Genetic and Environmental Influences on Antisocial Behaviors: Evidence from Behavioral–Genetic Research

Institute of Psychiatry, King's College London, London SE5 8AF, United Kingdom.
Advances in genetics (Impact Factor: 6.76). 02/2005; 55:41-104. DOI: 10.1016/S0065-2660(05)55003-X
Source: PubMed


This article reviews behavioral-genetic research into human antisocial behavior. The focus is on studies of antisocial behavior that have been leading the way in investigating environmental and genetic influences on human behavior. The first generation of studies, which provided quantitative estimates attesting that genes and environments each influence about half of the population's variation in antisocial behaviors is interpreted. Then how behavioral-genetic methods are being applied to test developmental theory and to detect environmental causes of antisocial behavior is illustrated. Evidence for interactions between genes and the environment in the etiology of antisocial behavior is also examined. The article ends by envisioning future work on gene-environment interplay in the etiology of antisocial behavior.

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    • "estimated as R 2 coefficients) in each of the three latent ASB measures explained by the pedigree risk factor. Based on the convergence of findings from a substantial number of studies employing twin-and adoption-based research designs to estimate the genetic and environmental influences on ASB (Ferguson, 2010; Mason & Frick, 1994; Miles & Carey, 1997; Moffitt, 2005; Rhee & Waldman, 2002 "
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    ABSTRACT: An impressive literature has revealed that variation in virtually every measurable phenotype is the result of a combination of genetic and environmental influences. Based on these findings, studies that fail to use genetically informed modeling strategies risk model misspecification and biased parameter estimates. Twin-and adoption-based research designs have frequently been used to overcome this limitation. Despite the many advantages of such approaches, many available datasets do not contain samples of twins, siblings or adoptees, making it impossible to utilize these modeling strategies. The current study proposes a measurement strategy for estimating the intergenerational transmission of antisocial behavior (ASB) within a nationally representative sample of singletons using an extended pedigree risk approach that relies on information from first-and second-degree relatives. An evaluation of this approach revealed a pattern of findings that directly aligned with studies examining ASB using more traditional twin-and adoption-based research designs. While the proposed pedigree risk approach is not capable of effectively isolating genetic and environmental influences, this overall alignment in results provides tentative evidence suggesting that the proposed pedigree risk measure effectively captures genetic influences. Future replication studies are necessary as this observation remains preliminary. Whenever possible, more traditional quantitative genetic methodologies should be favored, but the presented strategy remains a viable alternative for more limited samples.
    Full-text · Article · Sep 2015 · Twin Research and Human Genetics
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    • "The stability of the psychopathic personality trait and its strong genetic determination (Tielbeek et al., 2012; Yildirim and Derksen, 2013) would argue against the possibility to self-regulate brain activity in fearrelated regions. On the other hand, social and developmental factors also play a fundamental role in psychopathic behavior (Viding, 2004; Moffitt, 2005). These environmental factors suggest that modification of the fear circuitry is possible. "
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    ABSTRACT: This pilot study aimed to explore whether criminal psychopaths can learn volitional regulation of the left anterior insula with real-time fMRI neurofeedback. Our previous studies with healthy volunteers showed that learned control of the blood oxygenation-level dependent (BOLD) signal was specific to the target region, and not a result of general arousal and global unspecific brain activation, and also that successful regulation modulates emotional responses, specifically to aversive picture stimuli but not neutral stimuli. In this pilot study, four criminal psychopaths were trained to regulate the anterior insula by employing negative emotional imageries taken from previous episodes in their lives, in conjunction with contingent feedback. Only one out of the four participants learned to increase the percent differential BOLD in the up-regulation condition across training runs. Subjects with higher Psychopathic Checklist-Revised (PCL:SV) scores were less able to increase the BOLD signal in the anterior insula than their lower PCL:SV counterparts. We investigated functional connectivity changes in the emotional network due to learned regulation of the successful participant, by employing multivariate Granger Causality Modeling (GCM). Learning to up-regulate the left anterior insula not only increased the number of connections (causal density) in the emotional network in the single successful participant but also increased the difference between the number of outgoing and incoming connections (causal flow) of the left insula. This pilot study shows modest potential for training psychopathic individuals to learn to control brain activity in the anterior insula.
    Full-text · Article · Oct 2014 · Frontiers in Behavioral Neuroscience
    • "Secondly, taking advantage of the use of a twin sample, we examined the differences between the childhood-onset and adolescent-onset groups with respect to genetic influences. There is good evidence of genetic influences on the liability to Conduct Disorder (Moffitt, 2005; Rhee & Waldman, 2002) but a lack of evidence on whether these vary by age of onset (Moffitt et al., 2008). The issue is not just whether the age of onset groups vary in their level of heritability, but also whether they involve the same genetic influences. "
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    ABSTRACT: Background: Conduct Disorder (CD) is a markedly heterogeneous psychiatric condition. Moffitt (1993) proposed that subclassification of CD should be according to age of onset. Our goals were to compare childhood-onset and adolescent-onset CD in terms of differences in phenotypic risk factors, genetic analyses, and factors associated with the persistence of antisocial behavior into young adulthood. Methods: The data are from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) and Young Adult Follow-Up (YAFU). Childhood-onset CD was defined as CD beginning at or before age 11. Adolescent-onset CD was defined as having CD onset between ages 14 and 17. These subgroups were compared on ADHD, young adult antisocial behavior (ASB), family dysfunction, and parental depression. Genetic analyses compare childhood-onset and adolescent-onset CD, as well as their cooccurrence with ADHD and ASB. Finally, predictors of persistence were examined. Results: Childhood-onset CD was significantly associated with ADHD, ASB, family dysfunction, and parental depression. Adolescent-onset CD was marginally associated with parental depression (p = .05) but not with any of the other risk factors. Univariate genetic models showed that both childhood-onset and adolescent-onset CD involve a large genetic liability accounting for 62% and 65% of the variance, respectively. A common genetic factor (as well as an ADHD-specific factor) accounted for the cooccurrence of childhood-onset CD and ADHD. The cooccurrence of childhood-onset CD and ASB are reflected by a common genetic factor with genetic specific effects on ASB. There was no etiological link between adolescent-onset CD and either ADHD or ASB. Both ADHD and family dysfunction were significantly associated with the persistence of antisocial behavior into young adulthood. Conclusions: Phenotypic findings differentiated between childhood-onset and adolescent-onset CD. ADHD and family dysfunction predicted persistence of antisocial behavior into young adulthood.
    No preview · Article · Oct 2014 · Journal of Child Psychology and Psychiatry
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