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Social neural sensitivity as a susceptibility marker to family context in predicting adolescent externalizing behavior.

ABSTRACT: Adolescence represents a period of risk for developing patterns of risk-taking and conduct problems, and the quality of the family environment is one robust predictor of such externalizing behavior. However, family factors may not affect all youth uniformly, and individual differences in neurobiological susceptibility to the family context may moderate its influence. The current study investigated brain-based individual differences in social motivational processing as a susceptibility marker to family conflict in predicting externalizing behavior in early adolescent youth. 163 adolescents (M_age = 12.87 years) completed an fMRI scan during which they anticipated social rewards and social punishments. For adolescents with heightened ventral striatum and amygdala blood oxygen-level dependent (BOLD) response during the anticipation of social rewards and heightened ventral striatum BOLD response during the anticipation of social punishments, higher levels of family conflict were associated with greater externalizing behavior. BOLD response when anticipating both social rewards and punishments suggested increased susceptibility to maladaptive family contexts, highlighting the importance of considering adolescent social motivation in positive and negatively valenced contexts.

SUBMITTER: Turpyn CC

PROVIDER: S-EPMC8325100 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Evidence that gene×environment interactions can reflect differential sensitivity to the environmental context, rather than risk or resilience, is increasing. To test this model, we examined the genetic contribution to indiscriminate social behavior, in the setting of a randomized controlled trial of foster care compared to institutional rearing. Children enrolled in the Bucharest Early Intervention Project (BEIP) were assessed comprehensively before the age of 30 months and subsequently randomized to either care as usual (CAUG) or high quality foster care (FCG). Indiscriminate social behavior was assessed at four time points, baseline, 30 months, 42 months and 54 months of age, using caregiver report with the Disturbances of Attachment Interview (DAI). General linear mixed-effects models were used to examine the effect of the interaction between group status and functional polymorphisms in Brain Derived Neurotrophic Factor (BDNF) and the Serotonin Transporter (5htt) on levels of indiscriminate behavior over time. Differential susceptibility, relative to levels of indiscriminate behavior, was demonstrated in children with either the s/s 5httlpr genotype or met 66 BDNF allele carriers. Specifically children with either the s/s 5httlpr genotype or met66 carriers in BDNF demonstrated the lowest levels of indiscriminate behavior in the FCG and the highest levels in the CAUG. Children with either the long allele of the 5httlpr or val/val genotype of BDNF demonstrated little difference in levels of indiscriminate behaviors over time and no group×genotype interaction. Children with both plasticity genotypes had the most signs of indiscriminate behavior at 54 months if they were randomized to the CAUG in the institution, while those with both plasticity genotypes randomized to the FCG intervention had the fewest signs at 54 months. Strikingly children with no plasticity alleles demonstrated no intervention effect on levels of indiscriminate behavior at 54 months. These findings represent the first genetic associations reported with indiscriminate social behavior, replicate previous gene×gene×environment findings with these polymorphisms, and add to the growing body of literature supporting a differential susceptibility model of gene×environment interactions in developmental psychopathology.

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Social neural sensitivity as a susceptibility marker to family context in predicting adolescent externalizing behavior.

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