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AbstractSpecific environments and social relationships may alter the impact of genes. Previous studies have shown marriage to moderate heritability for depressive symptoms in females, suggesting that marriage provides protection or compensation against genetic risks. Similar mechanisms may be relevant for subjective wellbeing (SWB), which is considerably influenced by genes and almost universally associated with marital status. Questionnaire data on SWB from a population-based sample of 1250 monozygotic (MZ) and 981 dizygotic (DZ) male and female twin pairs (n= 4462) were analyzed using structural equation modeling by means of Mx to investigate genetic and environmental influences on SWB across marital status. Resemblance for SWB in MZ twins exceeded that of DZ twins, but the magnitude of this difference varied across marital status. Genetic factors explained 51% and 54% of the variance in SWB among unmarried males and females, and 41% and 39% in married or cohabitating respondents. Remaining variance was attributable to the nonshared environment. The genetic influences were partly different (rg= 0.64) across marital status in females, but overlapping in married and single males. Our findings show that marriage moderates the magnitude of genetic influences on SWB in both males and females, with a smaller estimate of genetic influences for those with a marital or equivalent partner. The genetic influences on SWB are thus clearly contingent on the environmental context.

Bidirectional pathways between twin relationship quality and friendship quality were investigated in a large longitudinal twin cohort. We examined negative and positive relationship features in 313 monozygotic (MZ) twins and 238 same-sex dizygotic (DZ) twins from ages 13 to 14 years, using latent structural modeling. Results showed stronger stability of the twin relationship quality compared to friendship quality. Positive features in the sibling relationship were associated with increased positive features in the relationship with the best friend a year later. In contrast, no significant association between negative sibling relationship features and change in negative friendship quality features was found. These findings speak to the important role of the sibling relationship in the development of good quality friendship relations in twins.

AbstractWhile snus has been the focus of increasing public health interest, twin studies have examined neither sources of individual variation for its use nor the sources of resemblance between snus and cigarette use. Twins from the Norwegian Institute of Public Health Panel were assessed by self-report questionnaire for the initiation of regular use and maximal quantity used for snus and cigarettes. Twin modeling was performed using OpenMx on data from 2767 twins including 856 complete pairs. Fitting univariate twin models produced similar results for cigarette initiation and quantity with estimates of additive genetic, shared environmental and unique environmental effects of approximately 77%, 0% and 23%, respectively. Estimates of snus initiation and quantity were, respectively, approximately 53%, 26% and 21%. Joint analyses suggested that the genetic, shared environmental and unique environmental correlations between cigarette and snus initiation and quantity were +.82, 0 and +.42, respectively. However, these results could not be statistically distinguished from a model which postulated that resemblance between cigarette initiation and quantity resulted from genetic and unique environmental correlations of +.47 and +.43. Compared with cigarette initiation and quantity of use in Norwegian twins, the role of genes was less prominent and shared environment more prominent for initiation and quantity of use of snus. Joint analyses of both tobacco phenotypes suggested, but did not confirm definitively, that genetic risk factors for cigarette and snus use were similar but not identical, while shared environmental factors existed that were specific to snus use.

In many Western countries, women now reach educational levels comparable to men, although their income remains considerably lower. For the past decades, it has become increasingly clear that these measures of socio-economic status are influenced by genetic as well as environmental factors. Less is known about the relationship between education and income, and sex differences. The aim of this study was to explore genetic and environmental factors influencing education and income in a large cohort of young Norwegian twins, with special emphasis on gender differences. National register data on educational level and income were obtained for 7,710 twins (aged 29–41 years). Bivariate Cholesky models were applied to estimate qualitative and quantitative gender differences in genetic and environmental influences, the relative contribution of genetic and environmental factors to the correlation between education and income, and genetic correlations within and between sexes and phenotypes. The phenotypic correlation between educational level and income was 0.34 (0.32–0.39) for men and 0.45 (0.43–0.48) for women. An ACE model with both qualitative and quantitative sex differences fitted the data best. The genetic correlation between men and women (rg) was 0.66 (0.22–1.00) for educational attainment and 0.38 (0.01–0.75) for income, and between the two phenotypes 0.31 (0.08–0.52) for men and 0.72 (0.64–0.85) for women. Our results imply that, in relatively egalitarian societies with state-supported access to higher education and political awareness of gender equality, genetic factors may play an important role in explaining sex differences in the relationship between education and income.

