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The BDNF gene val66met polymorphism and behavioral inhibition in early childhood
Author(s) -
Vandermeer Matthew R. J.,
Sheikh Haroon I.,
Singh Shiva S.,
Klein Daniel N.,
Olino Thomas M.,
Dyson Margaret W.,
Bufferd Sara J.,
Hayden Elizabeth P.
Publication year - 2018
Publication title -
social development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.078
H-Index - 91
eISSN - 1467-9507
pISSN - 0961-205X
DOI - 10.1111/sode.12292
Subject(s) - psychology , trait , allele , developmental psychology , neurotrophic factors , brain derived neurotrophic factor , context (archaeology) , anxiety , clinical psychology , gene , genetics , biology , receptor , psychiatry , paleontology , computer science , programming language
Abstract Stably elevated behavioral inhibition (BI) is an established risk factor for internalizing disorders. This stability may be related to genetic factors, including a valine‐to‐methionine substitution on codon 66 ( val66met ) of the brain‐derived neurotrophic factor (BDNF) gene. Past work on the BDNF met variant has inconsistently linked it to vulnerability to internalizing problems; some of this inconsistency may stem from the failure to consider gene‐trait interactions in shaping the course of early BI. Toward elucidating early pathways to anxiety vulnerability, we examined gene‐by‐trait interactions in predicting the course of BI over time in 476 children, assessed for BI using standardized laboratory methods. We found that children with the met allele showed lower stability of BI between ages 3 and 6 than those without this allele. While the mechanisms that underlie this effect are unclear, our findings are consistent with the notion that the met variant, in the context of early BI, influences the stability of this trait in early development.