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Serotonin transporter‐linked polymorphic region (5‐ HTTLPR ) genotype and stressful life events interact to predict preschool‐onset depression: a replication and developmental extension
Author(s) -
Bogdan Ryan,
Agrawal Arpana,
Gaffrey Michael S,
Tillman Rebecca,
Luby Joan L
Publication year - 2014
Publication title -
journal of child psychology and psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.652
H-Index - 211
eISSN - 1469-7610
pISSN - 0021-9630
DOI - 10.1111/jcpp.12142
Subject(s) - 5 httlpr , serotonin transporter , depression (economics) , genotype , major depressive disorder , psychology , context (archaeology) , allele , developmental psychology , clinical psychology , psychiatry , genetics , biology , gene , mood , paleontology , macroeconomics , economics
Background Scientific enthusiasm about gene × environment interactions, spurred by the 5‐ HTTLPR (serotonin transporter‐linked polymorphic region) × SLE s (stressful life events) interaction predicting depression, have recently been tempered by sober realizations of small effects and meta‐analyses reaching opposing conclusions. These mixed findings highlight the need for further research. Converging evidence suggests that the effects of 5‐ HTTLPR genotype may be neurodevelopmental in origin, but we are not aware of empirical studies that have investigated whether the 5‐ HTTLPR genotype × SLE interaction predicts preschool‐onset depression ( PO ‐ MDD ), the earliest validated form of depression. Methods Children ( n = 234) aged 3–5 were recruited for a longitudinal study designed to examine PO ‐ MDD . In a comprehensive baseline assessment, the child's primary caregivers completed questionnaires and were interviewed about their child's behaviors, psychiatric symptoms, and exposure to SLE s. Results A 5‐ HTTLPR × SLE s interaction emerged, such that children homozygous for the short allele were more susceptible to depression in the context of elevated SLE than long allele carriers. In contrast, at low SLE exposure, short allele homozygotes had fewer depressive symptoms. The data were best fit by a plasticity model with a substantial reduction in fit by diathesis‐stress models. Conclusions Extending studies in adult and adolescent populations, these data suggest that 5‐ HTTLPR genotype may provide plasticity to environmental influence, for better or worse. Specifically, children homozygous for the short allele were more susceptible to the depressogenic effects of SLE s but benefitted, in the form of reduced depressive symptoms, in the context of relatively benign environmental conditions (i.e. relatively low SLE exposure). These data highlight the importance of examining gene × environment interactions across development, environment, and outcome but should be interpreted cautiously given the small sample size.