واکنش به کورتیزول و آمیلاز آلفا و زمان بندی بلوغ: آسیب پذیری برای رفتار ضد اجتماعی در نوجوانان

Introduction Aggressive and antisocial behaviours may increase in some adolescents for a host of reasons including neuroendocrine and physical maturational changes, increasingly complex social roles, peer influences, and asynchronies between brain development and emotional and behavioural regulation. Recent studies suggest that these problems begin in later childhood and the early adolescent years (Andrews et al., 2003) and become more problematic in mid to late adolescence. The problem is that neuroendocrine developmental transitions are rarely examined as influences on behaviour problems even though major neuroendocrine changes are the mechanisms responsible for pubertal development. Early adolescence is considered an especially stressful and vulnerable period for the expression of antisocial behaviour problems because of the rapid, neuroendocrine, puberty-related changes that are differentially timed for males and females. A promising mechanism linking early vulnerabilities and antisocial behaviour is the putative stress of differential timing of puberty. The purpose of this report was to test hypotheses regarding psychobiological, stress system vulnerabilities and the interaction between these vulnerabilities and timing of puberty and antisocial behaviour includes parent reports of externalizing behaviour problems and conduct disorder and oppositional defiant disorder symptoms. The theoretical perspective upon which the study is based integrates multi-level processes: reactivity of the hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) response to stress, timing of puberty as indexed by pubertal physical maturation, and antisocial behaviour. 1.1. Psychobiological vulnerabilities and timing of puberty The specific heuristic model guiding this report proposes, first, that certain psychological risks (vulnerabilities) predispose adolescents to behaviour problems during puberty. This diathesis-stress model assumes that most individuals have some level of predisposing risk factors, or diatheses, for psychosocial problems ( Richters and Weintraub, 1990 and Abela and D’Alessandro, 2002). The tendency to develop psychosocial problems varies depending on the interaction between the degree to which risk factors are present and the degree of stress experienced by the individual ( Richters and Weintraub, 1990 and Monroe and Simons, 1991). We expanded this perspective by including HPA and SAM vulnerabilities as risks given the documented relation between these systems and antisocial behaviour ( McBurnett et al., 1991, Raine, 2005, Shirtcliff et al., 2005, Gordis et al., 2006, Granger et al., 2006 and Granger et al., 2007). Gordis et al. (2006) showed the importance of including both HPA and SAM stress regulation in understanding aggressive behaviour. Second, the heuristic model includes the concept of transitional stress and describes the stress imposed by ambiguity related to individualization and destandardization of roles that accompany periods of change like puberty. Transitional stress with regard to puberty is directly linked to neuroendocrine and physical-maturational changes and predicts that an increase in adrenal and gonadal hormones and the physical changes of maturation lead to an increase in antisocial behaviours ( Graber et al., 1997, Graber et al., 2004, Angold et al., 1999, Stoff and Susman, 2005 and Ge et al., 2006). Transitional stress is especially acute if there is an asynchrony between the timing of the physical changes relative to same-age peers. Specifically, an earlier or later pubertal transition biases vulnerable individuals toward behaviour problems ( Stattin and Magnusson, 1990 and Caspi and Moffitt, 1991) in some but not all adolescents. 1.2. Biological vulnerabilities A recent theoretical perspective (Bauer et al., 2002) suggests that arousal and recovery from reactivity, as reflected in reactivity to stressors entailing novelty and uncertainty, is representative of how individuals generally regulate their arousal. Difficulty in arousal regulation, including both high and/or sustained responsivity, is considered a vulnerability for behaviour problems (Kagan et al., 1994). Bauer et al. (2002) go on to suggest that differences in arousal may explain differences in susceptibility to the adverse effects of stressors. Variations in arousal, as indexed herein by cortisol and salivary alpha amylase (sAA) reactivity, reflect coordinated, yet distinct axes of the stress response system. Central components of the stress system are the corticotrophin-releasing-hormone (CRH) neurons of the endocrine HPA axis system and the locus coeruleus, norepinephrine system (LC/NE), and the sympathetic-adrenal-medullary (SAM) system (Chrousos and Gold, 1992). Individual differences in both HPA and SAM reactivity are expected to be related to antisocial behaviour. 1.2.1. Cortisol From the prenatal period onward, regulatory patterns of cortisol are related to psychological functioning. For instance, low basal, maternal prenatal cortisol levels predicted difficult infant temperament in 3-year-old children (Susman et al., 2001). At the older end of the life span, higher basal cortisol levels were related to cognitive declines (Seeman et al., 1997, Kudielka et al., 2004a and Kudielka et al., 2004b) and exaggerated cortisol reactivity (Préville et al., 2008). In addition, non-invasively collected salivary cortisol and its links to emotions and behaviours have been extensively validated in laboratory settings (Kirschbaum et al., 1992, Schwartz et al., 1998 and Dickerson and Kemeny, 2004). With regard to antisocial behaviour, lower basal salivary cortisol levels are characteristic of individuals exhibiting disruptive behaviour problems (McBurnett