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

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

Erfelijkheid en omgevingsinvloeden bij psychiatrische stoornissen

BACKGROUND: In recent years quantitative genetic research has addressed all the major psychiatric disorders. In order to interpret the results of this type of research one needs to be aware of its potential and its limitations. AIM: To discuss the basic concepts and the main results of quantitative genetic research and to consider how this can help us to better understand the aetiology of psychiatric disorders. METHODS: Using Medline (1990-February 2006) we reviewed the literature on the subject of quantitative genetic and psychiatric disorders. In addition we studied the standard books on the subject. RESULTS: A fairly large number of psychiatric disorders, namely about 30 to 85%, can be inherited. In addition, the non-shared environment has a considerable influence on the phenotype. The influence of the shared environment seems to have only a limited influence or it is totally absent. The results of quantitative genetic research are specific to a particular time or environment and therefore may not be applicable to other populations. There may be a correlation or interaction between genetic factors and the environment while the phenotype is being formed. However, because of the analytical methods used, this is only partly visible in the results. CONCLUSION: Quantitative genetic research has made an impressive contribution to our knowledge about the heritability of psychiatric disorders. By definition quantitative genetic research always provides information about environmental influences

Family based association analyses between the Serotonin Transporter Gene Polymorphism (5-HTTLPR) and Neuroticism, Anxiety and Depression

We studied the association between the short/long promotor-based length polymorphism of the serotonin transporter gene (5-HTTLPR) and neuroticism, anxiety and depression. Subjects included twins, their siblings and parents from the Netherlands Twin Register (559 parents and 1,245 offspring). Subjects had participated between one and five times in a survey study measuring neuroticism, anxiety and depression. Offspring of these families were also approached to participate in a psychiatric interview diagnosing DSM-IV major depression. Within-family and total association between 5-HTTLPR and these traits were tested. Only three of the 36 tests showed a significant effect of 5-HTTLPR (P < 0.05). These effects were in opposite directions, i.e. both negative and positive regression coefficients were found for the s allele. No additive effect of the s allele was found for DSM-IV depression. Our results strongly suggest that there is no straightforward association between 5-HTTLPR and neuroticism, anxiety and depression

Sociodemographic and clinical characteristics in child and youth mental health; comparison of routine outcome measurements of an Australian and Dutch outpatient cohort

Routine outcome measurement (ROM) data offer unique opportunities to study treatment outcomes in clinical practice, and can help to assess the real-world impact of mental health services for children and adolescents (youth). This is illustrated by studies using naturalistic data from specialist child and adolescent mental healthcare services (CAMHS), showing the proportion of patients with reliable improvement, recovery or deterioration (Burgess et al., 2015; Wolpert et al., 2016), and revealing specific subgroups of patients with greater risk of poor outcome (Garralda et al., 2000; Lundh et al., 2013; Murphy et al., 2015; Edbrooke-Childs et al., 2017). Naturalistic data are therefore undeniably necessary in addition to data derived from randomised clinical trials, which often have limited generalisability due to strict selection criteria (Rothwell, 2005; Van Noorden et al., 2014).New methods for child psychiatric diagnosis and treatment outcome evaluatio