engagement,









and involuntary disengagement) but subscales of coping, specifically, mapped onto other

standard measures of coping quite clearly. More important, however, was the finding that factors

within this model of responses to stress correlated with internalizing and externalizing behavior.

Thus, these exploratory analyses suggest that a model including both coping and involuntary

responses adequately captured how adolescents adapt to stressors. Additionally, how one copes

with stress was associated with emotional or behavioral outcomes.

Other studies examining the association between responses to stress and emotional and

behavioral outcomes have consistently demonstrated that style of response mediates the

relationship between stress, specifically family conflict and chronic pain, and anxiety,

depression, and aggression (Jaser et al., 2005; Wadsworth, Raviv, Compas, & Connor-Smith,

2005). Extrapolating to other realms of stress, it is likely that an individual's type of response to

social stress (e.g., peer stress) will mediate the relationship between social stress and

psychopathology during adolescence. However, little empirical work has examined the effects of

responses to stress on this relationship and even fewer studies have extended this research to

examining how coping may serve as a mechanism through which biological indicators of stress

(i.e., cortisol) and pubertal timing influence poor outcomes.

Proposed Study

This study investigated the impact of stress reactivity and social factors on negative

outcomes from a bio-psychosocial perspective as a means to explain emotional and behavioral

changes that occur during the transition into adolescence. By integrating several theoretical

models that focus on the context of peer stress, pubertal timing, adrenocortical activity, and

coping (Figure 1), this study aimed to provide a more comprehensive approach to understanding

the pathways to adjustment. Within this framework, this study examined physiological and

environmental indicators of social stress and how these indicators were associated with










symptoms of psychopathology, in particular internalizing distress and aggression. Additionally,

this study explored whether responses to stress mediated this relationship. Specifically, the study

examined the following questions:

Research question 1

Are physiological and environmental indicators of social stress associated with symptoms
of internalizing distress and aggression?

Specifically, is biological stress reactivity (i.e., pattern of cortisol levels) associated with
symptoms of psychopathology? Because of the exploratory nature of the study with
respect to the Eindings associated with cortisol, it was predicted that pattern of reactivity
was associated with symptoms of internalizing distress and aggression. However,
specific predictions about the association between particular patterns of cortisol and
behavioral outcomes were not made.


Is pubertal timing associated with symptoms of intemalizing distress and aggression?
This study predicted that girls who reported early pubertal timing would demonstrate
higher levels of internalizing distress and aggression compared to girls who reported
being on-time or late.

Are experiences of peer stress associated with symptoms of internalizing distress and
aggression? It was hypothesized that girls who reported a greater number of stressful peer
experiences would display more symptoms of intemalizing distress and aggression.

Research question 2

Do coping strategies mediate the association between biological and environmental
indicators of stress and symptoms of psychopathology?

Do coping strategies mediate the association between stress reactivity (i.e. cortisol
patterns) and symptoms of internalizing distress and aggression? It was hypothesized that
the 5 coping strategies or responses to stress (i.e., primary control, secondary control,
effortful disengagement, involuntary engagement, and involuntary disengagement) would
mediate the association between stress reactivity and symptoms of psychopathology.
More specifically, it was predicted that effortful disengagement and involuntary
disengagement would serve as mediators between stress reactivity and internalizing
distress, whereas involuntary engagement would mediate the association between stress
reactivity and aggression. It was expected that primary and secondary control coping
strategies would mediate the association between stress reactivity and internalizing
distress and aggression.










* Do coping strategies mediate the association between pubertal timing and symptoms of
internalizing distress and aggression? It was expected that coping strategies would
mediate the association between pubertal timing (i.e., early vs. on-time or late) and
symptoms of psychopathology in the same way that was described for stress reactivity.

* Do coping strategies mediate the association between peer stress and symptoms of
internalizing distress and aggression? It was hypothesized that coping strategies would
mediate the association between peer stress and symptoms of internalizing distress and
aggression in the same way that was described for stress reactivity and pubertal timing.







Social Stress
Pubertal timing
Peer Stress
Psychopathology
Coping Internalizing Distress
~IResponses Aggression


Figure 1-1. Bio-psychosocial framework









CHAPTER 2
METHOD S

Participants

Participants were 111 adolescent girls (Mage = 11.84, SD = .77), who were drawn from a

larger proj ect, the Girls Health and Development proj ect, that examined biological correlates of

girls' social and emotional health as they made the transition to puberty. Approximately 15% of

the girls were in 5th grade, 47% in 6th grade, 3 1% in 7th grade, and 2% in 8th grade. Of the 11 1

girls, 48% were Caucasian, 36% African American, and 16% Hispanic. Girls and their families

were originally recruited in 1995-1996 from public schools in ethnically integrated,

working-class and middle-class communities in the New York City area. The study included 138

girls at baseline; 1 11 of these girls participated in the final follow-up, approximately three years

later. Analyses for the current study were completed using only girls who participated in the final

follow-up .

Procedure

Girls and their families were recruited via their schools. Each time families participated,

parents signed informed consent forms at their homes, on their own behalf and for their child's

participation. Girls gave assent for their participation. Mothers and children completed several

tasks (Appendix A) during a home visit and completed surveys during the 3 consecutive days

following the home visit. Girls completed surveys on their own affect and behaviors. Surveys

were picked up from the families' homes 3 days after the home visit. Girls received a gift (tote

bag) for their participation and mothers were paid $75.









Measures


Demographic Data

Data concerning the characteristics of the participants were collected using standard items

concerning age, household structure, and race/ethnicity. Girls reported their date of birth, and

exact age was calculated from date of home visit. Mothers reported on family characteristics and

child race/ethnicity. Race/ethnicity was collapsed into three categories: White, African

American, and Hispanic. For regression analyses, two dummy coded variables were used:

African American versus others and Hispanic versus other, with White as the omitted group.

Family SES was assessed using the Hollingshead Scale (Hollingshead, 1975), a scale

based on survey data of social status tied to U.S. census categories. The standard scoring

protocols were used for different household types. Mothers reported on the education and

occupation of themselves and any other parent/caregiver in the household. For each head of

household, education (coded on a 7-point scale from 1 = less than 7th grade to 7 = graduate

professional) was multiplied by a weight of 3 and occupation (coded on a 9-point scale from

1 = farm labor and menial service workers to 9 = higher executives and major professionals) was

multiplied by a weight of 5. Thus the range of possible scores for family SES was 8 to 66

(Hollingshead, 1975). For one-parent households, the education score and occupation score were

summed to yield an SES score. In two-parent families, one parent in paid employment, the

family SES was derived by adding the mean of the parents' education scores to the occupation

score for the employed parent. If both parents were employed, the family SES score was the

mean of the parents' SES scores.









