Browsing by Subject "geenit"

Depression is a psychiatric disorder composed of several clusters of symptoms, which do not necessarily reflect common pathways of pathophysiological processes. Thus, a new conceptualization of depression has been proposed, which suggests that depression should be dissected to its key components instead of treating it as one homogeneous concept. Personality trait neuroticism is a risk factor that is consistently linked with depression. Several models have been suggested for the association between neuroticism and depression. One of them is a so-called common cause -model, which assumes that a shared etiology explains the co-occurrence of the two. Research from twin studies supports this notion, as neuroticism and depression have been found to share a large proportion of their genetic basis. However, earlier research has examined depression as a composite concept, and there are no studies to date which would have examined the shared genetic basis of specific symptoms of depression in relation with neuroticism. This study tests the common cause -model by estimating, whether the same genetic and environmental components are relevant in explaining the covariation between neuroticism and specific symptoms of depression. The data used in this study was from the Swedish Adoption/Twin Study (n = 1515, av. age = 62.0). Depression was measured with The Center for Epidemiological Studies - Depression Scale (CES-D), and separate analyses were conducted for three factors: somatic complaints, (lack of) positive affect and depressed affect. The results showed that all of the depressive symptoms shared the same genetic and environmental components when modeling the association with neuroticism, which supports the common cause -model. Over a half of the phenotypic correlation was explained by genetic influences between neuroticism and somatic complaints, as well as neuroticism and positive affect. Half of the co-variation between neuroticism and depressed affect was due to genetic influences. Findings of the current study suggest, that genetic and individual specific environmental influences are important in explaining the relationship in all of the symptoms. For future endeavors, it is suggested to search for concrete risk factors and neurobiological endophenotypes that are shared between specific symptoms and neuroticism. While the use of composite concept of depression was supported in this study, the research question has not been yet examined in molecular genetic studies. A twin model can only differentiate sources of variation, not concrete risk factors. Thus, the results presented here only apply in the context of twin modeling. Also, the robustness of the results should be tested by replicating the results among younger samples.