ABSTRACT
Child maltreatment is associated with increased risk for virtually all common mental disorders, but it is not yet clear why. One possible mechanism is emotion regulation ability. The present study investigated for the first time the influence of a BDNF Val66Met genotype × child maltreatment interaction on emotion regulation, and compared differential susceptibility and diathesis-stress models. A sample of N = 254 healthy volunteers were genotyped for the BDNF Val66Met polymorphism and underwent an experimental assessment of reappraisal ability (i.e. the success of using reappraisal to downregulate negative affect). A self-report instrument previously validated against a clinical interview was used to investigate child maltreatment. There was a significant BDNF Val66Met genotype × child maltreatment interaction (B = -0.31, P < 0.015), with Met carriers showing both the lowest level of reappraisal ability in maltreated participants, and the highest level of reappraisal ability in non-maltreated participants. By assessing alternative models, we found that the best fitting model was in line with strong differential susceptibility. As expected, reappraisal ability was negatively correlated with depressive symptoms. Therefore, the BDNF Val66Met polymorphism moderates the link between child maltreatment and emotion regulation ability. Future studies could investigate whether improving reappraisal in maltreated BDNF Met carriers results in reduced risk for mental disorders.
Subject(s)
Brain-Derived Neurotrophic Factor/genetics , Child Abuse/psychology , Cognition Disorders/etiology , Adult , Alleles , Brain-Derived Neurotrophic Factor/metabolism , Child , Cognition Disorders/genetics , Cognition Disorders/psychology , Depression/genetics , Emotions/physiology , Female , Gene-Environment Interaction , Genetic Predisposition to Disease , Genotype , Humans , Male , Polymorphism, Single Nucleotide , Self Report , Stress, Psychological/genetics , Stress, Psychological/psychology , Young AdultABSTRACT
This study investigated whether somatic markers mediate the effect of serotonin transporter genotype on Iowa Gambling Task (IGT) performance. Participants (N = 135) were genotyped for the insertion/deletion and single-nucleotide (rs25531) polymorphisms in the promoter region of the serotonin transporter gene (5-HTTLPR). The results of mediation analyses indicated that skin conductance responses that anticipated IGT card selections partially (i.e. 42% of the total effect) mediated the effect of genotype on IGT performance. In comparison with high-functioning 5-HTTLPR genotypes, the low-functioning genotypes were associated with higher total IGT scores. This suggests that the higher synaptic availability of serotonin, associated with the low-functioning 5-HTTLPR genotypes, may confer differential susceptibility to decision making under risk, and that almost half of this effect is explained by facilitated somatic markers during IGT.