Biological Response to Stress

During the in-home visit, 5 saliva samples were collected to assess cortisol levels

throughout a battery of tasks. See the Appendix A for a complete list of tasks. Approximately

15-20 min occurred between collections. The unit of measurement for cortisol assayed was Cpg/dl.

Saliva was collected via Salivettes. Girls kept the cotton roll in their mouths for 2 min,

resulting in sufficient amounts of saliva for repeat assays. Girls ingested a small amount of

sweetened Kool-Aid to stimulate saliva flow. Stimulating saliva flow with orally administered

substances such as powdered drink mix was recommended protocol at the time this protocol was

implemented (Granger et al., 1994; Gunnar & Vazquez, 2001; Hertsgaard, Gunnar, Larson,

Brodersen, & Lehman, 1992; Nachmias, Gunnar, Mangelsdorf, Parritz, & Buss, 1996).

Subsequent to the development of this procedure, it was found that Kool-Aid may alter the

results of the assay of cortisol from saliva samples (Schwartz, McFadyen-Ketchum, Dodge,

Pettit, & Bates, 1998). However, these effects were found to vary by assay kit used. The kit used

in the present study was not highly susceptible to this problem. Saliva samples were stored in a

refrigerator before being transported to Columbia-Presbyterian Reproductive Endocrinology

Department in New York City, where they were stored in a freezer at -20oC until assayed for

cortisol. Cortisol concentrations were determined using a radioimmunoassay adapted for

measurements in saliva (Diagnostic Products Company). The lower detection limit for this assay

was 0.02 Clg/dl per 200 Cll of saliva. Saliva samples were centrifuged at 3000 rpm for 10 min. A

200 Cll sample was used for duplicate analysis. All samples from a participant were analyzed in

one assay run, with inter- and intra-assay coefficients of variations less than 5 and 3%,

respectively.

Certain samples were excluded from analysis due to problems with the saliva sample. The

lab processing the samples excluded participants' samples if the samples were insufficient to










process. Log transformations were applied to the cortisol data to reduce the large positive skew,

which is consistent with standard procedures in cortisol research (Gunnar, 2000). However,

original units were reported for ease of interpretation.

Pubertal Timing

Pubertal timing was based on self-reported age of menarche obtained during the home

visit. A recent review of the use of self-reported menarche noted that accuracy of recall is

reduced as the time interval between menarche and recall is increased (Coleman & Coleman,

2002). However, if assessed within a period of 1 year from menarche, girls can typically recall

menarche within 1 month of the exact date. Given that the study's participants have recently

experienced menarche, the use of self-report can be considered a valid measure.

Using self-reported age of menarche, girls were classified as either early-maturers or other

(on-time or late). Cut-off ages by race (White, African American, and Latina) were derived from

a large, normative study of puberty (Herman-Giddens et al., 1997). Based on mean ages of

menarche reported by race in the Herman-Giddens study, girls that reported age of menarche

1/ SD below the mean were categorized as early. All other girls were in the other group (on-time

or late). According to an investigation of age at menarche for girls in the United States, age of

menarche for Hispanic girls tends to fall between ages for non-Hispanic white girls and

non-Hispanic black girls (Chumlea et al., 2003). Because the Herman-Giddens study only

examined White and African American girls, estimates for early Latinas were calculated as '/ SD

below the mean menarcheal age of the sample. Cut off ages for early maturing girls were: 12.28

y for White, 11.55 y for African American, and 11.97 y for Latina. Late maturation could not be

determined due to the mean age of assessment (just under 12 y) because the mean age of

menarche for each race as determined by Herman-Giddens et al. (1997) was greater than

12 years. Thirty five percent of the participants were classified as early maturers. Approximately









28% of White participants, 33% of African American participants, and 40% of Latina

participants were early maturers.

Experiences of Peer Stress

Participants' experiences of peer stress were assessed as part of the survey administered in

the days after the home visit using a stressful events checklist that was included in a version of

the Responses to Stress Questionnaire that was adapted for this study (RSQ; Connor-Smith,

Compas, Wadsworth, Thomsen, & Saltzman, 2000). The RSQ was developed to assess

experiences of stressful events and responses to stress in adolescent populations. The checklist

provided information about how many stressful experiences the participants had encountered

since the start of the school year. The RSQ can be tailored to specific stressors; this form of the

RSQ was tailored to assess peer stress. For the stressful events checklist, participants endorsed 9

items. Sum scores were calculated, with higher scores representing the experience of more

stressful events. Peer stress, as discussed in the study, was operationalized as the number of

stressful events a participant experienced.

Appraisal

Appraisal of stressful experiences was also assessed using the RSQ. Participants responded

to a single item that assessed overall how stressful the problems endorsed in the stressful events

checklist were for them on a likert scale (1 = not at all to 4 = very). Higher scores indicated that

the participant felt the experiences to be more stressful.

Coping

Coping was also assessed using the RSQ. Adapted from the original RSQ for the purposes

of this study, the measure consisted of 3 8 items rated on a 4-point likert scale (1 = not at all to

4 = a lot). The RSQ contains 5 sub scales: primary effortful control, secondary effortful control,

effortful disengagement, involuntary engagement and involuntary disengagement. In this study,










the primary effortful control subscale contained 7 items that assessed responses to stress

categorized as emotional expression, emotional regulation, and problem solving (a = .80). The

secondary effortful control subscale contained 4 items that measured responses to stress

categorized as acceptance, positive thinking, and cognitive restructuring (a = .70). The effortful

disengagement subscale contained 9 items and assessed denial, avoidance, and wishful thinking

(a = .75). The involuntary engagement sub scale contained 9 items, which assessed impulsive

action, physiological arousal, and intrusive thoughts or rumination (a = .78). Finally, the

involuntary disengagement subscale contained 9 items that measured inaction, emotional and

cognitive numbing, and involuntary avoidance or fleeing (a = .76). High scores on each sub scale

indicated that participants were more likely to engage in these types of responses in the face of

stress. Raw scores were reported as sum scores and used for reliability analyses. However, in

order to control for overall responding bias, factor scores reflecting the proportion of total

responses (e.g., sum of scores on primary control items/sum of all items) were used in analyzing

the associations with internalizing distress and aggression as recommended by Connor-Smith

and colleagues (2000).

