یک مطالعه طولی اجتماعی زیستی کورتیزول و تأثیر همسالان بر توسعه رفتار ضد اجتماعی نوجوانان

Introduction It is increasingly recognized that in order to understand the complex phenomenon of antisocial behavior, interrelations between biological and social risk factors should be taken into account (Bassarath, 2001, Dodge and Pettit, 2003, Raine, 2002 and Susman, 2006). A frequently hypothesized and examined biological risk factor for antisocial behavior, is a decreased level of hypothalamic-pituitary-adrenal (HPA) axis activity (e.g. McBurnett et al., 2000 and Popma et al., 2007). Associations between a decreased level of HPA axis activity and antisocial behavior have been confirmed, but less consistently for adolescent than for childhood samples (see review by Alink et al., 2008). At the same time, in adolescence deviant peer influence becomes a major social risk factor for antisocial behavior (Brown, 2004 and Gardner and Steinberg, 2005). Moreover, there are indications that deviant peers may mediate the association between the level of HPA axis activity and antisocial behavior (Raine et al., 2005 and Yanovitzky, 2005). To capture the developmental changes in HPA axis activity levels, peer relations, and antisocial behavior, which are characteristic for adolescence, longitudinal studies are required. Therefore, the current study focused on the mediating role of peer influences in longitudinal associations linking decreased levels of HPA axis activity to antisocial behavior. A biological perspective on the development of antisocial behavior is offered by the low arousal theories (Raine, 1993 and Zuckerman and Neeb, 1979). Low arousal is considered to constitute a negative physiological state, which could be increased (i.e., normalized) by seeking sensation through antisocial behavior (Zuckerman and Neeb, 1979). Alternatively, low arousal might reflect fearlessness, as a result of which youngsters may not fear the negative consequences of antisocial behavior (Raine, 1993). Although the exact mechanisms are unknown, it has been posed in theoretical models that low arousal may have resulted from genetic vulnerabilities or early life adversities. The amygdala is considered to link such early stressors to dysfunctions in arousal (Susman, 2006 and van Goozen et al., 2007). The HPA axis is one of the major physiological stress systems, and low arousal can be operationalized as low levels of HPA axis activity. As a measure of HPA axis activity, salivary cortisol levels are often assessed. For instance, McBurnett et al. (2000) found that persistent aggression in school aged boys was associated with lower day time cortisol levels. Popma et al. (2007) specifically studied the cortisol awakening response (CAR) in adolescent boys, and reported that the level of the CAR, but not the response to awakening, was decreased in antisocial boys compared to normal controls. In a meta-analysis, however, associations between the level of HPA axis activity and antisocial behavior were not found in adolescent samples (Alink et al., 2008). It is in adolescence when affiliation with deviant peers becomes an important social risk factor for developing antisocial behavior (Brown, 2004, Gardner and Steinberg, 2005 and Hartup and Stevens, 1997). Peer influences are dynamic and bidirectional (Dishion and Owen, 2002 and Popp et al., 2008): adolescents select friends who are similar to themselves in behavior and attitudes (selection), and friends become more similar to one another over time (socialization) (Brechwald and Prinstein, 2011 and Kandel, 1978). Imbalance or dissimilarity between mutual friends’ behavior and attitudes is likely to result in ending the friendship and seeking more similar friends, or to stay friends and modifying their own behavior to that of the friend (Kandel, 1978). Selection and socialization are not mutually exclusive, but can coexist and enhance one another. For instance, antisocial adolescents may select friends showing more antisocial behavior than themselves, which can exacerbate their own antisocial behavior (Gatti et al., 2005 and Thornberry et al., 1993). However, friends also tend to overestimate the similarity between their behaviors, that is, an adolescent may feel his/her friends are equally antisocial as he/she is, whereas in fact the friends may be less antisocial (Aseltine, 1995). To overcome this overestimating of the similarities, and provide an accurate view of the friends’ antisocial behavior, the best friends reported on their own behavior in the current study. Antisocial friendships may mediate associations between the level of HPA axis activity and antisocial behavior. It has for instance been shown that sensation seeking, as associated with lowered levels of HPA axis activity (cf. the low arousal theory, see above), is also associated with affiliating with deviant friends (Yanovitzky, 2005). These deviant friends in turn may influence the adolescent toward behaving antisocially (Moffitt, 1993 and Thornberry et al., 1994). Also, it has been shown that persistent antisocial youth show neurocognitive impairments compared to adolescence limited antisocial youth (Raine et al., 2005). This could imply that biological risk factors, including decreased levels of HPA axis activity, may be specific for persistent antisocial youths. As they are already involved in deviant behaviors, in adolescence they are more likely to select antisocial friends and influence others into antisocial behavior (Moffitt, 1993). Hence, two paths may be present linking the level of HPA axis activity to deviant friends: (1) influences of decreased levels of HPA axis activity may operate via deviant friends, and also (2) lower levels of HPA axis activity may first lead to adolescent antisocial behavior, which makes these adolescents more likely to have antisocial friends. Both pathways of influence will be tested in this study. To clarify when and how the influence of friends comes into play, and to compare the two paths, a longitudinal design is required. To the best of our knowledge, the only study which has investigated HPA axis activity levels and peer influences, was cross-sectional in nature (Dorn et al., 2009). Dorn et al. found that children with disruptive behavior disorders showed lowest levels of HPA axis activity if they had friends who showed low levels of antisocial behavior. As these children already showed antisocial behavior, these findings indicate that their behavior was not the result of peer influence. However, these children were aged 6–11 years, and deviant peers do not become a major risk factor for antisocial behavior until adolescence (Brown, 2004 and Gardner and Steinberg, 2005). To further investigate these promising findings, and incorporate the dynamics and bidirectionality of peer influences toward antisocial behavior in youths with decreased levels of HPA axis activity, a longitudinal design was applied in the current study. Furthermore, the relative influence of biological and social risk factors may differ by the type of antisocial behavior. Aggression and rule-breaking are two main types of behavior often recognized within adolescent antisocial behavior (e.g. Achenbach et al., 1989 and Burt, 2012). Both types are thought to result from biological as well as social risk factors (Moffitt, 1993 and Raine et al., 2005). However, there are indications that aggression may be more strongly related to decreased levels of HPA axis activity (Burt, 2012, McBurnett et al., 2000, Platje et al., 2013a and Platje et al., 2013b), whereas rule-breaking may be more strongly related to affiliation with and influence of deviant peers (Barnow et al., 2005 and Reitz et al., 2007). Therefore, both types of antisocial behavior were assessed in this study. For these reasons, in the current study, the role of deviant peer influences in longitudinal associations linking the level of HPA axis activity to aggression and rule-breaking was investigated in a general population sample of both boys and girls. Because within friendships bidirectional influences can occur, which may increase antisocial behavior, two indirect paths were examined: (1) do lower levels of HPA axis activity predict higher levels of antisocial behavior of the best friend, which in turn predicts higher levels of adolescent antisocial behavior, (2) do lower levels of HPA axis activity predict higher levels of adolescent antisocial behavior, which in turn predicts higher levels of antisocial behavior of the best friend? This was examined in a large sample of boys and girls, who participated in three annual assessments at ages 15, 16 and 17. As a measure of HPA axis activity, the CAR was assessed, and specified in two ways; firstly as cortisol levels at awakening, and secondly as the response in cortisol levels to awakening. The response to awakening has been shown to be influenced by situational factors (Fries et al., 2009 and Hellhammer et al., 2007), therefore associations are expected to be stronger for the cortisol level at awakening. The best friends of the adolescents also participated, reporting on their own aggressive and rule-breaking behavior over the years. The best friend could change from year to year, and stability of the friendship was examined to account for selection and socialization effects. As the sample consisted of both boys and girls, and gender differences may be present in antisocial behavior (Moffitt, 2001) and/or HPA axis activity (e.g. Fries et al., 2009), gender was taken into account in all analyses.

