Genetic factors in stress and major depression

2009 ◽  
pp. 55-66 ◽  
Author(s):  
Stephan Claes ◽  
Elisabeth B. Binder ◽  
Charles B. Nemeroff
1996 ◽  
Vol 168 (S30) ◽  
pp. 68-75 ◽  
Author(s):  
Kenneth S. Kendler

In both clinical and epidemiological samples, major depression (MD) and generalised anxiety disorder (GAD) display substantial comorbidity. In a prior analysis of lifetime MD and GAD in female twins, the same genetic factors were shown to influence the liability to MD and to GAD. A follow-up interview in the same twin cohort examined one-year prevalence for MD and GAD (diagnosed using a one-month minimum duration of illness). Bivariate twin models were fitted using the program Mx. High levels of comorbidity were observed between MD and GAD. The best-fitting twin models, when GAD was diagnosed with or without a diagnostic hierarchy, found a genetic correlation of unity between the two disorders. The correlation in environmental risk factors was +0.70 when GAD was diagnosed non-hierarchically, but zero when hierarchical diagnoses were used. Our findings provide further support for the hypothesis that in women, MD and GAD are the result of the same genetic factors. Environmental risk factors that predispose to ‘pure’ GAD episodes may be relatively distinct from those that increase risk for MD.


2013 ◽  
Vol 16 (5) ◽  
pp. 977-984 ◽  
Author(s):  
Giorgio Tettamanti ◽  
Daniel Altman ◽  
Anastasia N. Iliadou ◽  
Rino Bellocco ◽  
Nancy L. Pedersen

Previous studies have found that major depression and neuroticism are positively associated with urinary incontinence (UI). However, the genetic contribution to these associations has never been investigated. In 2005, a total of 14,094 female twins born 1959–1985 in the Swedish Twin Registry participated in a comprehensive survey on common exposures and complex diseases. Structured questions provided information on UI, depressive symptoms, major depression, and neuroticism. A logistic regression model based on generalized estimating equations (GEE) was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs). Environmental and genetic influences were assessed in co-twin control analyses and quantitative genetic analyses, which were also used to determine the proportion of the phenotypic correlation explained by familial factors. Major depression, depressive symptoms, and neuroticism were positively associated with all UI subtypes (overall, stress, urge, and mixed UI). In a trivariate Cholesky model with neuroticism, depressive symptoms (or depression), and UI a modest genetic correlation was found between indicators of depression and overall, or stress, UI. The majority of this correlation was independent from neuroticism. In contrast, the genetic factors shared between indicators of depression and urge or mixed UI were entirely in common with neuroticism. In conclusion, depression and neuroticism are associated with UI among premenopausal women: the associations are in part determined by genetic factors in common to the disorders.


1985 ◽  
Vol 15 (1) ◽  
pp. 63-69 ◽  
Author(s):  
Kathleen R. Merikangas ◽  
Myrna M. Weissman ◽  
David L. Pauls

SynopsisA twofold increase in the prevalence of depression among women has been consistently observed. Several possible explanations, including methodological, endocrine, psychosocial, and genetic factors, have been proposed for the increased rates of depression among women. This paper describes the analysis of data from a family-genetic study of depressed probands to examine whether genetic factors can explain the preponderance of depressed females. Our data indicate that the excess of females with major depression cannot be attributed to increased genetic loading for depression in women. Other factors which may explain increased rates of major depression in women are discussed.


2016 ◽  
Vol 46 (5) ◽  
pp. 525-534 ◽  
Author(s):  
Laura M. Thornton ◽  
Elisabeth Welch ◽  
Melissa A. Munn-Chernoff ◽  
Paul Lichtenstein ◽  
Cynthia M. Bulik

2013 ◽  
Vol 70 (6) ◽  
pp. 599 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Steven H. Aggen ◽  
Michael C. Neale

2011 ◽  
Vol 42 (3) ◽  
pp. 497-508 ◽  
Author(s):  
C. Blanco ◽  
J. Myers ◽  
K. S. Kendler

