Differential genetic and environmental influences on developmental trajectories of antisocial behavior from adolescence to young adulthood

Abstract

Little research has investigated differential genetic and environmental influences on different developmental trajectories of antisocial behavior. This study examined genetic and environmental influences on liabilities of being in life-course-persistent (LCP) and adolescent-limited (AL) type delinquent groups from adolescence to young adulthood while considering nonviolent and violent delinquency subtypes and gender differences. A genetically informative sample (n = 356, 15–16 years) from the first three waves of In-Home Interview of the National Longitudinal Study of Adolescent to Adult Health was used, with 94 monozygotic and 84 dizygotic pairs of same-sex twins (50% male). Biometric liability threshold models were fit and found that the male-specific LCP type class, chronic, showed more genetic influences, while the AL type classes, decliner and desister, showed more environmental influences. Genetic liability and shared environment both influence the persistence of antisocial behavior. The development of female antisocial behavior appears to be influenced more by shared environment.

Assessing the interplay between multigenic and environmental influences on adolescent to adult pathways of antisocial behaviors

“…Similar to the adolescence-peaked pathway of ASB, individuals in the high decline pathway exhibited peak rates of ASB during adolescence, but they also had the highest initial rate of ASB (even compared to the persistent class) and a much slower decline in their ASB throughout adulthood relative to the adolescence-peaked pathway. The existence of the high decline ASB class had been previously found for both males and females in a small Add Health subsample and other samples as well, despite focusing only on the first three waves of data (Nagin & Tremblay, 2005; Zheng & Cleveland, 2013, 2015). Prevalence rates were found to be roughly equivalent between sexes in a previous study (12% vs. 11% for males and females, respectively; Zheng & Cleveland, 2013), but the current results differed from the previous finding in that nearly 29% of males belonged in the high decline pathway versus only 12% of females.…”

“…There is evidence that genetic and environmental influences differentially contribute to developmental pathways of ASB across sexes (Van Hulle, Rodgers, D'Onofrio, Waldman, & Lahey, 2007; Zheng & Cleveland, 2015). Males and females may have different patterns of socialization that affect their engagement in ASB, and others have suggested that socialization processes and familial factors may be more relevant for females than for males (Fontaine, Carbonneau, Vitaro, Barker, & Tremblay, 2009; Zheng & Cleveland, 2015). Hence, the male-specificity of the G × E effect was unexpected, as prior studies have shown that adolescent girls may be more sensitive to social evaluation, acceptance, and connections with teachers and peers as it relates to general mental health outcomes than adolescent boys (Calvete & Cardenoso, 2005; Shochet et al, 2006).…”

“…For each of the five testing sets, beta regression models were conducted (and subsequently cross-validated) to examine associations between each polymorphism and the most severe GMM class that emerged (i.e., persistent ASB). This outcome was selected because the persistent ASB pathway has a high heritability relative to other ASB pathways (Burt, 2009; Zheng & Cleveland, 2015), and genetic influences for aggressive and persistent forms of ASB may be partially shared with other forms of ASB (Burt, 2013) as well as externalizing problems more generally (Lahey, Van Hulle, Singh, Waldman, & Rathouz, 2011). Separate cross-validations were conducted for males and females because the beta regression for females did not include MAOA genotype, given that MAOA is located on the X chromosome and heterozygosity can only be present in females but not males (Ficks & Waldman, 2014).…”

“…Four distinct adolescent ASB classes emerged from the analysis: normative, predatory (i.e., aggressive and violent), drug use, and pervasive (i.e., chronic offenders), and a significant proportion of adolescents who engaged in predatory, drug use, or pervasive ASB transitioned between these classes as they aged into adulthood, rather than having completely desisted in their ASB. Several studies have similarly identified unique groups of individuals who peak in ASB during adolescence but persist in modest levels of ASB well into their mid-20s (DiLalla & Gottesman, 1989; Moffitt, 2003; Nagin & Tremblay, 2005; Odgers et al, 2008), including studies using data from the National Longitudinal Study of Adolescent to Adult Health (Add Health; Barnes, Beaver, & Boutwell, 2011; Tung & Lee, 2016; Zheng & Cleveland, 2015). Taken together, these studies suggest that there are likely to be unique pathways of ASB from adolescence into adulthood.…”

Genetic and environmental influences on conduct and antisocial personality problems in childhood, adolescence, and adulthood

“…Furthermore, the sex differences in prevalences for conduct and antisocial personality problems [ 16 , 18 ] lead to the questions whether the influence of genetic and environmental influences also is different for males and females (i.e., quantitative sex differences) and whether there the same or different genes play a role (i.e., qualitative sex differences). Some twin studies have reported qualitative sex differences for conduct and antisocial problems [ 16 , 19 ], while others have not [ 15 , 17 , 20 – 23 ], just as some studies have detected quantitative sex differences [ 15 , 17 , 19 , 21 , 24 ], and others have not [ 12 , 16 , 20 , 22 , 25 ]. As the effect of sex might differ across age, we address this question by analyzing large samples of twins ranging from 8 to 65 years.…”