Introduction It is increasingly recognized that in order to understand the complex phenomenon of antisocial behavior, interrelations between biological and social risk factors should be taken into account (Bassarath, 2001, Dodge and Pettit, 2003, Raine, 2002 and Susman, 2006). A frequently hypothesized and examined biological risk factor for antisocial behavior, is a decreased level of hypothalamic-pituitary-adrenal (HPA) axis activity (e.g. McBurnett et al., 2000 and Popma et al., 2007). Associations between a decreased level of HPA axis activity and antisocial behavior have been confirmed, but less consistently for adolescent than for childhood samples (see review by Alink et al., 2008). At the same time, in adolescence deviant peer influence becomes a major social risk factor for antisocial behavior (Brown, 2004 and Gardner and Steinberg, 2005). Moreover, there are indications that deviant peers may mediate the association between the level of HPA axis activity and antisocial behavior (Raine et al., 2005 and Yanovitzky, 2005). To capture the developmental changes in HPA axis activity levels, peer relations, and antisocial behavior, which are characteristic for adolescence, longitudinal studies are required. Therefore, the current study focused on the mediating role of peer influences in longitudinal associations linking decreased levels of HPA axis activity to antisocial behavior. A biological perspective on the development of antisocial behavior is offered by the low arousal theories (Raine, 1993 and Zuckerman and Neeb, 1979). Low arousal is considered to constitute a negative physiological state, which could be increased (i.e., normalized) by seeking sensation through antisocial behavior (Zuckerman and Neeb, 1979). Alternatively, low arousal might reflect fearlessness, as a result of which youngsters may not fear the negative consequences of antisocial behavior (Raine, 1993). Although the exact mechanisms are unknown, it has been posed in theoretical models that low arousal may have resulted from genetic vulnerabilities or early life adversities. The amygdala is considered to link such early stressors to dysfunctions in arousal (Susman, 2006 and van Goozen et al., 2007). The HPA axis is one of the major physiological stress systems, and low arousal can be operationalized as low levels of HPA axis activity. As a measure of HPA axis activity, salivary cortisol levels are often assessed. For instance, McBurnett et al. (2000) found that persistent aggression in school aged boys was associated with lower day time cortisol levels. Popma et al. (2007) specifically studied the cortisol awakening response (CAR) in adolescent boys, and reported that the level of the CAR, but not the response to awakening, was decreased in antisocial boys compared to normal controls. In a meta-analysis, however, associations between the level of HPA axis activity and antisocial behavior were not found in adolescent samples (Alink et al., 2008). It is in adolescence when affiliation with deviant peers becomes an important social risk factor for developing antisocial behavior (Brown, 2004, Gardner and Steinberg, 2005 and Hartup and Stevens, 1997). Peer influences are dynamic and bidirectional (Dishion and Owen, 2002 and Popp et al., 2008): adolescents select friends who are similar to themselves in behavior and attitudes (selection), and friends become more similar to one another over time (socialization) (Brechwald and Prinstein, 2011 and Kandel, 1978). Imbalance or dissimilarity between mutual friends’ behavior and attitudes is likely to result in ending the friendship and seeking more similar friends, or to stay friends and modifying their own behavior to that of the friend (Kandel, 1978). Selection and socialization are not mutually exclusive, but can coexist and enhance one another. For instance, antisocial adolescents may select friends showing more antisocial behavior than themselves, which can exacerbate their own antisocial behavior (Gatti et al., 2005 and Thornberry et al., 1993). However, friends also tend to overestimate the similarity between their behaviors, that is, an adolescent may feel his/her friends are equally antisocial as he/she is, whereas in fact the friends may be less antisocial (Aseltine, 1995). To overcome this overestimating of the similarities, and provide an accurate view of the friends’ antisocial behavior, the best friends reported on their own behavior in the current study. Antisocial friendships may mediate associations between the level of HPA axis activity and antisocial behavior. It has for instance been shown that sensation seeking, as associated with lowered levels of HPA axis activity (cf. the low arousal theory, see above), is also associated with affiliating