بزاق کورتیزول و ابعاد اختلالات فکری و روانی در نوجوانان ضد اجتماعی بازداشت شده
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|34377||2013||10 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychoneuroendocrinology, Volume 38, Issue 9, September 2013, Pages 1586–1595
Previous research revealed hypothalamic–pituitary–adrenal (HPA) axis abnormalities in relation to antisocial and aggressive behavior. Some evidence suggests that low cortisol levels may serve as a biological marker for a severe antisocial subgroup with pronounced callous–unemotional (CU) traits. Children displaying the combination of severe antisocial behavior and CU traits appear to be particularly at risk of developing adult psychopathy. Given the lack of studies on the relationship between cortisol levels and CU traits in antisocial adolescents, the current study investigates whether cortisol levels are uniquely associated with CU traits as compared to other psychopathy dimensions (i.e., narcissism and impulsivity). Detained antisocial adolescents (n = 63) and a community comparison group (n = 62) completed diaries and collected three saliva samples daily on two days, with compliance monitored electronically. Psychopathy dimensions were assessed through self-report questionnaires. Externalizing symptoms were assessed by structured clinical interview. Multilevel regression analyses indicated no differences in cortisol levels or diurnal slopes between the two groups. Overall, cortisol levels were not significantly related to psychopathy dimensions. However, greater impulsivity was associated with lower cortisol levels in the community sample, but not in the antisocial group.
Childhood behavioral disorders are the most common diagnoses in child and adolescent psychiatric settings. Among these, conduct disorder (CD) describes the most severe form of antisocial and aggressive behavior, causing the highest mental health and public expenditures of all problem behaviors (Schmeck and Poustka, 2000 and Foster and Jones, 2005). Aside from the environmental risk factors that play a role in the development of severe antisocial and aggressive behavior, certain neurobiological factors may be of importance. The hypothalamic–pituitary–adrenal (HPA) axis and its end product, the stress hormone cortisol, are of particular interest in this respect (van Goozen et al., 1998 and McBurnett et al., 2000). It is theorized that low levels of arousal in the central nervous system are causally related to the development and maintenance of antisocial and aggressive behavior (van Goozen et al., 2000). According to this line of thought, low HPA axis activity, as reflected in low cortisol levels, may be a neurobiological marker of underarousal and thus of predisposition toward aggressive and antisocial behavior. The mechanisms through which underarousal and low cortisol contribute to antisocial behavior have been conceptualized in terms of two largely compatible theories. First, according to the fearlessness theory, the neurobiological systems that normally process threat information, including the amygdala and the prefrontal cortex, are believed to be compromised in highly antisocial and aggressive individuals (van Goozen and Fairchild, 2008). Fearless individuals are thus physiologically underaroused and less sensitive to stress (Raine, 1996). Being less afraid of negative consequences of their actions and less sensitive to punishment, they do not experience normal inhibitions against engaging in aggressive and antisocial behavior (Raine, 1993). Second, the stimulation-seeking theory suggests that a certain level of arousal or stress is needed in order to feel pleasant; underarousal thus represents an aversive condition. Chronically underaroused individuals are believed to seek physiological stimulation through aggressive and antisocial behavior in order to counteract this negative state (Zuckerman, 1979). In adults, studies have repeatedly found associations between antisocial, aggressive behavior and low cortisol levels (Woodman et al., 1978 and Virkkunen, 1985). Several studies in children and adolescents have also reported negative associations between CD symptoms and basal cortisol levels. For example, children with antisocial fathers showed both more CD symptoms and lower cortisol levels (Vanyukov et al., 1993). In particular, the severity and persistence of aggressive, antisocial behavior has been linked to low cortisol (McBurnett et al., 1996, McBurnett et al., 2000, Matthys et al., 2004, van de Wiel et al., 2004 and Popma et al., 2006). However, patterns appear to be less consistent than in adults, as a number of carefully conducted studies have reported mixed findings (van Goozen et al., 2000, Azar et al., 2004, McBurnett et al., 2005 and van Bokhoven et al., 2005). For example, van Bokhoven et al. (2005) reported that reactive aggression was positively associated with cortisol levels, whereas Azar et al. (2004) found no association of aggression or CD with cortisol. Sondeijker et al. (2007) found no evidence that disruptive behavior was associated with low basal cortisol levels in a community sample. They concluded that this aspect of HPA axis activity might not be a useful biological marker of disruptive, antisocial, aggressive behavior (Sondeijker et al., 2007). The same research group also investigated whether low cortisol levels might predict the development of disruptive behavior in pre-adolescent youth from the general population (Sondeijker et al., 2008). Interestingly, their longitudinal data suggest that low cortisol, although not a good predictor of future disruptive behavior, might help identify a severe subgroup among those children who already show disruptive behavior problems (Sondeijker et al., 2008). A recent meta-analysis of 82 studies in child and adolescent samples found a significant but small (d = −0.10) relationship between antisocial behavior and low cortisol levels; no association was found between antisocial behavior and cortisol reactivity ( Alink et al., 2008). Thus, despite inconsistent findings, the leading hypothesis – in line with underarousal theory – still postulates a negative relationship between aggressive, antisocial behavior and basal cortisol ( van Goozen et al., 2007 and Shirtcliff et al., 2009). At the same time, it is clear that this relationship is less strong and more complex than originally thought. Differences in sample characteristics and other methodological aspects have likely contributed to the observed