BackgroundRelatively little is known about the environmental and genetic contributions to gambling frequency and disordered gambling (DG), the full continuum of gambling-related problems that includes pathological gambling (PG).MethodA web-based sample (n=43 799 including both members of 609 twin and 303 sibling pairs) completed assessments of number of lifetime gambling episodes, DSM-IV criteria for PG, alcohol, nicotine and caffeine intake, and nicotine dependence (ND) and DSM-III-R criteria for lifetime major depression (MD). Twin modeling was performed using Mx.ResultsIn the entire cohort, symptoms of DG indexed a single dimension of liability. Symptoms of DG were weakly related to caffeine intake and moderately related to MD, consumption of cigarettes and alcohol, and ND. In twin and sibling pairs, familial resemblance for number of times gambled resulted from both familial–environmental (c2=42%) and genetic factors (a2=32%). For symptoms of DG, resemblance resulted solely from genetic factors (a2=83%). Bivariate analyses indicated a low genetic correlation between symptoms of DG and MD (ra=+0.14) whereas genetic correlations with DG symptoms were substantially higher with use of alcohol, caffeine and nicotine, and ND (ranging from +0.29 to +0.80). The results were invariant across genders.ConclusionsWhereas gambling participation is determined by shared environmental and genetic factors, DG constitutes a single latent dimension that is largely genetically determined and more closely related to externalizing than internalizing behaviors. Because these findings are invariant across genders, they suggest that the etiological factors of DG are likely to be similar in men and women.


1991 ◽  
Vol 21 (2) ◽  
pp. 329-335 ◽  
Author(s):  
Peter McGuffin ◽  
Randy Katz ◽  
Joan Rutherford

SYNOPSISWe studied a series of twins systematically ascertained through 214 probands (84 monozygotic, 130 dizygotic) who had had one or more episodes of hospital-treated major depression. A variety of definitions of depression were applied to the co-twins all of which resulted in (a) markedly higher rates of disorder than are found in the general population, (b) significantly higher monozygotic than dizygotic concordance. The results of applying a simple additive model in which depression is considered as a threshold trait suggested that both genetic factors and shared family environment make substantial and significant contributions to the familiality of depression.


2001 ◽  
Vol 31 (4) ◽  
pp. 605-616 ◽  
Author(s):  
K. S. KENDLER ◽  
C. O. GARDNER ◽  
M. C. NEALE ◽  
C. A. PRESCOTT

Background. Although women are at consistently greater risk for major depression (MD) than men, it is unclear whether sex modifies the aetiological impact of genetic factors on MD. Is the heritability of MD different in men and women? Do the same genetic risk factors predispose to MD in the two sexes?Methods. We obtained a lifetime history of MD by personal interview on two occasions from 6672 individual twins and 2974 complete twin pairs. Three diagnostic criteria of increasing narrowness were employed: DSM-III-R, DSM-III-R plus impairment and Washington University. To increase power by controlling for unreliability of assessment, we evaluated sex differences on genetic risk for MD using a structural equation measurement model.Results. Using DSM-III-R criteria, but not the two narrower definitions, heritability of MD was significantly greater in women than in men. In the three diagnostic systems, the genetic correlation in liability to MD in men and women was estimated at between +0·50 and +0·65. These estimates differed significantly from unity for the two broader definitions.Conclusion. Using broad but not narrower definitions of illness, genetic factors play a greater role in the aetiology of MD in women than in men. The genes that influence risk for MD in the two sexes are correlated but are probably not entirely the same. These results raise the possibility that, in linkage and association studies, the impact of some loci on risk for MD will differ in men and women.


2001 ◽  
Vol 31 (3) ◽  
pp. 411-423 ◽  
Author(s):  
KENNETH S. KENDLER ◽  
CHARLES O. GARDNER

Background. Genetic effects upon behaviour are pervasive. To what extent are the many correlates of major depression (MD) due to individual-specific environmental experiences versus genetic factors correlated with risk for MD?Methods. From a population-based twin registry, we identified 72 female monozygotic pairs discordant for a lifetime history of MD and compared the affected and unaffected members on a wide range of putative correlates of MD.Results. The affected twin differed from her unaffected co-twin on many variables, eight of which were maximally discriminating: (i) maternal protectiveness; (ii) conflictual parent–child relationship; (iii) low optimism; (iv) current stressful life events; (v) financial difficulties and a history of (vi) phobia, (vii) nicotine dependence; and (viii) divorce. A cluster analysis suggested three ‘environmental pathways' to MD characterized by: (i) childhood vulnerability and anxiety; (ii) acting-out and demoralization; and (iii) interpersonal difficulties.Conclusion. Important precursors and sequelae of MD originate in environmental experiences unique to the individual and are not mediated through genetic factors or family-of-origin effects. Such environmental factors cause pervasive differences in monozygotic twins discordant for MD, especially in the areas of interpersonal difficulties, psychopathology, social problems and self-concept. These findings should be interpreted in the context of possible retrospective recall bias and the difficulty of distinguishing risk factors from sequelae in co-twin–control studies.


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