Internalizing Distress

Internalizing distress was assessed during the home visit using the anxiety/depression

sub scale of the Youth Self Report (YSR/1 1-18) created by Achenbach (1991). The YSR for ages

11-18 is a self-report measure designed to measure competencies, adaptive functioning, and

problems in youth and adolescents ages 11-18. It can be completed by those having a fifth grade

reading level or administered orally. Participants were asked to report on behavior now or within

the past 6 months and rated items on a likert scale (0 = not true, 2 = very true or often true).

Scores for the anxiety/depression subscale were reported as sum scores. The anxiety/depression

sub scale contained 16 items, with a reliability of a = .83.










Aggression

Aggression was also assessed using the YSR/11-18 (Achenbach, 1991). Participants rated

items on a likert scale (0 = not true, 2 = very true or often true). Participants were asked to report

on behavior now or within the past 6 months. Scores for the subscale of aggression were reported

as sum scores. The aggression sub scale contained 19 items, with a reliability of a = .86.

Analysis Plan

The goal of this study was to examine physiological and environmental indicators of social

stress and how these indicators were associated with symptoms ofpsychopathology, specifically

internalizing distress and aggression. Additionally, this study explored whether responses to

stress mediated this association. First, attrition analyses were performed to determine if the

sample used in this study differed on key variables from the original sample of participants

recruited. Descriptive analyses were performed on key variables.

To address the first set of hypotheses, main effects were explored via ANCOVAs and

hierarchical linear regression. As a means to explore the main effect of stress reactivity on

internalizing distress and aggression, a combination of linear regression models and mixed

models was used. Within the cortisol literature, researchers use multiple approaches to examine

the association between stress reactivity (i.e., change in cortisol levels) and outcomes of interest.

The computation of the area under the curve (AUC) is a frequently used method in

endocrinological research and the neuroscience to explore information that is contained in

repeated measurements over time (Pruessner, Kirschbaum, Meinlschmid, & Hellhammer, 2003).

In the case of this study, AUC was employed to investigate task-dependent changes in cortisol

level over the period of the home visit. AUCoon-isol was calculated from zero and log

transformations were applied to the AUCoon-isolvalue for each participant to reduce the large










positive skew. To explore the main effects of stress reactivity, AUCoortisol was entered as the

independent variable in a linear regression model.

Although frequently used in endocrinological research to capture patterns of change over

time, the area under the curve as calculated from zero may neglect to capture idiosyncrasies of

change that occur regardless of one's absolute levels of cortisol. Also, as indicated, calculating

area under the curve requires data at each time point. Thus, in order to further explore potential

associations between patterns of change in cortisol production and symptoms of internalizing

distress and aggression, mixed effects models were used. These models addressed the question

of whether one' s pattern of production of cortisol over the 5 home visit samples changed in

association with one's symptoms of psychopathology. In addition, mixed models do not require

participants to have data at each time point. Thus, for this study, it was possible to estimate the

desired associations with fewer than 5 cortisol samples, allowing for a greater total sample size.

Addressing the remaining components of the first set of research questions, the main effect

of pubertal timing on internalizing distress and aggression was explored via a combination of

ANCOVAs and a hierarchical linear regression model. The main effect of peer stress was

explored using only a linear regression analysis.

Mediation was tested using the guidelines delineated by Baron and Kenny (1986). The

mediators were primary control coping, secondary control coping, disengagement coping,

involuntary engagement responses, and involuntary disengagement responses. Specifically,

separate regression models tested the effects of the social stress predictors (peer stress, pubertal

timing) or biological correlates of stress (cortisol) on each mediator and both internalizing

distress and aggression. A full model was then tested with the social stress predictor and all the

mediators entered on the same step. For mediation to occur, the predictor must have a significant









association with the mediator and the outcome variable, and, in the full model, the mediator must

predict the outcome variable and the size and significance of the association between the

predictor and the outcome variable must be reduced. In all models, race and family SES was

controlled for; in the models with peer stress as the predictor, appraisal was also controlled for.

Researchers comparing methods to test mediation have suggested that Baron and Kenny's

(1986) method neglects to provide a direct estimate of the size of the indirect effect of the

independent variable on the dependent variable (MacKinnon, Lockwood, Hoffman, West, &

Sheets, 2002; Preacher & Hayes, 2004). In turn they suggest supporting research findings with a

product of coefficients test, typically the Sobel Test, which states if ab (the indirect effect) is not

significantly different from zero, there is no effect of mediation (Sobel, 1982). However,

according to Preacher and Hayes (2004) this method is also misleading because there is reason to

be suspicious of the use of the normal distribution for computing the p value for the Sobel test

because the sampling distribution of ab may not be normal. To address this issue, Preacher and

Hayes (2006) recommend bootstrapping the sampling distribution of ab and deriving a

confidence interval with the empirically derived bootstrapped sampling distribution. This

approach has been suggested as a way of circumventing the power problem introduced by

asymmetries and other forms of non-normality in the sampling distribution of ab (Preacher &

Hayes, 2004; Shrout & Bolger, 2002). Given this recommendation, a test of the indirect effect

was performed to support mediation effects consistent with Baron and Kenny's (1986)

guidelines.









CHAPTER 3
RESULTS

Attrition Analyses

Due to the loss of 19.5% of the sample of girls from baseline (n = 13 8) to the final

follow-up 3 years later (n = 1 11), univariate analyses of non-response bias were

conducted to determine if the remaining sample differed on key demographic factors,

pubertal development variables, and outcomes (depression, peer problems, internalizing

and externalizing behavior) assessed at baseline. Results showed that families did not

differ on variables used in this study.

Some participants were excluded from particular analyses because they did not

have values for some variables. For analyses involving cortisol samples, some girls were

excluded because their saliva samples were insufficient to assay cortisol, whereas others

participated via phone interview and survey if they moved, and thus did not have a

cortisol sample. For the exact number of reports for each variable see Table 3-1.

