Social stress regulation in 4-month-old infants: Contribution of maternal social engagement and infants' 5-HTTLPR genotype

•Infant genetics and environment factors contribute to infants' stress regulation.•Four-month-old infants were exposed to a well-established social stress procedure.•5-HTTLPR S-carriers were more susceptible to social stress than L-homozygotes.•Maternal behavior acted as a buffer for S-carriers, but not for L-homozygotes.

BackgroundMaternal behavior and infant 5-HTTLPR polymorphism have been linked to infants' social stress reactivity and recovery at different ages. Nonetheless, Gene × Environment (G × E) studies focusing on early infancy are rare and have led to mixed results.AimTo investigate the contribution of maternal social engagement and infants' 5-HTTLPR polymorphism in predicting infants' negative emotionality in response to a social stressor, namely maternal unresponsiveness.Study designCross-sectional, G × E study.Subjects73 4-month-old infants and their mothers took part to the Face-to-Face Still-Face (FFSF) procedure.Outcome measuresA micro-analytical coding of negative emotionality was adopted to measure infants' reactivity to social stress (Still-Face episode) and infants' recovery after social stress (Reunion episode). Maternal contribution was measured as maternal social engagement during the Play episode. Infants were genotyped as S-carriers or L-homozygotes.ResultsThe interplay between maternal social engagement and infants' genotype was found to be predictive of infants' negative emotionality during both Still-Face and Reunion episodes of the FFSF paradigm. The interaction highlighted that maternal social engagement predicted minor negative emotionality during Still-Face and Reunion episodes for S-carrier infants, but not for L-homozygotes.ConclusionsFindings extend previous results on adults and children, highlighting that maternal behavior might be a protective factor for stress reactivity and regulation, especially for S-carrier infants who are at risk for heightened stress susceptibility.