Serotonin Transporter Gene as a Predictor of Stress Generation in Depression
Journal of Abnormal Psychology (Impact Factor: 4.86). 05/2012; 121(4). DOI: 10.1037/a0027952
Research suggests that a polymorphism in the promoter region of the serotonin transporter promoter (5-HTTLPR) interacts with stressful life events to predict depressive onset, with short (s) allele presence associated with greater susceptibility to stressors. However, this research has not considered that depressed individuals often actively generate stressful contexts. Furthermore, little is known about the genetic basis of stress generation. The current study explored the role of 5-HTTLPR genotype in stress generation in a longitudinal sample of 381 adolescents, oversampled for maternal depression, assessed at ages 15 and 20. Genotype did not correlate directly with number or ratings of stressful life events. However, 5-HTTLPR genotype interacted with depression at age 15 to predict dependent stressful events at age 20. Specifically, participants with one or more s alleles showed a stronger association between age 15 depression and age 20 dependent and interpersonal events than long allele homozygotes. Results imply that the 5-HTTLPR genotype predicts reciprocal associations between stress and depression, indicating a more complex relationship between stress, depression, and their genetic underpinnings than previously suggested. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
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ABSTRACT: Previous research demonstrates that carriers of the short allele of the serotonin transporter gene (5-HTTLPR) show both greater susceptibility to depression in response to stressful life events and higher rates of generation of stressful events in response to depression. The current study examines relational security (i.e., self-reported beliefs about attachment security) as a moderator of these effects, building on emerging research suggesting that the short allele acts as a marker of sensitivity to the social environment. Participants were 354 Caucasian adolescents oversampled for maternal depression (137 male, 217 female), assessed at ages 15 and 20. Results indicated that the short allele predicted increased stress generation at age 20 among those with low age 15 security but decreased stress generation among those with high security, and revealed a three-way interaction between age 15 depression, age 15 security, and genotype, where depression predicted stress generation only among short allele carriers with low security. Further, among boys only, security interacted with genotype to predict longitudinal changes in depression diagnosis, with the s-allele predicting relative increases in probability of depression among boys with low security but decreases among boys with high security. Results support the notion of the short allele as a marker of social reactivity, and suggest that attachment security may buffer against the genetic vulnerability introduced by the short allele, in line with predictions of the differential susceptibility theory.Journal of Abnormal Child Psychology 10/2012; 41(3). DOI:10.1007/s10802-012-9682-z · 3.09 Impact Factor
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ABSTRACT: Although the past two decades have seen increasing empirical interest in stress generation, the process whereby depressed or depression-prone individuals experience higher rates of life stress that are at least in part influenced by their own cognitive and behavioral characteristics, several important aspects of this phenomenon remain relatively unexamined, leaving open several promising opportunities for future advancement of the field. The current paper begins with a brief review of the extant literature on the influence of cognitive, behavioral and interpersonal, childhood maltreatment, and genetic factors on stress generation. An integrative theoretical model is then presented tying together these different lines of research in accounting for the stress generation effect and its potential depressogenic sequelae (i.e., depression recurrence and depression contagion). Drawing on this model, particular focus is given to the need to identify the behavioral processes through which cognitive factors confer risk for stress generation, as well as to the need for research assessing the full etiological chain posited by the stress generation hypothesis linking self-generated stress with subsequent depression. In addition, methodological issues of particular relevance to this area of research are discussed. The current review ends with a consideration of the clinical implications of the stress generation phenomenon.Clinical Psychology Review 01/2013; 33(3):406-416. DOI:10.1016/j.cpr.2013.01.005 · 7.18 Impact Factor
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ABSTRACT: Previous research supports gene-environment interactions for polymorphisms in the corticotropin hormone receptor 1 gene (CRHR1) and the serotonin transporter gene linked polymorphic region (5-HTTLPR) in predicting depression, but it has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life. The current study tested a gene-environment-environment interaction (G × E × E; specifically, gene-EA-proximal stress interaction) model of depression in a 20-year longitudinal study. Participants were assessed prospectively for EA up to age 5 and recent chronic stress and depressive symptoms at age 20 and genotyped for CRHR1 single nucleotide polymorphism rs110402 and 5-HTTLPR. EA predicted stronger associations between recent chronic stress and depression, and the effect was moderated by genes. CRHR1 A alleles and 5-HTTLPR short alleles were associated with greater stress sensitization (i.e., greater depressive reactivity to chronic stress for those also exposed to high levels of EA). The results are consistent with the notion that EA exposure results in neurobiological and cognitive-emotional consequences (e.g., altered hypothalamic-pituitary-adrenal axis functioning), leading to emotional distress in the face of recent stressors among those with certain genetic characteristics, although further research is needed to explore explanatory mechanisms.Development and Psychopathology 11/2014; 26(4 Pt 2):1241-54. DOI:10.1017/S0954579414000996 · 4.89 Impact Factor
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