Transition from stress sensitivity to a depressive state: longitudinal twin study (original) (raw)

Recent findings suggest that genetic liability to depression is in part expressed as the tendency to display negative affect in response to minor stressors in the flow of daily life. 1 Thus, a causal pathway from genetic risk of daily-life stress sensitivity to the development of affective symptoms may be hypothesised. Additional support for a causal pathway from daily-life stress sensitivity to the development of depression can be obtained by assessing the within-individual association between baseline dailylife stress sensitivity and the development of future affective symptoms. We examined this issue in a large general-population female twin sample using experience sampling methodology, 1 together with prospective dimensional and diagnostic follow-up measurements of depression. In addition, since not everyone with high levels of stress sensitivity will develop depression, factors that might moderate transition to depression were examined. We predicted that indirect measures of genetic risk and polymorphisms in the genes encoding the serotonin transporter (serotonintransporter-linked or 5-HTTLPR) and the gene encoding brainderived neurotrophic factor (BDNF Val66Met) 2-5 would moderate the transition from experiencing increased daily-life stress sensitivity to future affective symptoms. Furthermore, we hypothesised that the occurrence of negative life events would moderate this transition.