This study examined the extent to which rumination and depression share genetic and environmental influences in a community sample of adult twins (= 663). than genes can explain alone). In contrast nonshared environmental influences (E; those that contribute to twins’ behavior being uncorrelated such as individual-specific life events) are indicated when ranged from .40-.82 and ranged from .22-.49. Genetic and environmental correlations can be used Rabbit polyclonal to HNRNPH2. to compute the phenotypic correlations predicted by the model and to calculate the percentages of those phenotypic correlations that are due to overlapping genetic and environmental influences. Results of these calculations (Appendix A3) suggest that genetic and nonshared environmental influences account for approximately LDN193189 equal proportions (~50%) of the phenotypic correlation between rumination and depressive disorder. Physique 3 AE correlational model for RLV and CESD (A) and MDD (B) (standard errors in parentheses). Parameters for women in italics. For simplicity the indicators for the RLV are not shown. RLV=Rumination Latent Variable; CESD=Center for Epidemiological Studies-Depression; … Discussion We examined genetic and environmental influences on rumination depressive disorder and their association in a community sample of adult twins. Three novel findings have important implications for our understanding of the etiology of rumination. First we found that rumination is usually moderately heritable with the remaining variance due to nonshared environmental influences. Furthermore results were comparable across multiple rumination steps suggesting that this genetic structure of rumination LDN193189 is not measure-dependent. Second nonshared environmental influences on rumination (as measured by the RRS) were significantly larger for women. Third there was a large overlap in the genetic influences on rumination and depressive disorder suggesting a shared genetic etiology. Importantly this obtaining was consistent across gender and across steps of depressive symptoms and diagnosis of MDD suggesting this etiological overlap is not dependent on a continuous or categorical definition of depressive disorder. Etiology of Rumination Our results that rumination is usually moderately heritable in adulthood extend those from prior research (Chen & Li 2013 Moore et al. 2013 in two ways. First we examined multiple steps of rumination including a latent variable so we are confident that our results extend beyond a specific measure of rumination. Second results suggest that the heritability of rumination may LDN193189 be higher in adulthood than early adolescence. Our heritability estimate for the RLV in men (up to .82) suggest that rumination may serve as a cognitive mediator between genetic risk for depressive disorder and the onset and course of depressive disorder. This interpretation is usually consistent with recent theoretical models of risk for psychopathology in which individuals’ genetic predispositions for depressive disorder interact with cognitive risk factors (e.g. rumination) and environmental exposure to trigger the onset of depressive disorder (Gibb et al. 2013 Nolen-Hoeksema & Watkins 2011 Our results support these models suggesting that certain individuals are genetically predisposed to depressive disorder and also at risk for rumination thus further LDN193189 increasing their risk for depressive disorder. There are plausible mechanisms linking genetic predispositions to the development of rumination and depressive disorder. First high stress reactivity (e.g. hypothalamic-pituitary-adrenal axis dysfunction) has been linked to depressive disorder and low resilience to stress in adults and depressive behaviors in mice and rats (for a review see Southwick Vythilingam & Charney 2005 Individuals with a genetic propensity for high stress reactivity who are exposed to adverse events may be more likely to engage in rumination in an attempt cope with this intense reactivity increasing their risk for depressive disorder (Disner Beevers Haigh & Beck 2011 Second deficits in executive function (EF) may also increase risk for rumination and depressive disorder. Highly heritable (Friedman et al. 2008 EF deficits have been linked to rumination in that ruminators have more difficulty disengaging from stimuli that is no longer.