Background The previous decades have shown increased symptoms of depression and anxiety among adolescents. To promote mental health and reduce mental illness, the government of Norway has, as in other countries, pledged that all schools must incorporate life-skills education. We report results from an evaluation of MindPower, a modification of the Coping With Depression (CWD) course, delivered universally in the classroom to secondary high school students, aged 15–16 years, in one county in Norway. The aim of the study was to evaluate the effect of MindPower on symptoms of depression and anxiety. Methods We utilized a two-groups` delayed intervention design where 110 first year high school classes were randomized into one of two intervention groups (IG1 and IG2). IG1 participated in MindPower while IG2 served as a control group for four months until the intervention started also in this group. IG1 and IG2 responded to questionnaires before and after the eight weeks course, at the start of the first and the second booster session, and at the five months follow up. Questionnaires, including online versions of the Hopkins Symptom Checklist (SCL-8) and the Reynolds Adolescent Depression Scale (RADS-2:SF), were administered to 1673 out of a total of 2384 students. SCL-levels were also compared with those from a large population study (UngData). Results According to mixed model analyses, SCL-8 and RADS-2:SF showed significant baseline differences between IG1 and IG2. In IG1 and IG2, both SCL-8 and RADS-2:SF showed a small but significant increase in mean scores throughout the study period, with markedly lower mean scores among boys. The SCL-levels were first lower for both girls and boys and then after the completion of MindPower the SCL-levels, equal to the SCL-levels in UngData. Conclusions No effects of the intervention were found. This large universal school-based trial suffered from considerable drop-out of participants. Experiences from implementation and evaluation of universal mental health promotion and preventive school interventions are thoroughly discussed, including, preparation, resources, support, time, realistic expectations, teacher selection and training, implementation, research designs and more. Several empirically based, practical advices are presented. Clinical Trial registration 27/08/2018. Registration number NCT03647826.

Self-report scales for symptoms of anxiety and depression are frequently used for screening and research purposes. A moderate phenotypic association between disorders measured by diagnostic interviews and symptoms of anxiety and depression measured by self-report scales has been shown, but little is known about the overlap in these phenotypes' genetic and environmental variance. In the present study, we used twin modeling to identify common genetic and environmental liabilities underlying the phenotypic association between the self-report Symptom Checklist-5 (SCL-5) and lifetime internalizing disorders derived from the Composite International Diagnostic Interview (CIDI). The sample consisted of 7,992 young adult twins from the Norwegian Institute of Public Health Twin Panel (NIPHT), who all responded to a questionnaire. A subset of 2,793 individuals later underwent structured interviews. The best fitting model showed a strong genetic correlation of 0.82 (95% confidence interval; 0.61–1.0) between current self-report symptoms of anxiety and depression, and lifetime internalizing disorders, which suggests an almost complete overlap in genetic liability. The correlation between environmental factors was much lower: 0.16 (0.00–0.34, 95% CI). This implies that brief self-report scales capture genetic variance that is highly overlapping with the genetic variance common to internalizing disorder diagnoses. It thus follows that SCL-5 and similar instruments may be used as screening instruments for genetic risk factors that influence liability to internalizing disorders. In addition, existing data on self-report symptoms of anxiety and depression can be used with increased confidence to specify models including effects from genes coding for internalizing disorders.

BACKGROUND: The previous decades have shown increased symptoms of depression and anxiety among adolescents. To promote mental health and reduce mental illness, the government of Norway has, as in other countries, pledged that all schools must incorporate life-skills education. We report results from an evaluation of MindPower, a modification of the Coping With Depression (CWD) course, delivered universally in the classroom to secondary high school students, aged 15–16 years, in one county in Norway. The aim of the study was to evaluate the effect of MindPower on symptoms of depression and anxiety. METHODS: We utilized a two-groups` delayed intervention design where 110 first year high school classes were randomized into one of two intervention groups (IG1 and IG2). IG1 participated in MindPower while IG2 served as a control group for four months until the intervention started also in this group. IG1 and IG2 responded to questionnaires before and after the eight weeks course, at the start of the first and the second booster session, and at the five months follow up. Questionnaires, including online versions of the Hopkins Symptom Checklist (SCL-8) and the Reynolds Adolescent Depression Scale (RADS-2:SF), were administered to 1673 out of a total of 2384 students. SCL-levels were also compared with those from a large population study (UngData). RESULTS: According to mixed model analyses, SCL-8 and RADS-2:SF showed significant baseline differences between IG1 and IG2. In IG1 and IG2, both SCL-8 and RADS-2:SF showed a small but significant increase in mean scores throughout the study period, with markedly lower mean scores among boys. The SCL-levels were first lower for both girls and boys and then after the completion of MindPower the SCL-levels, equal to the SCL-levels in UngData. CONCLUSIONS: No effects of the intervention were found. This large universal school-based trial suffered from considerable drop-out of participants. Experiences from implementation and evaluation of universal mental health promotion and ...