with deviant friends (Yanovitzky, 2005). These deviant friends in turn may influence the adolescent toward behaving antisocially (Moffitt, 1993 and Thornberry et al., 1994). Also, it has been shown that persistent antisocial youth show neurocognitive impairments compared to adolescence limited antisocial youth (Raine et al., 2005). This could imply that biological risk factors, including decreased levels of HPA axis activity, may be specific for persistent antisocial youths. As they are already involved in deviant behaviors, in adolescence they are more likely to select antisocial friends and influence others into antisocial behavior (Moffitt, 1993). Hence, two paths may be present linking the level of HPA axis activity to deviant friends: (1) influences of decreased levels of HPA axis activity may operate via deviant friends, and also (2) lower levels of HPA axis activity may first lead to adolescent antisocial behavior, which makes these adolescents more likely to have antisocial friends. Both pathways of influence will be tested in this study. To clarify when and how the influence of friends comes into play, and to compare the two paths, a longitudinal design is required. To the best of our knowledge, the only study which has investigated HPA axis activity levels and peer influences, was cross-sectional in nature (Dorn et al., 2009). Dorn et al. found that children with disruptive behavior disorders showed lowest levels of HPA axis activity if they had friends who showed low levels of antisocial behavior. As these children already showed antisocial behavior, these findings indicate that their behavior was not the result of peer influence. However, these children were aged 6–11 years, and deviant peers do not become a major risk factor for antisocial behavior until adolescence (Brown, 2004 and Gardner and Steinberg, 2005). To further investigate these promising findings, and incorporate the dynamics and bidirectionality of peer influences toward antisocial behavior in youths with decreased levels of HPA axis activity, a longitudinal design was applied in the current study. Furthermore, the relative influence of biological and social risk factors may differ by the type of antisocial behavior. Aggression and rule-breaking are two main types of behavior often recognized within adolescent antisocial behavior (e.g. Achenbach et al., 1989 and Burt, 2012). Both types are thought to result from biological as well as social risk factors (Moffitt, 1993 and Raine et al., 2005). However, there are indications that aggression may be more strongly related to decreased levels of HPA axis activity (Burt, 2012, McBurnett et al., 2000, Platje et al., 2013a and Platje et al., 2013b), whereas rule-breaking may be more strongly related to affiliation with and influence of deviant peers (Barnow et al., 2005 and Reitz et al., 2007). Therefore, both types of antisocial behavior were assessed in this study. For these reasons, in the current study, the role of deviant peer influences in longitudinal associations linking the level of HPA axis activity to aggression and rule-breaking was investigated in a general population sample of both boys and girls. Because within friendships bidirectional influences can occur, which may increase antisocial behavior, two indirect paths were examined: (1) do lower levels of HPA axis activity predict higher levels of antisocial behavior of the best friend, which in turn predicts higher levels of adolescent antisocial behavior, (2) do lower levels of HPA axis activity predict higher levels of adolescent antisocial behavior, which in turn predicts higher levels of antisocial behavior of the best friend? This was examined in a large sample of boys and girls, who participated in three annual assessments at ages 15, 16 and 17. As a measure of HPA axis activity, the CAR was assessed, and specified in two ways; firstly as cortisol levels at awakening, and secondly as the response in cortisol levels to awakening. The response to awakening has been shown to be influenced by situational factors (Fries et al., 2009 and Hellhammer et al., 2007), therefore associations are expected to be stronger for the cortisol level at awakening. The best friends of the adolescents also participated, reporting on their own aggressive and rule-breaking behavior over the years. The best friend could change from year to year, and stability of the friendship was examined to account for selection and socialization effects. As the sample consisted of both boys and girls, and gender differences may be present in antisocial behavior (Moffitt, 2001) and/or HPA axis activity (e.g. Fries et al., 2009), gender was taken into account in all analyses.

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