Interacting effect of MAOA genotype and maternal prenatal smoking on aggressive behavior in young adulthood

Abstract

Findings on the etiology of aggressive behavior have provided evidence for an effect both of genetic factors, such as variation in the monoamine oxidase A (MAOA) gene, and adverse environmental factors. Recent studies have supported the existence of gene × environment interactions, with early experiences playing a key role. In the present study, the effects of prenatal nicotine exposure, MAOA genotype and their interaction on aggressive behavior during young adulthood were examined. In a sample of 272 young adults (129 males, 143 females) from an epidemiological cohort study, smoking during pregnancy was measured with a standardized parent interview at the offspring's age of 3 months. Aggressive behavior was assessed between the ages of 19 and 25 years using the Young Adult Self-Report. DNA was genotyped for the MAOA 5' untranslated region variable number of tandem repeats polymorphism (VNTR). Results revealed a significant interaction between MAOA and smoking during pregnancy, indicating higher levels of aggressive behavior in young adults carrying the MAOA low-expressing genotype who had experienced prenatal nicotine exposure (n = 8, p = .025). In contrast, in carriers of the MAOA high-expressing genotype, maternal smoking during pregnancy had no effect on aggressive behavior during young adulthood (n = 20, p = .145). This study extends earlier findings demonstrating an interaction between MAOA genotype and prenatal nicotine exposure on aggressive behavior into young adulthood. The results point to the long-term adverse effects of smoking during pregnancy on the offspring's mental health, possibly underlining the importance of smoking cessation during pregnancy. According to the nature of the study (particularly sample size and power), analyses are exploratory and results need to be interpreted cautiously.

Interacting Effect of Catechol-O-Methyltransferase (COMT) and Monoamine Oxidase A (MAOA) Gene Polymorphisms, and Stressful Life Events on Aggressive Behavior in Chinese Male Adolescents

“…In line with previous findings that a single gene polymorphism was not on its own related to aggressive behavior (e.g., Hygen et al, 2015 ; Hohmann et al, 2016 ; Tuvblad et al, 2016 ; Zhang Y. et al, 2017 ), our results didn’t show the main effect of MAOA T941G or COMT Ala22/72Ser polymorphism. However, MAOA T941G polymorphism was found to moderate the effect of interpersonal problems experienced by adolescents on aggressive behavior, specifically, adolescents with T allele were more likely to evince aggressive behavior when exposed to interpersonal problems.…”

“…MAOA knockout mice have been shown to exhibit elevated aggressive behavior ( Cases et al, 1995 ), but results from studies of the association between MAOA and aggressive behavior in humans were still inconsistent. A broader literature has shown that the low-activity MAOA genotype is associated with more aggressive behavior ( Caspi et al, 2002 ; Hart and Marmorstein, 2009 ; McDermott et al, 2009 ; Hohmann et al, 2016 ), while some other work has come to the opposite conclusion – that the high-activity MAOA genotype is associated with more aggressive behavior ( Manuck et al, 2000 ; Beitchman et al, 2004 ; Kinnally et al, 2009 ; Mcgrath et al, 2012 ). Still other studies have indicated that MAOA gene polymorphisms are not associated with aggressive behavior ( Fresan et al, 2007 ).…”

“…In addition, the majority of extant studies ( Manuck et al, 2000 ; Caspi et al, 2002 ; Beitchman et al, 2004 ; Kinnally et al, 2009 ; Mcgrath et al, 2012 ; Hohmann et al, 2016 ) on MAOA gene have focused on the effects of a variable number tandem repeat (VNTR) polymorphism of 30-bp located in the upstream promoter region ( MAOA -VNTR), which is associated with differences in MAOA activity. Another polymorphism, T941G (rs6323) is a common functional polymorphism in exon 8 of the MAOA gene; the TG or GG genotype codes for the higher activity form of the enzyme.…”

Respiratory sinus arrhythmia in the fourth decade of life depends on birth weight and the DRD4 gene: Implications for understanding the development of emotion regulation

“…Our understanding of the roles genes play in disease pathogenesis has been enhanced by the study of interactions between genetic risk factors and the environment. Studies of these gene by environment interactions further highlight the importance of the environment in the development of physiological variability, and more recently, in keeping with the developmental origins of health and disease (DOHaD) hypothesis, pre and early postnatal exposures have been implicated as important to the development of neuropsychiatric disorders and their endophenotypic markers (Fortier et al, ; Hohmann et al, ).…”

Behavioral Genetics in Criminal and Civil Courts

“…For instance, an emerging body of literature has indicated an interactive effect of MAOA genotype and prenatal adverse environments (e.g., mother’s smoking during pregnancy) on aggressive behavior in young adulthood. 54,55 The research literature also suggests that these individuals’ genetic sensitivity to the environment is for better and for worse: they are as likely to benefit disproportionately from supportive environments as to be disadvantaged by adverse ones. 56–58 And while initial studies on this so-called differential-susceptibility thesis—which has now mostly (but not always 59 ) been confirmed 60,61 by correlational studies, 62 a few randomized trials, 62 and a meta-analysis 62 —have focused primarily on family-based childhood adversity, more recent research demonstrates that adverse childhood environments may also include broader societal settings, such as conditions in schools and neighborhoods.…”