A foundational question in the social sciences concerns the interplay of underlying causes in the formation of people's political beliefs and prejudices. What role, if any, do genes, environmental influences, or personality dispositions play? Social dominance orientation (SDO), an influential index of people's general attitudes toward intergroup hierarchy, correlates robustly with political beliefs. SDO consists of the subdimensions SDO-dominance (SDO-D), which is the desire people have for some groups to be actively oppressed by others, and SDO-egalitarianism (SDO-E), a preference for intergroup inequality. Using a twin design (n = 1,987), we investigate whether the desire for intergroup dominance and inequality makes up a genetically grounded behavioral syndrome. Specifically, we investigate the heritability of SDO, in addition to whether it genetically correlates with support for political policies concerning the distribution of power and resources to different social groups. In addition to moderate heritability estimates for SDO-D and SDO-E (37% and 24%, respectively), we find that the genetic correlation between these subdimensions and political attitudes was overall high (mean genetic correlation 0.51), while the environmental correlation was very low (mean environmental correlation 0.08). This suggests that the relationship between political attitudes and SDO-D and SDO-E is grounded in common genetics, such that the desire for (versus opposition to) intergroup inequality and support for political attitudes that serve to enhance (versus attenuate) societal disparities form convergent strategies for navigating group-based dominance hierarchies.

A foundational question in the social sciences concerns the interplay of underlying causes in the formation of people's political beliefs and prejudices. What role, if any, do genes, environmental influences, or personality dispositions play? Social dominance orientation (SDO), an influential index of people's general attitudes toward intergroup hierarchy, correlates robustly with political beliefs. SDO consists of the subdimensions SDO-dominance (SDO-D), which is the desire people have for some groups to be actively oppressed by others, and SDO-egalitarianism (SDO-E), a preference for intergroup inequality. Using a twin design (n = 1,987), we investigate whether the desire for intergroup dominance and inequality makes up a genetically grounded behavioral syndrome. Specifically, we investigate the heritability of SDO, in addition to whether it genetically correlates with support for political policies concerning the distribution of power and resources to different social groups. In addition to moderate heritability estimates for SDO-D and SDO-E (37% and 24%, respectively), we find that the genetic correlation between these subdimensions and political attitudes was overall high (mean genetic correlation 0.51), while the environmental correlation was very low (mean environmental correlation 0.08). This suggests that the relationship between political attitudes and SDO-D and SDO-E is grounded in common genetics, such that the desire for (versus opposition to) intergroup inequality and support for political attitudes that serve to enhance (versus attenuate) societal disparities form convergent strategies for navigating group-based dominance hierarchies.

A foundational question in the social sciences concerns the interplay of underlying causes in the formation of people's political beliefs and prejudices. What role, if any, do genes, environmental influences, or personality dispositions play? Social dominance orientation (SDO), an influential index of people's general attitudes toward intergroup hierarchy, correlates robustly with political beliefs. SDO consists of the subdimensions SDO-dominance (SDO-D), which is the desire people have for some groups to be actively oppressed by others, and SDO-egalitarianism (SDO-E), a preference for intergroup inequality. Using a twin design (n = 1,987), we investigate whether the desire for intergroup dominance and inequality makes up a genetically grounded behavioral syndrome. Specifically, we investigate the heritability of SDO, in addition to whether it genetically correlates with support for political policies concerning the distribution of power and resources to different social groups. In addition to moderate heritability estimates for SDO-D and SDO-E (37% and 24%, respectively), we find that the genetic correlation between these subdimensions and political attitudes was overall high (mean genetic correlation 0.51), while the environmental correlation was very low (mean environmental correlation 0.08). This suggests that the relationship between political attitudes and SDO-D and SDO-E is grounded in common genetics, such that the desire for (versus opposition to) intergroup inequality and support for political attitudes that serve to enhance (versus attenuate) societal disparities form convergent strategies for navigating group-based dominance hierarchies.

