Serotonin transporter gene variation and its association with cognitive vulnerability to depression
MetadataShow full item record
Depression is a serious condition that affects a significant proportion of the population and causes substantial life impairment (Kessler et al., 2003). Cognitive models of depression vulnerability (e.g., Teasdale, 1988) posit that information processing biases for negative and positive stimuli play a critical role in the disorder. Change in negative thinking in response to dysphoric moods is referred to as cognitive reactivity and has been shown to be a risk factor for future increases in depression (e.g., Beevers & Carver, 2003; Segal et al., 2006). Interestingly, recent behavioral genetics research indicates that certain genes may influence cognitive factors associated with depression. The short allele of a polymorphism of the serotonin transporter gene (5-HTTLPR) has been associated with increased risk for depression in the context of life stress (Caspi et al., 2003); however, the psychological mechanisms that increase depression risk for short 5-HTTLPR allele-carriers have not been definitively identified. Recent work has begun to reveal an association between the 5-HTTLPR and cognitive factors associated with depression such as attention bias for emotional information (Beevers et al., 2007) and negative thinking style (Hayden et al., 2007). A pilot study (n = 156) revealed an association between 5-HTTLPR and cognitive reactivity for attention bias for happy faces. The current study (n = 180) extended and improved upon the pilot study’s methodology and examined the relationship between the 5-HTTLPR and cognitive reactivity for attention to sad and happy faces as well as cognitive reactivity for dysfunctional attitudes. Cognitive variables were assessed after a neutral mood induction and after a sad mood induction at two laboratory sessions separated by at least 24 hours. There was a significant association between the 5-HTTLPR and cognitive reactivity for attention bias for emotional faces among Caucasian participants. Specifically, the short allele was associated with increased bias for emotional faces after the sad mood induction compared to the neutral mood induction. There was a linear relationship between number of short alleles possessed by participants and increase in bias for emotional information. The 5-HTTLPR was not significantly associated with cognitive reactivity for dysfunctional attitudes, but the effect was in the expected direction. Results are discussed in the context of recent neuroimaging research and plasticity models of behavior genetics. Implications for a model of depression vulnerability integrating genetic, neural, and cognitive factors and future directions for similar behavioral genetics studies are discussed.