inconsistencies. First, heterogeneity arises from divergent operationalizations of antisocial behavior, which include delinquency, covert and overt aggressive, oppositional behavior, and psychiatric externalizing disorders like CD or ADHD. Second, the research population and settings have varied widely, with participants drawn from healthy community samples, at-risk community samples, clinically referred samples with diverse diagnoses, and samples of incarcerated offenders. Third, the samples have differed in age and gender (see Alink et al., 2008, for a more detailed discussion). Fourth, studies have differed in how cortisol was assessed: most importantly, some investigated basal cortisol levels, whereas others measured cortisol reactivity to experimental stressors. Furthermore, the timing, frequency, and method of cortisol assessment as well as the applied statistical analyses need to be taken into account. These methodological differences, which occur not only between studies conducted by different research groups but also within large research consortia, complicate the comparison of findings (Rosmalen and Oldehinkel, 2011). Inconsistent findings may also be due to heterogeneity within aggressive, antisocial samples. Low cortisol might not be related to all types of aggression and antisocial behavior, but particularly to severe forms associated with stimulation seeking, reward dominance, fearlessness, and insensitivity to punishment (O’Brien and Frick, 1996, Mitchell et al., 2002 and van Honk et al., 2003). O’Brien and Frick (1996) found the strongest evidence for a reward-dominant response style, in which behavior is stimulated by the gain of quickly available short-term rewards, rather than by the avoidance of punishment, in children with conduct problems and psychopathic traits. At present, research suggests that the combination of severe aggressive, antisocial and impulsive behavior, as often seen in youth with a diagnosis of CD, together with callous–unemotional (CU) traits delineates a highly severe behavioral group, with a close resemblance to the adult picture of psychopathy (e.g. Barry et al., 2000 and Frick and White, 2008). In addition to severe antisocial and aggressive behavior, the construct of psychopathy includes deviant personality features (Porter and Woodworth, 2006). There is still substantial debate about how many dimensions best capture the construct (e.g., Cooke et al., 2007), but at least three dimensions consistently emerge. In adults, these are (1) an affective deficient dimension comprising CU traits (including a lack of empathy, emotion, and guilt), believed to be at the core of the disorder, (2) an interpersonal, arrogant, deceitful, and narcissistic behavior dimension, and (3) an irresponsible, impulsive, and aggressive behavior dimension. In children and adolescents, similar dimensions are often described as CU traits, narcissism, and impulsivity (Salekin et al., 2004 and Frick and White, 2008). Understanding the causes and correlates of psychopathic traits in children and adolescents has become an increasingly important research topic. In this regard, the role of HPA axis abnormalities in psychopathy remains to be clarified. In studies of incarcerated individuals, initial evidence indicated low cortisol levels in psychopathic offenders as compared to non-psychopathic offenders (Cima et al., 2008). In adolescent males, there is evidence that low cortisol levels as well as an attenuated cortisol response to stress may be biological markers for CU traits: low cortisol was related to higher CU traits, even after controlling for conduct problems (Loney et al., 2006). The same study found no significant associations between the narcissistic or impulsive psychopathy dimensions with cortisol levels. However, in clinically referred boys with behavioral problems, low cortisol predicted the combined CU traits/narcissistic dimension later in life (Burke et al., 2007). Similarly, in young adult offenders high scores on the combined callous/narcissistic dimension were associated with low cortisol levels (Holi et al., 2006). In contrast, recent community findings showed no relationship between CU traits and basal cortisol in youth (Poustka et al., 2010). Although findings are still sparse, research to date thus suggests that low basal cortisol levels might play a more important role in the etiology of psychopathy through a particularly severe and aggressive antisocial pathway than in the etiology of aggressive, antisocial behavior in general (Hawes et al., 2009). If cortisol abnormalities can be clearly linked to the development of antisocial behavior and psychopathy, the HPA axis might be a promising target for pharmacological interventions, as raising low cortisol levels might increase sensitivity to behavioral treatments that are otherwise ineffective (Glenn, 2009 and Stadler et al., 2010). A number of questions still need to be addressed. As mentioned above, meta-analytic evidence supports the association between youth antisocial behavior and low cortisol levels. Nevertheless, those studies that included relevant control samples found no differences in basal cortisol between antisocial youths and controls (Popma et al., 2007 and Fairchild et al., 2008). These studies did not, however, investigate the possible association of different psychopathy dimensions with cortisol. The few studies that did examine the psychopathy dimensions did so predominantly in small, non-clinical samples (Loney et al., 2006), thereby failing to consider those youths who are most at risk for developing psychopathy. Thus, whereas there are at least preliminary findings concerning CU traits, the role of the remaining psychopathy dimensions, narcissism and impulsivity, in relation to cortisol is as yet largely unknown. The present study aimed to bridge this gap in knowledge by investigating the associations of all three psychopathy dimensions (CU traits, narcissism and impulsivity) with cortisol levels. Given the lack of studies on the relationship between diurnal cortisol patterns and psychopathy dimensions in antisocial youth, the design incorporated a detained antisocial group and a comparison group from the community. We addressed the following questions: (1) Do detained antisocial adolescents differ from a healthy comparison group in patterns of basal cortisol secretion and diurnal slopes? (2) Do the three psychopathy dimensions (CU traits, narcissism, and impulsivity) show different patterns of association with cortisol