The purpose of the present study was to examine the relative association of genetic and environmental factors with individual differences in each of the proximal, jointly necessary, and sufficient causes for suicidal behavior, according to the Interpersonal-Psychological Theory of Suicide (IPTS; Joiner, 2005). We examined data on derived scales measuring acquired capability, belongingness, and burdensomeness (the determinants of suicidal behavior, according to theory) from 348 adolescent male twins. Univariate biometrical models were used to estimate the magnitude of additive genetic (A), non-additive genetic (D), shared environmental (C), and nonshared environmental (E) effects associated with the variance in acquired capability, belongingness, and burdensomeness. The best fitting model for the acquired capability allowed for additive genetic and environmental effects, whereas the best fitting model for burdensomeness and belongingness allowed for shared and nonshared environmental effects. The present research extends prior work by specifying the environmental and genetic contributions to the components of the IPTS, and our findings suggest that belongingness and burdensomeness may be more appropriate targets for clinical intervention than acquired capability as these factors may be more malleable or amenable to change.

Though initially conceptualized as resulting from peer imitation of child-onset or life-course-persistent youth [Moffitt, 1993], there is mounting evidence from twin studies that adolescent-onset or adolescent-limited antisocial behavior may also be genetically influenced. This study sought to provide preliminary molecular genetic evidence in support of these findings. We further evaluated whether genetic associations varied between behavioral subtypes of ASB (i.e., physical aggression and nonaggressive rule-breaking), given that only the latter has been found to characterize adolescent-onset ASB. The sample consisted of 211 undergraduate men of European-American ancestry. Three polymorphisms with theoretical and/or empirical ties to ASB or related traits (i.e., tryptophan hydroxylase-A218C, 5HT(2A) His452Tyr, and the DAT1 variable nucleotide tandem repeat) were genotyped. Analyses revealed that two of the three polymorphisms (i.e., His452Tyr and DAT1) were associated with adolescent ASB. Moreover, these associations appeared to be specific to the nonaggressive, rule-breaking form of ASB, and did not extend to physical aggression, further supporting ties to adolescent ASB in particular. Such results thus constructively replicate earlier findings of genetic influence on adolescent ASB. They also offer preliminary evidence that the genetic processes underlying aggressive and nonaggressive antisocial behavior may be (at least partially) distinct.

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There is mounting evidence that physical aggression and nonaggressive, rule-breaking delinquency constitute two separable though correlated subtypes of antisocial behavior. Even so, it remains unclear whether these behavioral subtypes have meaningfully different interpersonal correlates, particularly as they are subsumed within the same broad domain of antisocial behavior. To evaluate this, we examined whether hostile perceptions of others (assessed via exposure to a series of neutral unknown faces) were linked to level and type of antisocial behavior aggression vs. rule-breaking, and moreover, whether this association persisted even when also considering the common association with negative affect (as manipulated via written recollection of one's best and worst life experiences). Analyses revealed that aggression, but not rule-breaking, was uniquely tied to hostile perceptions of others. Furthermore, this association persisted over and above the common association of both hostile perceptions and aggression with negative affect (at both trait and state levels). Such results provide additional support for clinically meaningful differences between the behavioral subtypes of aggression and nonaggressive rule-breaking and for the independent role of hostile perceptions in aggressive behavior.

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