Descriptive Analyses

Descriptive information (i.e., M and SD) are shown in Table 3-1 and correlations

among the variables of interest are shown in Table 3-2.

Contrary to the hypotheses, stress reactivity (AUCoor-tisol) was not associated with

internalizing distress or aggression (r = .02, ns, and r = .12, ns, respectively). In fact, only

two variables demonstrated significant correlations with stress reactivity: pubertal timing

(r = .23, p < .05), and involuntary engagement (r = .27, p < .05).

Pubertal timing also demonstrated significant associations with the outcomes. For

the dichotomous pubertal timing variable (early vs. Other), ANCOVAs (controlling for

SES and race) were conducted, as the F-values, means, and standard deviations for the










effects may be more illuminating than correlations. As expected, girls who were early

maturers reported more internalizing distress, F (1, 104) = 4.83, p < .05, with an average

score of 6.63 (SD = 4.76) compared to other girls (M = 4.57, SD = 4.44), and more

aggressive symptoms, F (1, 104) = 4.54, p < .05, with an average score of 8.77

(SD = 6.39) compared to other girls (M = 6.29, SD = 4.96).

Peer stress was positively associated with both internalizing distress (r = .40,

p < .01) and aggression (r = .23, p < .05). Appraisal of the stressful experiences was

positively associated with both peer stress (r = .41, p < .01) and internalizing distress

(r = .28, < .05 .

As anticipated, the potential mediators of the association between biological and

environmental indicators of social stress and adjustment demonstrated consistent

associations with the outcomes of interest. Internalizing distress was positively associated

with voluntary disengagement, involuntary engagement, and involuntary disengagement

responses (Table 3-2). Additionally as predicted, internalizing distress was negatively

associated with primary control strategies (r = -.48, p < .01), meaning that girls who used

problem solving and emotional expression and regulation tactics to cope with peer stress

reported fewer symptoms of anxiety and depression. The use of secondary control

strategies, such as acceptance or cognitive restructuring, was also negatively associated

(r = -.45, p < .01) with internalizing distress. This suggested that adolescent girls who

attempted to manage stressful peer experiences by using positive self-talk or accepting

these stressors as something from which to learn experienced fewer anxious and

depressive symptoms than girls were less likely to use these strategies.










Similar to the findings for internalizing distress, aggression was positively

correlated with involuntary engagement responses, and involuntary disengagement

responses (Table 3-2). As hypothesized, primary control engagement coping and

secondary control engagement coping were negatively correlated with aggression. The

use of disengagement coping strategies, such as denial, avoidance, and wishful thinking,

was not correlated with aggression.

Tests of Main Effects

As indicated, in order to test whether or not physiological and environmental

indicators of social stress were associated with symptoms of internalizing distress and

aggression, a series of hierarchical regression analyses were performed. All analyses

controlled for race/ethnicity (African American versus other, Hispanic versus other,

White as omitted group) and family SES.

Biological Response to Stress

Controlling for race and family SES, AUCoon-isol was not significantly associated

with internalizing distress, F (4, 65) = .59, p = .67, or aggression, F (4, 65) = .33, p = .86,

meaning amount of total stress reactivity over the 5 points of cortisol assessment were not

associated with symptoms of intemalizing distress or aggression. Sample sizes for these

analyses were much lower than the main group of participants (N= 111). This occurred

because in order to calculate an AUCoon-isol score, participants needed to have 4 out of the

5 samples and were not missing sample 1 or sample 5, in addition to needing race, SES,

internalizing distress, and aggression scores.

An unrestricted covariance structure was used for each model and all continuous

between-person variables were centered on the grand mean. Because race and family SES

were shown not to be significant predictors of AUCoon-isol, they were not included in the









mixed effect models. Researchers claim that including covariates that do not exhibit

associations with the dependent variable can generate spurious significant associations in

models, and thus it is recommended to exclude covariates from the analyses that would

otherwise be included in typical regression and ANCOVA analyses (Rovine, von Eye, &

Wood, 1988; Weisberg, 1979). One set of analyses was performed for each set of

symptoms (i.e., internalizing distress and aggression), resulting in 2 sets of analyses.

However, because internalizing distress and aggression showed not to be significant

predictors of participants' patterns of change in cortisol, results from the 2 sets of

analyses will be discussed in combination.

In Model 1 (see Tables 3-3 and 3-4), the variance in cortisol was partitioned into

within- and between-person variance; 41.18% of the variance was due to within-person

variability and 58.82% was due to between-person variability. In Models 2 and 3, fixed

effects were added in a systematic fashion and pseudo R2 -Staltistics were calculated to

determine the amount of variance these models accounted for relative to the baseline

model .

In Model 2, time was included as a level-1 predictor of cortisol. Results

demonstrated that time was a significant predictor of cortisol levels and accounted for

43% of the within-person variance. In Model 3, the effects of internalizing distress

(Table 3-3) or aggression (Table 3-4) were added. Both internalizing distress and

aggression were not significant predictors and did not account for any between-person

variance. In addition, the interactions between time and internalizing distress and time

and aggression were not significantly associated with cortisol levels. Thus, although

results showed that cortisol levels changed over the 5 in-home collections, symptoms of










psychopathology were not associated with how cortisol levels changed over time. These

results corroborate the findings from the area under the curve analyses.

Pubertal Timing

To test whether or not pubertal timing was associated with symptoms of

internalizing distress and aggression, a series of hierarchical regression models was

performed (Table 3-5). Controlling for race/ethnicity and SES, pubertal timing was

significantly associated with internalizing distress, such that girls who were early

maturers demonstrated higher levels of internalizing distress compared to other girls.

Controlling for race/ethnicity and SES, pubertal timing was also significantly associated

with aggression, such that girls who reported early maturation demonstrated higher levels

of aggression compared to other girls. These findings were consistent with bivariate

correlations reported in Table 3-2.

Peer Stress

As expected, results indicated that peer stress was significantly associated with

both internalizing distress and aggression (Tables 3-7 and 3-8). Controlling for race,

SES, and appraisal, higher levels of peer stress were associated with greater symptoms of

internalizing distress and aggression.

Tests of Mediation

As indicated, a series of regression models were performed to test effects of

mediation as specified by Baron and Kenny (1986), with subsequent examination of tests

of mediation as proposed by Preacher and Hayes (2006).

