Familial clustering in burnout: a twin-family study

BACKGROUND: Research on risk factors for burnout has mainly focused on circumstances at work and on personal characteristics. The aim of this study was to investigate whether burnout clusters within families and, if so, whether this is due to genetic influences or to environmental factors shared by family members. Finally, we tried to identify specific risk factors for burnout. METHOD: In 2707 twins, 736 of their siblings and 575 of their spouses from a population-based twin-family sample, burnout was measured using a self-report questionnaire. Correlations in burnout scores were obtained for monozygotic and dizygotic twin pairs and sibling pairs conditional on the pairs' sex. Correlations for twins and their spouses were derived conditional on the length of the relationship. RESULTS: In the final model, correlations of the monozygotic and dizygotic twin pairs and sibling pairs were significantly different from zero, but not significantly different from each other. The correlation was estimated at 0.22. The correlation between spouses was also significant. This was mainly due to the group with a relationship longer than 5 years in which the correlation was 0.24. Burnout scores were higher in subjects whose parents had a high level of education. CONCLUSIONS: There is familial clustering for burnout due to environmental factors shared by family members, explaining 22 % of the variance. Genetic factors do not seem to be of importance. The significant correlation between spouses supports the conclusion that common environment plays a role in burnout. A high parental education is one of the familial risk factor

Twin and genetic effects on life events

Twin studies that examine the effect of specific environmental risk factors on psychiatric disorders assume that there are no differences in prevalences of these risk factors between twins and singletons. Violation of this assumption signifies that the results from twin studies might not generalize to singletons. Another assumption, not only underlying twin studies but also epidemiological research, is that life-events are not influenced by familial factors. We tested differences in prevalences of experienced life events in a Dutch sample of 1086 monozygotic (MZ) twins, 2090 dizygotic (DZ) twins and 1307 of their siblings. Self reported data on life events (illness of self, illness of a significant other, spouse/romantic relationship, divorce/break-up of a relationship, death of a significant other, traffic accident, robbery, violent assault, sexual assault) were available from a survey-study. We further investigated whether familial resemblance was present for the exposure to these life events and, if so, whether this resemblance was due to genetic or common environmental factors. No differences were found in the prevalences of life events between MZ twins, DZ twins and their siblings. There was evidence for familial aggregation of all life events, except for traffic accidents in women. Results indicated genetic control on the presence of a spouse or involvement in a relationship. Familial resemblance of illness and death of a significant other was mainly due to common environment. For the other life events, it was not possible to distinguish between genetic and common environmental effect

Twin studies on obsessive-compulsive disorder: a review

Genetic factors have historically been thought of as important in the development of obsessive-compulsive disorder (OCD). For the estimation of the relative importance of genetic and environmental factors, twin studies are an obvious approach. Twin studies of OCD have a long history, starting in 1929. In this review, over 70 years of twin research of OCD is presented, using four different approaches that represent the steps in the twin research of OCD from past to present. These steps include (1) case-studies of twins with OCD from the old literature; (2) twin studies of OCD using Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria; (3) twin studies of OCD using a dimensional approach, comparing resemblances in monozygotic and dizygotic twins; and (4) twin studies of OCD using a dimensional approach, analyzing the data with Structural Equation Modeling. It is concluded that only the studies using the last method have convincingly shown that, in children, obsessive-compulsive (OC) symptoms are heritable, with genetic influences in the range of 45% to 65%. In adults, studies are suggestive for a genetic influence on OC symptoms, ranging from 27% to 47%, but a large twin study using a biometrical approach with continuous data is still needed to provide conclusive evidence. Strategies for future twin studies of OCD are discusse

The co-morbidity of anxiety and depression in the perspective of genetic epidemiology. A review of twin and family studies

