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      The environment and schizophrenia.

      Nature

      Cities, Cognition Disorders, complications, etiology, Environment, Genetic Predisposition to Disease, Humans, Marijuana Smoking, adverse effects, Minority Groups, Phenotype, Psychotic Disorders, Translational Medical Research, genetics, physiopathology, psychology, Schizophrenia, Stress, Psychological, Substance-Related Disorders, Animals

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          Abstract

          Psychotic syndromes can be understood as disorders of adaptation to social context. Although heritability is often emphasized, onset is associated with environmental factors such as early life adversity, growing up in an urban environment, minority group position and cannabis use, suggesting that exposure may have an impact on the developing 'social' brain during sensitive periods. Therefore heritability, as an index of genetic influence, may be of limited explanatory power unless viewed in the context of interaction with social effects. Longitudinal research is needed to uncover gene-environment interplay that determines how expression of vulnerability in the general population may give rise to more severe psychopathology.

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          Most cited references 4

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          Biologic synergism and parallelism.

           J Darroch (1997)
          In epidemiologic studies of two binary exposure factors, much attention has been given to the concept of synergism of the factors. The leading dictionary of epidemiology offers two definitions of synergism, one of which this author labels statistical and the other biologic. The epidemiologic literature has been largely concerned with statistical synergism, which is typically measured using additive or multiplicative interaction. This paper focuses on biologic synergism, on the related concept of biologic parallelism, and on the question of how much information can be gleaned about population amounts of biologic synergism and parallelism--information which is of vital interest to epidemiologists. A fundamental identity equates the difference between the amounts of biologic synergism and parallelism to the additive interaction. Two biologic models, the multistage model and the no-hit or immunity model, enhance the interpretation of multiplicative interaction as a measure of statistical synergism, but it is pointed out here that, unfortunately, both models incorporate the strong assumption that there is no parallelism. A third model, the single-hit or vulnerability model, makes the even stronger assumption that there is no biologic synergism and consequently that the additive interaction is equal to minus the amount of parallelism. A consequence of this fact is that a link which has been perceived in the literature to exist between the single-hit model and the additive interaction is false.
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            Is our concept of schizophrenia influenced by Berkson's bias?

            If both positive and negative dimensions of schizophrenia independently influence need for care, a higher estimate of the comorbidity between these dimensions is expected in clinical samples than would be the case if non-clinical cases were investigated (i.e. Berkson's bias). The present paper investigates whether positive and negative dimensions independently contribute to mental health care use in a general population sample. A prospective cohort study was conducted, in which 7076 individuals were interviewed with the Composite International Diagnostic Interview Schedule at baseline and 1 and 3 years later. Lifetime positive and negative psychotic experiences (PPE, NPE) were assessed at baseline. Mental health care use (MHC) was assessed at baseline, and prospectively 1 and 3 years later. The rating of MHC was strongly associated with NPE and PPE, both retrospectively and prospectively and the effects of both variables remained strong and significant in the analyses with both variables included. These results, therefore, suggest that the concept of schizophrenia, as a unitary entity with high comorbidity between positive and negative dimensions, is in part the result of Berkson's bias.
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              Sources of individual differences in depressive symptoms: analysis of two samples of twins and their families.

              Self-reported symptoms of depression are commonly used in mental health research to assess current psychiatric state, yet wide variation in these symptoms among individuals has been found in both clinical and epidemiologic populations. The authors sought to understand, from a genetic-epidemiologic perspective, the sources of individual differences in depressive symptoms. Self-reported symptoms of depression were assessed in two samples of twins and their spouses, parents, siblings, and offspring: one sample contained volunteer twins recruited through the American Association of Retired Persons and their relatives (N = 19,203 individuals) and the other contained twins from a population-based twin registry in Virginia and their relatives (N = 11,242 individuals). Model fitting by an iterative, diagonal, weighted least squares method was applied to the 80 different family relationships in the extended twin-family design. Independent analyses of the two samples revealed that the level of depressive symptoms was modestly familial, and familial resemblance could be explained solely by genetic factors and spousal resemblance. The estimated heritability of depressive symptoms was between 30% and 37%. There was no evidence that the liability to depressive symptoms was environmentally transmitted from parents to offspring or was influenced by environmental factors shared either generally among siblings or specifically between twins. With correction for unreliability of measurement, genetic factors accounted for half of the stable variance in depressive symptoms. Depressive symptoms in adulthood partly reflect enduring characteristics of temperament that are substantially influenced by hereditary factors but little, or not at all, by shared environmental experiences in the family of origin.
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                Author and article information

                Journal
                21068828
                10.1038/nature09563

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