Pubertal Timing

Figure 3-2-1 shows the model testing mediated pathways of pubertal timing (early

vs. Other) to internalizing distress. The standardized P coefficients are shown in the










figures. In all, 5 tests of mediation (one for each mediator) were performed for

internalizing distress. As can be seen in Figure 3-2-1, there was evidence for full

mediation of the effect of timing on internalizing distress via primary control and

involuntary engagement responses. As per specifications of Baron and Kenny (1986), the

coefficient of pubertal timing predicting internalizing distress was reduced and was no

longer significant when the mediators were included in the model (i.e., P for pubertal

timing to internalizing distress, when mediated by primary control, was reduced from .20,

p < .10, to .08, ns, and was reduced from .20, p < .10, to .11, ns, when mediated by

involuntary engagement). Results from Preacher and Hayes (2006) test of the indirect

effect found that the indirect effect (ab = .1 1) of pubertal timing on internalizing distress

through primary control was estimated to lie between .03 and .27 with 95% confidence.

Also, the indirect effect (ab = .10) of pubertal timing on internalizing distress through

involuntary engagement was estimated to lie between .03 and .20 with 95% confidence.

For both indirect effects, mediation was said to occur because the indirect effects (ab)

were significantly different from zero.

The tests of mediation demonstrated that early pubertal timing predicted less use of

primary control strategies which subsequently predicted fewer symptoms of internalizing

distress. Conversely, early timing predicted greater use of involuntary engagement

responses, which subsequently predicted greater symptoms of internalizing distress.

Pubertal timing was not associated with secondary control strategies, voluntary

disengagement strategies, and involuntary disengagement responses.

Potential mediation effects on the association between pubertal timing and

aggression were not examined. Although initial analyses demonstrated that pubertal










timing was significantly associated with aggression (Table 3-6), analyses for tests of

mediation demonstrated that pubertal timing did not demonstrate a significant association

with aggression (P = .15, p = .14). In the tests of mediation, listwise deletion was

utilized, thus excluding participants who did not have scores for all the necessary

variables needed to illustrate mediation (i.e., pubertal timing, internalizing distress,

coping scores, and all covariates). This difference in analysis between the general

regression and the tests of mediation accounts for the emergence of a significant

association between pubertal timing and aggression in the original regression analysis

and the non-signifieant association that emerged in the test of mediation.

Peer Stress

Figure 3-2 shows the model testing mediated pathways of peer stress to

internalizing distress; and Figure 3-3 shows the model examining the association between

peer stress and aggression. As shown in Figure 3-2 and 4, peer stress was positively

associated with voluntary disengagement; however, because voluntary engagement

strategies were not associated with either internalizing distress or aggression, mediation

effects did not emerge. Peer stress was not associated with involuntary engagement and

disengagement responses.

Two mediation effects emerged for both internalizing distress and aggression. As

can be seen in Figure 3-2, there was evidence for partial mediation of the effect of peer

stress on internalizing distress via primary control and secondary control strategies. The

coeffieient of peer stress predicting internalizing distress was reduced and was no longer

significant when the mediators were included in the model (i.e., P for peer stress to

internalizing distress, when mediated by primary control, was reduced from .35, p < .01,

to .26, p < .05, and was reduced from .35, p < .01, to .25, p < .05, when mediated by









secondary control). Noteworthy was the fact that the association between peer stress and

primary control was only a trend. However, using Preacher and Hayes' (2006) test of the

indirect effect supported the Einding of partial mediation, demonstrating that ab was

significantly different from zero with 95% confidence for primary control, ab = .10, CI

(.02, .21), and for secondary control strategies, ab = .10, CI (.01, .23).

Figure 3-3 shows evidence for full and partial mediation of the effect of peer stress

on aggression via primary control and secondary control strategies, respectively. The

coefficient of peer stress predicting aggression was reduced and was no longer significant

when the mediators were included in the model (i.e., P for peer stress to aggression, when

mediated by primary control, was reduced from .25, p < .05, to .20, p < .10, and was

reduced from .25, p < .05, to .17, p = .13, when mediated by secondary control).

Supporting these Eindings, ab was significantly different from zero with 95% confidence

for primary control, ab = .06, CI (.01, .16), and for secondary control strategies, ab = .08,

CI (.01, .24). For tests of the indirect effect, ab was significantly different from zero,

which demonstrated mediation. This means that greater peer stress predicted less use of

primary and secondary control strategies which subsequently predicted fewer symptoms

of internalizing distress and aggression.










Table 3-1 Means and standard deviations of adolescents' demographic information,
health, stress, coping, and psychological symptoms


SD
.78
6.72
.16
.16
.17
.12
.14
0.20
.87
1.96
1.00
.05
.03
.05
.04
.04
4.62
5.54


Variable N M
Age 111 11.84
SES 110 33.07 11
Cortisol sample 1 89 .17
Cortisol sample 2 84 .14
Cortisol sample 3 80 .12
Cortisol sample 4 71 .09
Cortisol sample 5 73 .10
Cortisol AUC 72 9.72 11
Age of menarche 46 1 1.26
Peer stress 98 2.60
Degree of hassle 96 2.16
Primary control 101 .23
Secondary control 100 .13
Effortful disengagement 101 .24
Involuntary engagement 100 .20
Involuntary disengagement 100 .19
Internalizing distress 109 5.21
Aggression 109 7.07
Note. Coping and stress responses are reported as proportional scores.