et al., 1991, Susman et al., 1997, McBurnett et al., 2000 and Oosterlaan et al., 2005), including oppositional defiant behaviour (van Goozen et al., 1998), conduct disorder (Vanyukov et al., 1993 and Pajer et al., 2001;), habitual violence (Virkkunen, 1985), and abuse of others (Bergman and Brismar, 1994). Furthermore, low basal cortisol is both a concurrent correlate and risk factor for future alcohol use (Moss et al., 1995) and externalizing behaviour problems (Shirtcliff et al., 2005). With regard to cortisol reactivity, hyper-reactivity characterized the HPA axis response to stressors in some studies (Susman et al., 1997), whereas hyporeactivity was characteristic of antisocial boys in other studies (Fairchild et al., 2008). The precise mechanisms whereby inconsistencies occur are unknown (Dickerson and Kemeny, 2004). Nonetheless, age, dysfunction in the serotonin system, developmental differences between children and adults, composition of the sample and outcome measures are explanations of the inconsistencies (van Goozen et al., 2007), Given the similarity of our methods with those of previous studies that used a cognitive and social evaluative stressor, we expected that higher cortisol reactivity would be associated with antisocial behaviour. 1.2.2. Salivary alpha amylase A new marker of stress reactivity, sAA is considered a surrogate marker of SAM activity (Granger et al., 2007 and Stroud et al., 2009). SAA is an enzyme produced in the oral mucosa and is an assumptive marker of the adrenergic component of the stress response. SAA levels are associated with SAM activity and increase under stressful conditions that are also associated with increases in plasma catecholamines, heart rate, systolic blood pressure, preinjection period (PEP), and cardiac output (Chatterton et al., 1996 and Skosnik et al., 2000). However, sAA can be elevated in response to a stressor independently of serum catecholamines and may reflect a general marker of SAM activity (van Stegeren et al., 2006). The validity of salivary sAA as an index of SAM activity additionally is supported by the suppression of sAA secretion after experiencing periods of emotionally charged stressors by the adrenergic blocker propranolol (van Stegeren et al., 2006). Increases in sAA also are evident in response to laboratory stressors that include adolescents (Nater et al., 2005, Gordis et al., 2006, Gordis et al., 2008 and Stroud et al., 2009). In addition, in four independent studies intra-individual sAA responses to challenge differed distinctly from salivary cortisol responses, particularly, in associations with social behaviour, negative affectivity, cognitive problems, and cardiovascular activity. Similarly, Gordis et al. (2006) show that sAA levels increased post-stressor in adolescents. If stress reactivity in the SAM system is parallel to that of HPA reactivity, we expected to see an increase in sAA post-stressor to be associated with antisocial behaviour. 1.3. Transitional stress: timing of puberty Young adolescents experience multiple changing social contexts (Stroud et al., 2009) as well as rapid neuroendocrine risks. The early years of puberty entail transitioning from a childlike to youthful appearance that is accompanied by changing social demands, role changes and expectations for more mature behaviour. Timing of puberty is primarily under genetic and neuroendocrine control. Those genetic factors that are associated with timing of puberty also may be associated with antisocial behaviour (Comings et al., 2002). Although under genetic control there is a great deal of developmentally significant variability in timing around a normative age. Earlier or later puberty has implications for multiple dimensions of adjustment and behaviour during adolescence and beyond (Stattin and Magnusson, 1990, Ge et al., 1996, Ge et al., 2003, Ge et al., 2006 and Graber et al., 2004). In general, girls who mature earlier than their peers are at elevated risk for emotional and behaviour problems (e.g. Stattin and Magnusson, 1990), whereas for boys, effects of early maturation are variable across studies with some positive (e.g. popularity, self-confidence) and some negative outcomes (e.g. delinquency) (Huddleston and Ge, 2003, Collins and Steinberg, 2006 and Steinberg et al., 2006). Off-time puberty is assumed to be a transitional stressor given that being asynchronous with peers in morphological characteristics can be emotionally arousing. Shirtcliff and Essex (2008) were the first to show that stressors associated with a developmental transition are associated with different patterns of cortisol reactivity prior to and after the transition. In stable, nonschool transition years, reflected in the cross-sectional analyses, hypoarousal at 5th grade predicted increasing severity of mental health problems and hyperarousal at 7th grade after the school transition had occurred. The diathesis-stress model in the current instance suggests that HPA and SAM vulnerabilities, specifically, cortisol reactivity, will interact with the transitional stressor of timing of puberty to place individuals at risk for antisocial behaviour problems. Specifically, we hypothesized that earlier or later puberty in combination with higher cortisol or sAA reactivity would be related to antisocial behaviour in young adolescents. It was expected that: (1) Higher reactivity of the stress system based on cortisol or sAA independently would be related to antisocial behaviour. (2) However, timing of puberty was expected to moderate the relation between cortisol and sAA reactivity and antisocial behaviour such that adolescents with high reactivity and off-time maturation would exhibit the most antisocial behaviour, although these relations may vary for boys and girls.

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