Objective: To test whether individuals with at least one copy of the short (S) or long (L) G allele of the serotonin transporter polymorphism (5-HTTLPR) exhibit greater increases in anxiety, compared with L A L A individuals, under periods of high daily stress. Although this common polymorphism in the serotonin transporter gene has been identified as a vulnerability factor for anxiety, findings in the literature are mixed. Discrepant findings could be explained by recent research showing that

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... HTTLPR is functionally triallelic (L A versus L G or S), rather than biallelic (L versus S). Mixed findings could also result from a lack of attention to diathesis-stress models, whereby genetic vulnerability is considered latent until activated by stress (gene-environment interplay). Based on this model, we argue that genotype differences in anxiety should be stronger in the presence of stress. Methods: A total of 350 college students recorded their daily stressors and mood for two 30-day periods, separated by 1 year. Results: Across both years, diathesis-stress patterns were observed for reports of anxious mood as a function of 5-HTTLPR. Individuals with at least one copy of the S or L G allele at 5-HTTLPR experienced elevated anxious mood on days with more intense stressors, as compared with those who were L A homozygotes. Genotype differences in anxiety were less apparent on low stress days. No consistent allelic association of 5-HTTLPR was observed with any other mood states, trait anxiety, or neuroticism. Conclusion: Our findings highlight the potential value of focusing on genetic vulnerability in the context of everyday environmental triggers.