Table 3-2 Intercorrelations among demographic information, health, stress, coping, and psychological symptoms
1 2 3 4 5 6 7 8 9 10 11 12
1. SES--
2. Cortisol AUC -.02 --
3. Pubertal Timing -.06 .23* -
4. Peer Stress .05 -.05 .02 --
5. Degree of Hassle .16 .06 -.09 .41 --
6. Primary Control .11 -.13 -.22* -.23* -. 18t
7. Secondary Control -.03 .20 -.05 -.27* -.20t .48 --
8. Vol. Disengagement -.05 -.09 .07 .19 .04 -.59* -.26--
9. Inv. Engagement .03 .27* .21* .17 .26* -.44* -.57* -. 19t
10. Inv. Disengagement -.08 -.11 .06 .13 .10 -.62* -.64* .01 .35*
11. Internalizing Distress .10 .02 .21* .40* .28* -.48* -.45* .19t .40* .42 --
12. Aggression -.04 .12 .21* .23 .13 -.34 -.4 -.05 .46~ .43 .56~ ---
Note. p <.10; p<.05; ** p<.01









Table 3-3 Mixed effects models examining the association of internalizing distress and cortisol
Parameter Model 1 Model 2 Model 3
Fixed Effects
Initial status
Intercept Too -1.12*** -0.96*** -0.96***
(0.04) (0.04) (0.04)
Internalizing Distress 70, -.002
(0.01)
Rate of change
Intercept 710 -0.09*** -0.09***
(0.01) (0.01)
Time X Internalizing 7,, -0.003
Distress (0.002)
Variance Components
Level 1
Within-person residual eij 0.07*** 0.04*** 0.04***
(0.02) (0.004) (0.004)
Level 2
In initial status PUo, 0.10*** 0.11*** 0.12***
(0.65) (0.02) (0.02)
In rate of change p 0.006*** 0.005***
(0.002) (0.002)
Pseudo R2 and Goodness of Fit

R2 E (within person variance) 0.43 0.00
R20 (variance in initial
0.00 0.00
status)
R21 (variance in rate of 01
change)
Deviance (-2LL) 260.4 135.1 153.4
ADeviance (-2LL) 125.3*** -18.3
Note. *** p<.001










Table 3-4 Mixed effects models examining the association of aggression and cortisol
Parameter Model 1 Model 2 Model 3


Fixed Effects
Initial status
Intercept


-1.12***
(0.04)


-0.96***
(0.04)


-0.96***
(0.04)
-.002
(0.01)

-0.09***
(0.01)
-0.003
(0.002)


0.04***
(0.004)

0.12***
(0.02)
0.005***
(0.002)


Aggression 70

Rate of change
Intercept 7,

Time X Aggression 7,3

Variance Components
Level 1
Within-person residual eg

Level 2
In initial status Uo

In rate of change p,

Pseudo R2 and Goodness of Fit

R2 E (within person variance)
R20 (variance in initial
status)
R21 (variance in rate of
change)
Deviance (-2LL)
ADeviance (-2LL)
Note. *** p<.001


-0.09***
(0.01)


0.07***
(0.02)

0.10***
(0.65)


0.04***
(0.004)

0.11***
(0.02)
0.006***
(0.002)


0.43

0.00

0.00


0.00

0.00

0.17


260.4


135.1 155.3
125.3*** -20.2










Table 3-5 Pubertal timing predicting internalizing distress
Variable R2 AR2 B SEE B


Step 1
African American
Latina
Family SES
Step 2
African American
Latina
Family SES
Pubertal Timing
Note. p <.05


.006


-.10 .99
-.07 1.30
.02 .03


-.01
-.01
.08

-.02
-.02
.09
.21*


.051* .045*


-.19
-.21
.03
2.12


.97
1.28
.03
.95










Table 3-6 Pubertal timing predicting aggression
Variable R2 AR2 B SEE B


Step 1
African American
Latina
Family SES
Step 2
African American
Latina
Family SES
Pubertal Timing
Note. p <.05


.028


1.06 1.17
-.84 1.55
-.04 .04


.09
-.06
-.11

.08
-.07
-.10
.20*


.068* .04*


.95
-1.00
-.04
2.40


1.15
1.52
.04
1.13


















.173* .094**


.08 1.02 .01
.50 1.35 .04
.01 .03 .03
.64 .51 .14
.81 .26 .38**


Table 3-7 Peer stress predicting internalizing distress
Variable R2 AR2 B SEE B


.08


Step 1
African American
Latina
Family SES
Degree of Hassle
Step 2
African American
Latina
Family SES
Degree of Hassle
Peer Stress
Note. ** p <.01


.07 1.08
.48 1.41
.01 .03
1.29 .47


.01
.04
.03
.28**










Table 3-8 Peer stress predicting aggression
Variable R2 AR2 B SEE B
Step 1 .031
African American .72 1.26 .06
Latina -.15 1.66 -.01
Family SES -.03 .04 -.09
Degree of Hassle .75 .57 .14
Step 2 .082* .051*
African American .73 1.23 .06
Latina -.13 1.62 -.01
Family SES -.03 .03 -.09
Degree of Hassle .20 .61 .04
Peer Stress .68 .31 .25
Note. p <.05




























a) .20t / .08 for primary control


b) .20t /.11 for involuntary engagement


Figure 3-1. Path model for pubertal timing to internalizing distress. Each pathway controls for
race and family SES. At the top of the model, the P value was calculated for the
pathway between pubertal timing and internalizing distress. On the left side of the
model, the P values were calculated separately for each pathway for pubertal timing
to each potential mediator. The P values on the right side of the model were
calculated with all variables (covariates, predictors, and mediators) entered
simultaneously into the model. (a) On the right side, change in P values for pathway
between pubertal timing and internalizing distress when primary control is
simultaneously entered; (a) On the right side, change in P values for pathway between
pubertal timing and internalizing distress when involuntary engagement is
simultaneously entered. "f p < .10, p < .05, ** p < .01, *** p < .001




























a) .35 / .26* for primary control


b) .35 / .26* for secondary control



Figure 3-2. Path model for peer stress to internalizing distress. Each pathway controls for race,
family SES, and degree of hassle. At the top of the model, the P value was calculated
for the pathway between peer stress and internalizing distress. On the left side of the
model, the P values were calculated separately for each pathway for peer stress to
each potential mediator. The P values on the right side of the model were calculated
with all variables (covariates, predictors, and mediators) entered simultaneously into
the model. (a) On the right side, change in P values for pathway between peer stress
and internalizing distress when primary control is simultaneously entered; (b) On the
right side, change in P values for pathway between peer stress and internalizing
distress when secondary control is simultaneously entered. "f p < .10, p < .05,
** p <.01, *** p <.001






























a) .25* /.19t for primary control
b) .25 / .17 for secondary control


Figure 3-3. Path model for peer stress to aggression. Each pathway controls for race, family SES,
and degree of hassle. At the top of the model, the P value was calculated for the
pathway between peer stress and aggression. On the left side of the model, the P
values were calculated separately for each pathway for peer stress to each potential
mediator. The P values on the right side of the model were calculated with all
variables (covariates, predictors, and mediators) entered simultaneously into the
model. (a) On the right side, change in P values for pathway between peer stress and
aggression when primary control is simultaneously entered; (b) On the right side,
change in P values for pathway between peer stress and aggression when secondary
control is simultaneously entered. "f p < .10, p < .05, ** p < .01, *** p < .001









