Developmental Patterns of Child Emotion Dysregulation as Predicted by Serotonin Transporter Genotype and Parenting

Abstract

Individual differences in emotion regulation are central to social, academic, occupational, and psychological development, and emotion dysregulation (ED) in childhood is a risk factor for numerous developmental outcomes. The present study aimed to (a) describe the developmental trajectory of ED across early childhood (3–6 years) and (b) examine its sensitivity to youth serotonin transporter genotype, positive and negative parenting behaviors, and their interaction. Participants were 99 families in the Collaborative Family Study, a longitudinal study of children with or without developmental delays. Child ED and early parenting were coded from parent–child interactions.

To examine serotonin transporter genotype as a moderator between parenting and child emotion dysregulation (ED), children with the homozygous short (SS) genotype were compared to children with the homozygous long (LL) or heterozygous (SL) genotype. We used latent growth curve modeling (LGCM) to model yearly change in ED from child age 3 to 6 years. LGCM revealed that ED decreased overall across early childhood. In addition, we observed separate Genotype × Positive and Genotype × Negative parenting behavior interactions in predictions of ED growth curves. Children with the SL/LL genotype had ED trajectories that were minimally related to positive and negative parenting behavior, whereas ED decreased more precipitously among children with the SS genotype when exposed to low negative parenting or high positive parenting. These findings provide evidence for Gene × Environment interactions (G×Es) in the development of ED in a manner that is conceptually consistent with vantage sensitivity, and they improve inferences afforded by prospective designs.

Acknowledgments

We are indebted to our staff and doctoral student colleagues, and especially to the families who participated in our research study.

Funding

This research was supported by the National Institute of Child Health and Human Development, Grant number 34879-1459 (PIs: Bruce Baker, Jan Blacher, Keith Crnic). This work was also supported by a National Science Foundation Graduate Student Fellowship to the first author.

Notes

¹ Although we obtained a measure of IQ at age 3 and acknowledge that a covariate before or at the baseline measure is ideal, we elected to use the age 5 measure given the variability in earlier measures. Within our research center, we have found that the age 5 Stanford Binet index is more consistent with assessment of DD at older ages. In addition, previous researchers have urged caution in drawing predictive conclusions regarding delay using the Bayley Scales (Crowe, Deitz, & Bennett, 1987; Hack et al., 2005).

Additional information

Funding

This research was supported by the National Institute of Child Health and Human Development, Grant number 34879-1459 (PIs: Bruce Baker, Jan Blacher, Keith Crnic). This work was also supported by a National Science Foundation Graduate Student Fellowship to the first author.