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      Unraveling the Genetic and Environmental Relationship Between Well-Being and Depressive Symptoms Throughout the Lifespan

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          Abstract

          Whether well-being and depressive symptoms can be considered as two sides of the same coin is widely debated. The aim of this study was to gain insight into the etiology of the association between well-being and depressive symptoms across the lifespan. In a large twin-design, including data from 43,427 twins between age 7 and 99, we estimated the association between well-being and depressive symptoms throughout the lifespan and assessed genetic and environmental contributions to the observed overlap. For both well-being (range 31–47%) and depressive symptoms (range 49–61%), genetic factors explained a substantial part of the phenotypic variance across the lifespan. Phenotypic correlations between well-being and depressive symptoms across ages ranged from −0.34 in childhood to −0.49 in adulthood. In children, genetic effects explained 49% of the phenotypic correlation while in adolescents and young adults, genetic effects explained 60–77% of the phenotypic correlations. Moderate to high genetic correlations (ranging from −0.59 to −0.66) were observed in adolescence and adulthood, while in childhood environmental correlations were substantial but genetic correlations small. Our results suggest that in childhood genetic and environmental effects are about equally important in explaining the relationship between well-being and depressive symptoms. From adolescence onwards, the role of genetic effects increases compared to environmental effects. These results provided more insights into the etiological underpinnings of well-being and depressive symptoms, possibly allowing to articulate better strategies for health promotion and resource allocation in the future.

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          Most cited references 35

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          'Mendelian randomization': can genetic epidemiology contribute to understanding environmental determinants of disease?

          Associations between modifiable exposures and disease seen in observational epidemiology are sometimes confounded and thus misleading, despite our best efforts to improve the design and analysis of studies. Mendelian randomization-the random assortment of genes from parents to offspring that occurs during gamete formation and conception-provides one method for assessing the causal nature of some environmental exposures. The association between a disease and a polymorphism that mimics the biological link between a proposed exposure and disease is not generally susceptible to the reverse causation or confounding that may distort interpretations of conventional observational studies. Several examples where the phenotypic effects of polymorphisms are well documented provide encouraging evidence of the explanatory power of Mendelian randomization and are described. The limitations of the approach include confounding by polymorphisms in linkage disequilibrium with the polymorphism under study, that polymorphisms may have several phenotypic effects associated with disease, the lack of suitable polymorphisms for studying modifiable exposures of interest, and canalization-the buffering of the effects of genetic variation during development. Nevertheless, Mendelian randomization provides new opportunities to test causality and demonstrates how investment in the human genome project may contribute to understanding and preventing the adverse effects on human health of modifiable exposures.
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            Mental Illness and/or Mental Health? Investigating Axioms of the Complete State Model of Health.

             Corey Keyes (2005)
            A continuous assessment and a categorical diagnosis of the presence (i.e., flourishing) and the absence (i.e., languishing) of mental health were proposed and applied to the Midlife in the United States study data, a nationally representative sample of adults between the ages of 25 and 74 years (N = 3,032). Confirmatory factor analyses supported the hypothesis that measures of mental health (i.e., emotional, psychological, and social well-being) and mental illness (i.e., major depressive episode, generalized anxiety, panic disorder, and alcohol dependence) constitute separate correlated unipolar dimensions. The categorical diagnosis yielded an estimate of 18.0% flourishing and, when cross-tabulated with the mental disorders, an estimate of 16.6% with complete mental health. Completely mentally healthy adults reported the fewest health limitations of activities of daily living, the fewest missed days of work, the fewest half-day work cutbacks, and the healthiest psychosocial functioning (low helplessness, clear life goals, high resilience, and high intimacy). (c) 2005 APA, all rights reserved.
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              Mendelian randomization: prospects, potentials, and limitations.

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                Author and article information

                Contributors
                Journal
                Front Psychiatry
                Front Psychiatry
                Front. Psychiatry
                Frontiers in Psychiatry
                Frontiers Media S.A.
                1664-0640
                14 June 2018
                2018
                : 9
                Affiliations
                1Department of Biological Psychology, Vrije Universiteit Amsterdam , Amsterdam, Netherlands
                2Amsterdam Public Health Research Institute, Vrije Universiteit Amsterdam , Amsterdam, Netherlands
                3Neuroscience Amsterdam , Amsterdam, Netherlands
                Author notes

                Edited by: Fotios C. Papadopoulos, Uppsala University, Sweden

                Reviewed by: Andres Ricardo Schneeberger, Psychiatrische Dienste Graubünden, Switzerland; Erika Comasco, Uppsala University, Sweden

                *Correspondence: Bart M. L. Baselmans b.m.l.baselmans@ 123456vu.nl

                This article was submitted to Public Mental Health, a section of the journal Frontiers in Psychiatry

                †These authors have contributed equally to this work.

                Article
                10.3389/fpsyt.2018.00261
                6010548
                Copyright © 2018 Baselmans, Willems, van Beijsterveldt, Ligthart, Willemsen, Dolan, Boomsma and Bartels.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 3, Tables: 4, Equations: 0, References: 69, Pages: 12, Words: 8252
                Funding
                Funded by: Nederlandse Organisatie voor Wetenschappelijk Onderzoek 10.13039/501100003246
                Award ID: NWO/SPI 56-464-14192
                Award ID: NWO 480-04-004
                Award ID: NWO/ZonMW 91210020
                Award ID: NWO 463-06-001
                Award ID: NWO-VENI 451-04-034
                Award ID: NWO 406-15-132
                Award ID: NWO 480-15-001/674
                Funded by: European Research Council 10.13039/501100000781
                Award ID: ERC-230374
                Funded by: Foundation for the National Institutes of Health 10.13039/100000009
                Award ID: NIH-1R01DK092127-01
                Categories
                Psychiatry
                Original Research

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