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Depression and anxiety are highly comorbid due to shared genetic risk factors, but less is known about whether burnout shares these risk factors. We aimed to examine whether the covariation between major depressive disorder (MDD), generalized anxiety disorder (GAD), and burnout is explained by common genetic and/or environmental factors. This cross-sectional study included 25,378 Swedish twins responding to a survey in 2005–2006. Structural equation models were used to analyze whether the trait variances and covariances were due to additive genetics, non-additive genetics, shared environment, and unique environment. Univariate analyses tested sex limitation models and multivariate analysis tested Cholesky, independent pathway, and common pathway models. The phenotypic correlations were 0.71 (0.69–0.74) between MDD and GAD, 0.58 (0.56–0.60) between MDD and burnout, and 0.53 (0.50–0.56) between GAD and burnout. Heritabilities were 45% for MDD, 49% for GAD, and 38% for burnout; no statistically significant sex differences were found. A common pathway model was chosen as the final model. The common factor was influenced by genetics (58%) and unique environment (42%), and explained 77% of the variation in MDD, 69% in GAD, and 44% in burnout. GAD and burnout had additive genetic factors unique to the phenotypes (11% each), while MDD did not. Unique environment explained 23% of the variability in MDD, 20% in GAD, and 45% in burnout. In conclusion, the covariation was explained by an underlying common factor, largely influenced by genetics. Burnout was to a large degree influenced by unique environmental factors not shared with MDD and GAD.

Background:Previous research indicates that liability to disability pension (DP) due to mental diagnoses is moderately influenced by genetic factors. This study investigates whether genetic contributions to the liability to DP due to mood and neurotic diagnoses overlap with the genetic influences on major depression (MD), generalized anxiety disorder (GAD), or chronic fatigue (CF).Method:A prospective cohort study including 9,985 female twins born in Sweden 1933–1958. The presence of MD, GAD, and CF was assessed by computer-assisted telephone interviews conducted in 1998–2002. Data on DP due to mood and neurotic diagnoses were obtained from nationwide registers for the years 1998–2010. Common genetic and environmental influences on the phenotypes were estimated by applying structural equation modeling.Results:The prevalence of MD/GAD was 30%, CF 8%, and DP due to mood and neurotic diagnoses 3% in 2010. Genetic effects on MD/GAD explained 31% of the total genetic variation in DP, whereas genetic contributions in common with CF were small and not significant. The majority of the total non-shared environmental variance in DP (85%) was explained by the factors that were unique to DP.Conclusions:Large proportions of genetic and non-shared environmental influences in DP due to mood and neurotic diagnoses were not explained by the contributions from MD/GAD or CF. The results suggest that the process leading to DP is complex and influenced by factors other than those related to the disorder underlying DP.

Despite agreement on the negative effects of job insecurity, more knowledge needs to be generated on the health effects in terms of burnout and depressive symptoms and for whom job insecurity has these negative effects. The present study aims to investigate the associations between job insecurity and burnout and depressive symptoms respectively, by studying the moderation influences of performance-based self-esteem (PBSE), a form of contingent self-esteem. A population-based sample with 4145 twins was used. The results showed that job insecurity was significantly associated with both burnout and depressive symptoms, and that PBSE acted as a moderator, so that the associations were stronger for individuals with high PBSE than for individuals with low PBSE. The study contributes by including a personality characteristic to gain more knowledge about the mechanisms of job insecurity on mental ill-health, and by illustrating that job insecurity has an impact on severe health outcomes in terms of burnout and depressive symptoms.

Background: This study aims to assess whether the associations between burnout and sick leave due to stress-related mental disorders, other mental disorders, and somatic conditions are influenced by familial (genetic and shared environmental) factors.Methods: In this prospective cohort study, 23,611 Swedish twins born between 1959 and 1985, who answered a web-based questionnaire, including the Pines Burnout Measure 2004–2006, were included. Registry data on sick leave spells from the response date until December 31, 2010 were obtained from the Swedish Social Insurance Agency. Logistic regression analysis was performed to assess odds ratios with 95% confidence intervals for the association between burnout and sick leave for the whole sample, while conditional logistic regression of the same-sex discordant twin pairs was used to estimate the association between burnout and sick leave, adjusting for familial confounding. The Bivariate Cholesky models were used to assess whether the covariation between burnout and sick leave was explained by common genetic and/or shared environmental factors.Results: Burnout was a risk factor for sick leave due to stress-related and other mental disorders, and these associations were explained by familial factors. The phenotypic correlation between burnout and sick leave due to somatic conditions was 0.07 and the association was not influenced by familial factors. The phenotypic correlations between burnout and sick leave due to stress-related (0.26) and other mental disorders (0.30) were completely explained by common genetic factors.Conclusions: The association between burnout and sick leave due to stress-related and other mental disorders seems to be a reflection of a shared genetic liability.