CHAPTER 4
DISCUSSION

Although much is known about stress and coping during adolescence, few studies have

examined the influence of coping strategies on the relationship between social stress and

adjustment. More specifically, relatively little is known as to how adolescents cope with being

"off-time" with respect to puberty, and how responses to being off-time influence psychosocial

outcomes (Compas et al., 1999; Connor-Smith et al., 2000; Ge et al., 2001; Jaser et al., 2005;

Klimes-Dougan et al., 2001). The goal of this study was to examine the association of biological

and psychosocial indicators of stress and psychopathology from an integrated bio-psychosocial

perspective and to expand upon the current understanding of how biological and social factors

work in combination to influence negative outcomes during adolescence.

This study examined the effect of peer stress on adjustment and why the impact of peer

stress on adjustment varies among young adolescent girls. Consistent with prior research, girls

who experienced more peer stress reported higher levels of internalizing distress and aggression

(Deater-Deckard, 2001; Nansel et al., 2004; Rudolph, 2002). Moreover, as expected, coping

strategies, specifically primary and secondary control strategies, mediated both of these

associations. Specifically, girls who experienced more peer stress used fewer primary and

secondary control strategies, which are typically considered to be adaptive and effective means

of coping, such as problem solving, positive thinking, emotional regulation, etc. This association,

in turn, accounted for greater levels of internalizing distress and aggression. Recently studies

examining the impact of social stress on adjustment during adolescence have begun to explore

how stress responses influence this relationship; however, most of these studies have focused on

the direct association between stress responses and adjustment or examined how coping and

stress responses moderated the association between stressful life events and adjustment










(Connor-Smith, et al., Hampel & Petermann, 2006). Building upon prior research, the present

study focused specifically on peer stress and demonstrated that how an adolescent responds to

peer stress mediates the association between stressful experiences and adjustment during

adolescence. These findings are important because they provide a more thorough understanding

of how stressful experiences with peers impact adolescents' psychosocial well-being.

This study also examined the effect of pubertal timing on adjustment. As anticipated, girls

who were early maturers, compared to those who were on-time or late, demonstrated higher

levels of internalizing distress and aggression. This finding is consistent with prior research that

has demonstrated that experiencing puberty earlier than one's peers may place girls at a

heightened risk for a variety of behavioral and emotional problems (Graber, 2003; Weichold,

Silbereisen, & Schmitt-Rodermund, 2003). However, based on findings from this study, this

association may be partially accounted for by the way girls deal with being early maturers. The

use of primary control strategies (i.e., emotional expression, emotional regulation, and problem

solving) has been shown to attenuate the effects of stressful experiences, whereas, the use of

involuntary engagement (i.e., impulsive action, physiological arousal, and intrusive thoughts or

rumination) has been shown to intensify the effects of stress on the individual (Compas, et al.,

1999; Wadsworth, Raviv, Compas, & Connor-Smith, 2005). In this study, these two responses to

stress mediated the association between early pubertal timing and internalizing distress.

Meaning, early maturers used fewer primary control strategies and more involuntary engagement

strategies, which in turn accounted for greater levels of internalizing distress.

Although main effects of pubertal timing were demonstrated for both internalizing distress

and aggression, these effects were reduced in the full regression (i.e., when stress response

factors were included). The main effect of pubertal timing on internalizing distress was reduced,









but remained statistically significant, thus allowing for mediation effects of stress responses to be

examined, as recommended by Baron and Kenny (1986). However, the main effect of pubertal

timing on aggression was reduced to the point that it was no longer significant, hindering tests of

mediation. According to Baron and Kenny (1986), mediation effects cannot be tested if a

significant effect between the independent variable pubertall timing) and the dependent variable

(aggression) does not exist. The drop in significance was likely due to the exclusion of

participants that did not have responses to stress scores. Five of these participants were early

maturers and 5 of them were on-time or late. Proportionally, there was a greater drop in the

number of early maturers included in the analyses. For this reason, it likely became more

difficult to demonstrate significance. Because the inability to test mediating effects of coping

and stress responses on the association between pubertal timing and aggression was likely due to

an attrition effect, future research should revisit this issue in order to demonstrate whether or not

using particular coping strategies benefits early maturers.

Although an abundance of research exploring the relationship between pubertal timing and

maladjustment exists, few studies have attempted to explore exactly how pubertal timing relates

to adjustment and how girls cope with the social and emotional ramifications of being earlier

than their peers (Brooks-Gunn et al., 1994; Caspi et al., 1993; Ge et al., 2002; Graber et al.,

2005). The Eindings from this study are important because they demonstrate that some of the

association between early timing and adjustment may be accounted for by how adolescents cope

with or react to the stress of being "off-time."

Although examining the influence of individual coping strategies and stress responses is

useful and informative, future research exploring coping and peer stress should also examine

coping styles and how they impact adjustment. Recent research exploring coping has suggested









that individuals have a tendency to respond to stress using a particular set of coping strategies

and involuntary responses rather than responding with one strategy (Reinhard, Wolff, &

Wadsworth, 2006). Research that focuses on one type of stress response may be missing the big

picture of how individuals deal with stress. Thus, it may be informative to understand how these

different combinations of strategies (i.e., coping styles) either attenuate or exaggerate the effects

of peer stress.

Contrary to expectation, this study failed to demonstrate an association between stress

reactivity and symptoms of internalizing distress and aggression; as a result, potential mediating

effects of coping strategies could not be explored. This study found no connection between how

cortisol levels changed over the course of a home visit (that included a variety of tasks) and

symptoms of psychopathology. Much of the current literature has found associations between

cortisol reactivity and psychopathology, but mostly in samples reporting borderline or clinical

levels of internalizing and externalizing behaviors (Angold, 2003; Klimes-Dougan, et al., 2001;

Oosterlaan, et al., 2005). In a study similar in design to the current study (i.e., normative

adolescent samples exposed to social challenge tasks), Klimes-Dougan and colleagues (2001)

demonstrated links between stress reactivity and internalizing symptoms, but were unable to find

clear associations between stress reactivity and aggression. It was only until adolescents

displayed clinical levels of aggression that a significant association with stress reactivity

emerged. Thus, because most of the girls in this study displayed low or at most marginally high

levels of internalizing distress and aggression, associations between stress reactivity and

symptoms of psychopathology may not have emerged. In turn, further research examining

adrenocortical activity in normative adolescent samples should be conducted in order to provide









a more thorough understanding of whether or not a reliable connection between stress reactivity

and symptoms of psychopathology exists.

