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Volume 60, Issue 7, Pages 671-676 (1 October 2006)


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Early Family Environment, Current Adversity, the Serotonin Transporter Promoter Polymorphism, and Depressive Symptomatology

Shelley E. TayloraCorresponding Author Informationemail address, Baldwin M. Waya, William T. Welcha, Clayton J. Hilmerta, Barbara J. Lehmana, Naomi I. Eisenbergerb

Received 4 January 2006; received in revised form 24 April 2006; accepted 25 April 2006. published online 25 August 2006.

Background

Mixed evidence has suggested that homozygous carriers of the short allele (s/s) of the serotonin transporter gene-linked polymorphic region (5-HTTLPR) may be at increased risk for depression, if they have also been exposed to early or current adversity/stress. We address this debate by examining the relation of a stressful early family environment, recent adversity/stress, and the 5-HTTLPR to depressive symptomatology in a normal sample.

Methods

A nonclinical sample of 118 young adult men and women completed assessments of early family environment, recent stressful events, psychosocial resources, and psychological distress, including depressive symptomatology. The 5-HTTLPR was genotyped using a standard protocol with DNA extracted from oral fluid.

Results

A stressful early family environment was significantly related to depressive symptomatology. In addition, gene-by-environment (G×E) interactions were observed between the 5-HTTLPR and both early family environment and current adversity/stress. Individuals homozygous for the short allele had greater depressive symptomatology if they had experienced early or recent adversity but significantly less depressive symptomatology if they reported a supportive early environment or recent positive experiences, compared with participants with the s/l or l/l genotype.

Conclusions

Early or current environment, in conjunction with the serotonin transporter polymorphism, predicts depressive symptomatology.

a Department of Psychology, University of California, Los Angeles, California

b Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, California.

Corresponding Author InformationAddress reprint requests to Dr. Shelley E. Taylor, Department of Psychology, University of California, 1282A Franz Hall, 405 Hilgard Avenue, Los Angeles, CA 90095

PII: S0006-3223(06)00530-0

doi:10.1016/j.biopsych.2006.04.019


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