BACKGROUND: Co-morbidity within anxiety disorders, and between anxiety disorders and depression, is common. According to the theory of Gray and McNaughton, this co-morbidity is caused by recursive interconnections linking the brain regions involved in fear, anxiety and panic and by heritable personality traits such as neuroticism. In other words, co-morbidity can be explained by one disorder being an epiphenomenon of the other and by a partly shared genetic etiology. The aim of this paper is to evaluate the theory of Gray and McNaughton using the results of genetic epidemiological studies. METHOD: Twenty-three twin studies and 12 family studies on co-morbidity are reviewed. To compare the outcomes systematically, genetic and environmental correlations between disorders are calculated for the twin studies and the results from the family studies are summarized according to the method of Klein and Riso. RESULTS: Twin studies show that co-morbidity within anxiety disorders and between anxiety disorders and depression is explained by a shared genetic vulnerability for both disorders. Some family studies support this conclusion, but others suggest that co-morbidity is due to one disorder being an epiphenomenon of the other. CONCLUSIONS: Discrepancies between the twin and family studies seem partly due to differences in used methodology. The theory of Gray and McNaughton that neuroticism is a shared risk factor for anxiety and depression is supported. Further research should reveal the role of recursive interconnections linking brain regions. A model is proposed to simultaneously investigate the influence of neuroticism and recursive interconnections on co-morbidit

Cognitive and Experienced Flexibility in Patients With Anorexia Nervosa and Obsessive Compulsive Disorder

Objective: Anorexia nervosa (AN) and obsessive-compulsive disorder (OCD) share a neuropsychological profile characterized by cognitive inflexibility as evident in set-shifting problems, and by strong detail focus. Clinically, both patient groups display a strong rigidity which may be explained by these neurocognitive difficulties. Cognitive inflexibility may hinder treatment uptake and help explain suboptimal treatment outcomes in both AN and OCD. This is the first study to compare clinical AN and OCD groups and to examine similarities and differences in cognitive flexibility. Specifically, this study aims to investigate neuropsychological outcomes and self-reported difficulties in both clinical groups and a control group, and explore associations between the different flexibility outcomes and illness. Method: Two hundred participants (61 AN, 72 OCD and 67 HC) performed neuropsychological tasks on set-shifting abilities (Trail Making Task, Stroop color-word interference, Intradimensional-Extradimensional shift task), detail focus (Group Embedded Figures Test) and self-reported set-shifting abilities and attention to detail (DFlex). Results: Similarities between patient groups were found in terms of reduced set-shifting ability on the Trail Making Task and detail focus. Moreover, both patient groups self-reported more set-shifting problems but a less strong detail focus than HC, which in turn were not related to neuropsychological task outcomes in either of the groups. In both patient groups longer illness duration was associated to longer reaction times in the switching tasks and for both groups symptom severity was associated to higher experienced inflexibility and attention to detail. Conclusion: Cognitive inflexibility processes are largely similar in patients with AN and OCD. Both patient groups report inflexibility, yet this is unrelated to neuropsychological outcomes. Illness duration seems to contribute to poorer set-shifting and higher illness severity is linked to more experienced inflexibility. Findings highlight the need for entangling different domains of cognitive flexibility and detail focus and examining self-report measures for a cohesive understanding of clinically relevant flexibility weaknesses in AN and OCD

Synaptic processes and immune-related pathways implicated in Tourette syndrome.

Tourette syndrome (TS) is a neuropsychiatric disorder of complex genetic architecture involving multiple interacting genes. Here, we sought to elucidate the pathways that underlie the neurobiology of the disorder through genome-wide analysis. We analyzed genome-wide genotypic data of 3581 individuals with TS and 7682 ancestry-matched controls and investigated associations of TS with sets of genes that are expressed in particular cell types and operate in specific neuronal and glial functions. We employed a self-contained, set-based association method (SBA) as well as a competitive gene set method (MAGMA) using individual-level genotype data to perform a comprehensive investigation of the biological background of TS. Our SBA analysis identified three significant gene sets after Bonferroni correction, implicating ligand-gated ion channel signaling, lymphocytic, and cell adhesion and transsynaptic signaling processes. MAGMA analysis further supported the involvement of the cell adhesion and trans-synaptic signaling gene set. The lymphocytic gene set was driven by variants in FLT3, raising an intriguing hypothesis for the involvement of a neuroinflammatory element in TS pathogenesis. The indications of involvement of ligand-gated ion channel signaling reinforce the role of GABA in TS, while the association of cell adhesion and trans-synaptic signaling gene set provides additional support for the role of adhesion molecules in neuropsychiatric disorders. This study reinforces previous findings but also provides new insights into the neurobiology of TS