Some of the inconsistency in findings may be due to analytic differences. Most studies

examining stress reactivity in child and adolescent samples utilize reactivity categories (i.e.,

increased dramatically, remained stable, decreased slightly, etc.) to explore stress reactivity and

adjustment (Granger, et al., 1994; Klimes-Dougan, et al., 2001; Schmidt et al., 1999). This study

utilized area under the curve and mixed modeling to explore patterns of change. There exists a

debate as to what method is most appropriate to utilize when exploring adrenocortical activity

and adjustment. Thus further research exploring the method of AUC and mixed modeling in

different age groups of both boys and girls is necessary to understand the implications of using

these methods of analysis.

This study has taken informative steps in understanding better how social stress influences

psychosocial development; however, some limitations of the study exist. The examination of

stress and coping was based solely on adolescent girls, rather than both boys and girls. Although

researchers have suggested that social stress may be more detrimental to adolescent girls'

psychosocial well-being (Rudolph, 2002), it would be beneficial to examine further if gender

differences during early adolescence emerge with respect to how girls and boys cope with social

stress, and whether particular coping strategies are more problematic for one gender versus the

other. In addition, the study focused on early adolescence, particularly 12 year olds, which

prevented exploration of developmental changes in coping and stress responses over the course

of adolescence and the impact of late pubertal timing. Additionally, due to the fact that data were

only collected at a single time point, the direction of associations between social stress, coping,

and psychopathology were inferred from theoretical perspectives and previous research










exploring stress, coping and adjustment. Thus, results should be interpreted with some caution.

For example, it is unclear if girls who utilize particular types of coping strategies such as primary

and secondary control are more socially skilled and experience less peer stress. A Einal limitation

was the fact that participants were drawn from a large metropolitan area, limiting generalization

to adolescents in suburban and rural areas.

Despite the limitations, results of this study provide useful information regarding the

identification of specific coping strategies and stress responses that mediate the relationship

between stress and internalizing distress, and aggression. These Eindings speak to skills that

could be taught in programs that emphasize how to effectively adapt to the social and

psychological demands of transitioning into adolescence. Although the present study focuses on

negative outcomes, potential also exists to understand better what factors promote positive

development (i.e., prosocial behavior, academic success, positive self-esteem) in the face of

stressful social situations. Understanding these factors and how they affect psychosocial

development may ultimately expand our current understanding of resilience in the face of stress.











APPENDIX A
HOME DATA COLLECTION PROCEDURE AND SALIVA SAMPLE COLLECTION

1. Consents

2. Specimen and questionnaire delivery details

3. Saliva #1

4. Maze task

5. Neighborhood/peer questions

6. Saliva #2

7. Cold pressor task #1

8. Cold pressor questions

9. Cold pressor task #2

10. Cold pressor questions

11. Disagreement Questions

12. Saliva #3

13. Daily routines/ nutrition/ sleep questions

14. Physical exam

15. Menstruation & social activities questions

16. Saliva #4

17. Peer issues interaction task

18. Disagreement interaction task

19. Saliva #5









APPENDIX B
MIXED EFFECTS MODELS EXAMINING THE IMPACT OF TIME AND SYMPTOMS OF
PSYCHOPATHOLOGY ON PATTERNS OF CORTISOL PRODUCTION











Table B l. Impact of time and internalizing distress on patterns of cortisol
Model Level-1 Model Level-2 Model Composite Model
A Cortisol, = Ri, + e, ~ io, = 700 + 90, Cortisol,, = 700 + (ez, + 903,)
B Cortisol, = Ri, + zzTime, + e, or~ = 700 + 90, Cortisol,, = 700 + 710Time,
%, =710 Ae, + 90,, + Au, Timer; )
C Cortisol, = RT0 + n,Timell + ell ioz = Too, +,v01(Anlx/Dep Anzx/Dep) + 0,I Cortisol at = 700 + Trolime v +

ri,1 = 70 + 7,,(Anx/Dep -Anx/Dep)+ #0, 70,[( Anx /Dnep Anx /Dnep)(Time ii )
(ez, +o #u,+ ,Time, )
Note. (A) unconditional means model (partitions variance into between and within variance); (B) unconditional growth model (do
cortisol levels vary over time); (C) examines effect of internalizing distress on initial status and rate of change of cortisol


Table B2. Impact of time and aggression on patterns of cortisol
Model Level-1 Model Level-2 Model Composite Model
A Cortisol, = Ri, + e, ~ io, = 700 + 90, Cortisol,, = 700 + (ez, + 903,)
B Cortisol, = or~ + zzTimeO + ez, or = 700 + 90, Cortisolet = 700 + y0Time0 +
=710+A,(eO + 90, + Au,Timer,
C CortisEol = or, + %,~Timelj + ej no2 = 700 + 70, (Agg Agg)+ +, Cortisol at = 700 + 7/,0Tim~e I

Z11 = 710 + 7,(Agg-Agg)+ #1, 70, [(Agg Agg )(Time 23)
eO u, + Po;,,1Timery)
Note. (A) unconditional means model (partitions variance into between and within variance); (B) unconditional growth model (do
cortisol levels vary over time); (C) examines effect of aggression on initial status and rate of change of cortisol










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BIOGRAPHICAL SKETCH

Lisa M. Sontag is a third-year developmental psychology graduate student at the

University of Florida. She received a Bachelor of Science in Psychology at Tulane University.

Her research focuses on adolescent development from a bio-psychosocial orientation. In

particular, her research explores how peer relations, stress reactivity, pubertal timing, and coping

contribute to both healthy adjustment and emotional and behavioral problems. Currently she is

the co-investigator of the APEX (Adolescent Peer Experiences) Study that investigates how peer

relationships influence psychosocial development during the middle school years.