واکنش های عاطفی افتراقی در افراد مبتلا به رفتارهای تهاجمی در مقابل غیرتهاجمی ضد اجتماعی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|37208||2007||12 صفحه PDF||سفارش دهید||5036 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Personality and Individual Differences, Volume 43, Issue 6, October 2007, Pages 1481–1492
Abstract Affective dysfunction has been robustly tied to antisocial behavior, but little research has evaluated whether affective responses vary differentially with its aggressive (AGG) and rule-breaking (RB) subtypes. We therefore examined whether changes in negatively valenced affect (elicited via written recollection of one’s best and worst life experiences) were linked to level (i.e., low, average, high) and type (i.e., AGG, RB) of antisocial behavior. The sample consisted of 288 undergraduate men. Results suggested a general trait-like association between negative affect and AGG. However, this association varied across experimental conditions. In particular, the potentiation of negative affect following an aversive task was consistently associated with AGG. RB, by contrast, demonstrated little to no association with negative affect in any condition. Such findings imply that the link between antisocial behavior and affective dysregulation is largely specific to its aggressive subtype, and does not persist to non-aggressive antisocial behavior.
. Introduction Antisocial behavior (ASB) describes actions and attitudes that violate societal norms and the personal or property rights of others. Though generally operationalized via aggressive and rule-breaking behaviors, emotional shallowness and callousness are also considered core components. Consistent with this conceptualization, there is strong evidence of a link between ASB and dysfunctional affective processing/regulation of negatively valenced emotions (Davidson et al., 2000 and Lorber, 2004), an association that persists across the lifespan (Herpertz et al., 2005 and Sterzer et al., 2005) and extends to related constructs such as psychopathy (Deeley, Daly, Surguladze, Tunstall, & Mezey, 2006). Specifically, there appear to be functional and morphologic abnormalities in the frontal and limbic regions in those with aggressive/antisocial behaviors. As these areas of the brain play a primary role in the recognition and regulation of emotions (Davidson et al., 2000 and Sterzer et al., 2005), and therefore may act to constrain affective outbursts/emotional behavior, such deficits likely increase vulnerability to aggressive and behavioral outbursts. Importantly, however, studies of affective dysfunction have yet to fully consider differences within ASB. Indeed, given the pronounced heterogeneity within ASB, such studies would offer a significant refinement of current theories ( Raine, 2002). Physical aggression is found largely in males and decreases precipitously from early childhood to adulthood, with only a slight increase during mid-adolescence ( Stranger, Achenbach, & Verhulst, 1997). In contrast, non-aggressive rule-breaking increases sharply over the course of adolescence ( Burt, Carter, McGue, & Iacono, 2007), and is found in males and females ( Moffitt, 2003 and Stranger et al., 1997). Factor analytic studies ( Frick et al., 1993) further support this distinction, finding evidence for independent but correlated aggressive and rule-breaking dimensions within ASB. Aggression also appears to be more heritable than rule-breaking ( Eley et al., 2003 and Hudziak et al., 2003), while rule-breaking may be more highly influenced by shared environmental factors ( Deater-Deckard and Plomin, 1999 and Eley et al., 2003) (though the magnitude of non-shared environmental influences, generally 40–50% of the variance, does not differ across sub-types). To date, however, studies have only indirectly considered whether affective dysfunction varies by sub-type. Raine and colleagues (1997) found that low resting heart rate (a variable tied to disinhibition) at age 3 predicts aggressive but not non-aggressive ASB at age 11 (Raine, Venables, & Mednick, 1997), offering tentative (but provocative) support for differences in affective regulation across sub-type. Similarly, studies have found that aggressive ASB is more closely linked to indices of autonomic and neuroendocrine functioning than is non-aggressive ASB (Lahey, Hart, Pliszka, Applegate, & McBurnett, 1993). As low autonomic arousal and lack of autonomic responsiveness represent a form of affective deficit (Raine, 2002), such findings offer additional support for aggression-specific affective dysfunction. Finally, recent work suggests that affect dysregulation may be particularly important for precipitating aggressive behavior (Verona, Patrick, & Lang, 2002), again supporting an aggression-specific role for affective dysfunction. The above findings provide strong circumstantial evidence that affective dysfunction may be specific to aggressive ASB. The current study sought to more explicitly evaluate this hypothesis, examining whether affective responses were differentially associated with aggressive and non-aggressive ASB. We expected that those with high levels of aggression would exhibit both higher levels of negative affect in general and a more pronounced negatively valenced affective response to an aversive task (i.e., recollection of their worst memory) than those with lower aggression, and that these associations would not persist to rule-breaking.
نتیجه گیری انگلیسی
Conclusion The current results serve to further illuminate etiological distinctions between aggressive and non-aggressive antisocial behavior. Namely, the faulty affective regulation previously linked to antisocial behavior in general appears instead to be specific to its aggressive sub-type. Previous work indicates that unpleasant stimuli or events, such as pain or social stress, increase impulsive aggressive behaviors via the activation of high state-NA (Berkowitz, 2003). Within this formulation, the present study’s finding of affect dysregulation only in those higher in AGG is suggestive of an AGG-specific vulnerability for NA-mediated aggression. Moreover, as gene–environment interactions appear to contribute to NA-mediated aggression (Verona, Joiner, Johnson, & Bender, 2006), the current results further imply that gene-environment interplay may also vary by ASB sub-type (at least in men). Future research should further explore the possibility of differential gene–environment interplay within ASB.