Personality disorders (PDs) reduce global functioning, are associated with high levels of work disability, and are thus also likely to influence long-term sick leave (LTSL). Previous research has indicated significant genetic influence on both DSM-IV PDs and LTSL. To what degree genes contributing to PDs also influence LTSL has not been investigated. The aims of the current study were to investigate which PDs were significantly associated with LTSL, to what extent the genetic contributions to these PDs account for the heritability of LTSL, and to explore the hypothesis of a causal association between PDs and LTSL. The sample consisted of 2,771 young, adult Norwegian twins, born 1967–1979. PDs were assessed using the Structured Interview for DSM-IV Personality (SIDP-IV). The age range for the interview was 20–32. The data were subsequently linked to public records of LTSL (sick leave >16 days) up to 11 years later. The odds ratio for being in the highest LTSL category (>15% sick leave) when fulfilling the DSM-IV criteria for any PD diagnosis was 2.6 (1.8–3.8, 95% CI). Dimensional representations of schizotypal, paranoid, and borderline PD were independently and significantly associated with LTSL. The heritability of LTSL was 0.50. Genetic factors shared with the PDs accounted for 20% of this. The association between PDs and LTSL was due to shared genetic and not environmental influences, and was mainly explained by one common genetic factor. The hypothesis of a causal association was not supported, indicating that the association is explained by overlapping genetic liability between PDs and LTSL.

This study investigates the degree to which internalizing disorders (anxiety and mood disorders) are prospectively associated with sick leave granted for mental and somatic disorders, and the extent to which common genetic and environmental risk factors influence these relationships. Data include self-reported symptoms of psychological distress from 7,598 young adult twins and diagnostic interviews on a subsample of 2,766 adult twins, subsequently linked to registry data on sick leave. Regression analyses and multivariate twin models were used to investigate the relationship between internalizing disorders and sick leave. Internalizing disorders were associated with sick leave granted for both mental disorders and somatic disorders. The association between internalizing disorders and sick leave granted for mental disorders was influenced by genetic and non-shared environmental factors, while the association between internalizing disorders and sick leave granted for somatic disorders could be explained by common genetic factors alone. Monozygotic twins discordant for internalizing disorders differed significantly in rates of sick leave granted for mental but not somatic disorders. In conclusion, internalizing disorders in young adults predict sick leave granted for both mental and somatic disorders. Environmental risk factors for internalizing disorders seem to influence sick leave granted for mental disorders, but not sick leave granted for somatic disorders.

Although exclusion from the workforce due to long-term sick leave (LTSL) and disability pension (DP) is a major problem in many Western countries, the etiology of LTSL and DP is not well understood. These phenomena have a strong association as most patients receiving DP have first been on LTSL. However, only a few of those on LTSL end up with DP. The present study aimed to investigate the common and specific genetic and environmental risk factors for LTSL and DP. The present study utilizes a population-based sample of 7,710 young adult twins from the Norwegian Institute of Public Health Twin Panel, which has been linked to the Historical-Event Database (FD-Trygd; 1998–2008). Univariate and bivariate twin models were fitted to determine to what degree genetic and environmental factors contribute to variation in LTSL and DP. The estimated heritabilities of LTSL and DP were 0.49 and 0.66, respectively. There was no evidence for shared environmental or sex-specific factors. The phenotypic-, genetic-, and non-familial environmental correlations between the variables were 0.86, 0.82, and 0.94, respectively. Our results indicate that familial transmission of LTSL and DP is due to genetic and not environmental factors. The risk factors contributing to LTSL and DP were mainly shared, suggesting that what increases risk for LTSL also increases risk for DP. However, a non-negligible part of the genetic variance was not shared between the variables, which may contribute to explaining why some progress from LTSL to DP, whereas others return to work.

Until now, data have not been available to elucidate the genetic and environmental sources of comorbidity between all 10 DSM-IV personality disorders (PDs) and cocaine use. Our aim was to determine which PD traits are linked phenotypically and genetically to cocaine use. Cross-sectional data were obtained in a face-to-face interview between 1999 and 2004. Subjects were 1,419 twins (µage= 28.2 years, range = 19–36) from the Norwegian Institute of Public Health Twin Panel, with complete lifetime cocaine use and criteria for all 10 DSM-IV PDs. Stepwise multiple and Least Absolute Shrinkage and Selection Operator (LASSO) regressions were used to identify PDs related to cocaine use. Twin models were fitted to estimate genetic and environmental associations between the PD traits and cocaine use. In the multiple regression, antisocial (OR= 4.24, 95% CI [2.66, 6.86]) and borderline (OR= 2.19, 95% CI [1.35, 3.57]) PD traits were significant predictors of cocaine use. In the LASSO regression, antisocial, borderline, and histrionic were significant predictors of cocaine use. Antisocial and borderline PD traits each explained 72% and 25% of the total genetic risks in cocaine use, respectively. Genetic risks in histrionic PD were not significantly related to cocaine use. Importantly, after removing criteria referencing substance use, antisocial PD explained 65% of the total genetic variance in cocaine use, whereas borderline explained only 4%. Among PD traits, antisocial is the strongest correlate of cocaine use, for which the association is driven largely by common genetic risks.