Abstract Background Occupations and psychosocial working conditions have rarely been investigated as predictors of disability pension in population-based samples. This study investigated how occupational groups and psychosocial working conditions are associated with future disability pension due to musculoskeletal diagnoses, accounting for familial factors in the associations. Methods A sample of 24 543 same-sex Swedish twin individuals was followed from 1993 to 2008 using nationwide registries. Baseline data on occupations were categorized into eight sector-defined occupational groups. These were further used to reflect psychosocial working conditions by applying the job strain scores of a Job Exposure Matrix. Cox proportional hazard ratios (HR) were estimated. Results During the 12-year (average) follow-up, 7% of the sample was granted disability pension due to musculoskeletal diagnoses. Workers in health care and social work; agriculture, forestry and fishing; transportation; production and mining; and the service and military work sectors were two to three times more likely to receive a disability pension than those in the administration and management sector. Each single unit decrease in job demands and each single unit increase in job control and social support significantly predicted disability pension. Individuals with high work strain or an active job had a lower hazard ratio of disability pension, whereas a passive job predicted a significantly higher hazard ratio. Accounting for familial confounding did not alter these results. Conclusion Occupational groups and psychosocial working conditions seem to be independent of familial confounding, and hence represent risk factors for disability pension due to musculoskeletal diagnoses. This means that preventive measures in these sector-defined occupational groups and specific psychosocial working conditions might prevent disability pension due to musculoskeletal diagnoses.

Previous studies of risk factors for sickness absence (SA) focus primarily on psychosocial and work environmental exposures. The aim of this study was to investigate the relative contribution of genetic influences on SA among women and men. The population-based study sample of Swedish twins (34,547) included 13,743 twin pairs of known zygosity, 3,495 monozygotic, 5,073 same-sexed dizygotic, and 5,175 opposite sexed. The point prevalence of long-term SA (≥15 days) in each zygosity and sex group was calculated. The risk of SA was estimated as an odds ratio (OR) with 95% confidence intervals (CI) where the odds for twins on SA to have a co-twin on SA was compared to the OR for SA in twins whose co-twin were not sickness absent. Intrapair correlations and probandwise concordance rates were calculated and standard biometrical genetic model-fitting methods were used to estimate the heritability of SA. The prevalence of SA was 8.8% (women 10.7%; men 6.5%). Intrapair similarity was higher among monozygotic than dizygotic twin pairs. The best-fitting model showed no sex differences in genetic effects or variance components contributing to SA. The heritability estimate was 36% (95% CI: 35–40%). Results suggest genetic contribution to the variation of SA and that environmental factors have an important role, for women and men. As SA seem to be influenced by genetic factors, future studies of associations between risk factors and SA should consider this potentially confounding effect.

AbstractStudies have shown that familial aggregation is of importance for abdominal symptoms including irritable bowel syndrome and there are a few reports of a moderate heritability for irritable bowel syndrome. Sex differences in prevalence and incidence of irritable bowel syndrome have been demonstrated however less is known about sex differences in heritability. The objective was to investigate whether there were sex differences in heritability of irritable bowel syndrome while accounting for different prevalences among women and men in different age groups. A sample of 45,750 Swedish twins, whereof 16,961 were complete twin pairs, participated in a telephone interview. The sample was divided into three age groups (40–54, 55–64 and 65 years and older) and the diagnosis of irritable bowel syndrome was operationally defined with a number of disorder specific symptoms. Standard biometrical model fitting analyses were conducted using raw ordinal data from same-sex and opposite-sex twins. The prevalence of irritable bowel syndrome was greater among women than men and more prevalent at younger ages (e.g., women 10.3%, men 6.3% at ages 40–54 years vs. women 6.1%, men 4% at ages over 65 years). The heritability of the disorder was approximately 25% in all age groups. We found no evidence for sex differences in heritability in any of the age groups, however, models allowing prevalences of irritable bowel syndrome to differ between sexes and age groups fitted best.

AbstractWork incapacity is a major public health challenge and an economic burden to both society and individuals. Understanding the underlying causes is becoming ever more relevant as many countries face an aging workforce. We examined stability and change in genetic and environmental factors influencing work incapacity from age 18 until retirement, and sex differences in these effects. The large population-based sample comprised information from 28,759 twins followed for up to 23 years combined with high-quality national registry data. We measured work incapacity as the total proportion of potential workdays lost due to sickness absence, rehabilitation and disability benefits. Structural equation modeling with twin data indicated moderate genetic influences on work incapacity throughout life in both men and women, with a high degree of genetic stability from young to old adulthood. Environmental influences were mainly age-specific. Our results indicate that largely the same genetic factors influence individual differences in work incapacity throughout young, middle and older adulthood, despite major differences in degree of work incapacity and probable underlying medical causes.