Introduction English is the lingua franca of science. How well doctors understand English is therefore crucial for their understanding of scientific articles. However, only 5% of the world’s population have English as their first language.Methods Objectives: To compare doctors’ comprehension of a scientific article when read in their first language (Norwegian) versus their second language (English). Our hypothesis was that doctors reading the article in Norwegian would comprehend the content better than those reading it in English.Design: Parallel group randomised controlled trial. We randomised doctors to read the same clinical review article in either Norwegian or English, before completing a questionnaire about the content of the article.Setting: Conference in primary care medicine in Norway, 2018.Participants: 130 native Norwegian-speaking doctors, 71 women and 59 men. One participant withdrew before responding to the questionnaire and was excluded from the analyses.Interventions: Participants were randomly assigned to read a review article in either Norwegian (n=64) or English (n=66). Reading time was limited to 7 min followed by 7 min to answer a questionnaire.Main outcome measures: Total score on questions related to the article content (potential range −9 to 20).Results Doctors who read the article in Norwegian had a mean total score of 10.40 (SD 3.96) compared with 9.08 (SD 3.47) among doctors who read the article in English, giving a mean difference of 1.32 (95% CI 0.03 to 2.62; p=0.046). Age was independently associated with total score, with decreased comprehension with increasing age.Conclusion The difference in comprehension between the group who read in Norwegian and the group who read in English was statistically significant but modest, suggesting that the language gap in academia is possible to overcome.

Work 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.

Background:Sickness absence (SA) among pregnant women is high. The aim of this study was to examine whether factors known to predict SA in general also predict SA during pregnancy by estimating the association between prior mental distress and musculoskeletal pain and SA during pregnancy, and to assess the influence of familial (genetic and shared environmental) factors. In this prospective cohort study, data from 2076 female twins born 1967-79 who participated in a questionnaire study in 1998 were linked to register data on SA and childbirth during the years 1998-2008. Baseline measures included mental distress (symptoms of anxiety and depression; SCL-5) and musculoskeletal pain (lumbar spine, neck/shoulder and/or persisting muscular pain). SA was measured as a ratio of days on SA divided by potential working days. Negative binomial regression was performed for individual and within-pair effects. Musculoskeletal pain, but not mental distress, was prospectively associated with overall SA during pregnancy in the adjusted individual-level analyses. With each standard deviation increase in musculoskeletal pain, SA granted for any disorder increased with 12% (IRR 1.12, 95% CI = 1.07-1.17) and SA granted for pregnancy related disorders increased with 9% (IRR 1.09, 95% CI = 1.02-1.17). Within-pair estimates were similar, suggesting little or no familial confounding. Women with previous musculoskeletal pain are at increased risk of SA during pregnancy, whereas no increased risk in women with previous symptoms of mental distress could be demonstrated. SA during pregnancy seems partly to be associated with different factors than SA in general.

Background Maternal alcohol use during pregnancy has repeatedly been associated with development of attention-deficit hyperactivity disorder (ADHD) in the offspring. It is, however not known whether this reflects a direct casual intra-uterine effect or a non-causal relationship due to confounding. We used three different approaches to control for measured and unmeasured confounding: statistical adjustment for covariates, negative control comparison against maternal pre-pregnancy alcohol use, and comparison among differentially exposed siblings. Methods The sample comprised 114 247 children (34 283 siblings) from 94 907 mothers, recruited to the Norwegian Mother and Child Birth Cohort Study between 1999 and 2008. Self-reported measurements of alcohol use were obtained in week 30 during the pregnancy. Mothers rated offspring ADHD symptoms at 5 years on two measures. Clinical ADHD diagnoses were obtained from the Norwegian Patient Registry. Results We found an overall positive association between maternal alcohol use during pregnancy and offspring ADHD symptoms, which was only marginally attenuated after inclusion of measured covariates. Both the negative control and the sibling comparison analysis further attenuated the estimated association, but it remained greater than zero [β = 0.017, 95% confidence interval (CI) = 0.005-0.030). No association was found between maternal alcohol use during pregnancy and offspring ADHD diagnosis. Conclusions For offspring ADHD symptoms we found a weak, but possibly causal association with maternal alcohol use during pregnancy, but no such effect was observed for clinical ADHD diagnosis.

The Norwegian Twin Registry (NTR) is a large population based twin cohort for research purposes. At present, the registry has 14 692 complete twin pairs with information on zygosity and to varying degree information on somatic and mental health, lifestyle and demographics. The registry covers birth years 1895-1960 and 1967- 1991. NTR was established in 2009, at the Norwegian Institute of Public Health, as a merger of three major twin panels, the oldest originating in the 1960s. Since then Norwegian twin research has been a notable contributor to twin research internationally. Norwegian twin researchers have published over 250 papers based on Norwegian twin data, spanning a broad range of somatic and mental health phenotypes. In twin studies of heritability a data structure with both variance within and between pairs is required. Therefore a large sample is necessary, especially when studying rare diseases and conditions, and it is of vital importance to expand the registry. NTR is actively recruiting new twins, both young and older, but declining response rates are a challenge. The value of NTR is greatly enhanced through the linkage possibilities offered by Norway’s many nationwide registries (medical, demographic, and socio-economic). Access to data is permitted by the NTR steering group and will in most instances need permission from the Regional Ethics Committee.

Linking national registries with twin data represents an opportunity to produce epidemiological research of high quality. National registries contain information on a broad array of variables, some of which cannot be measured reliably in regular health surveys. By taking kinship into consideration, twin studies have the benefit of being able to identify confounding stemming from genetic or shared environmental sources. In this paper, we use examples from our own interview and questionnaire-based twin studies from the Norwegian Twin Registry (NTR) on mental disorders, alcohol use and socioeconomic status linked to registry data on medical benefits to demonstrate the value. In the first example, we examined to what extent genetic and environmental factors contributed to sick leave and disability pension and the association between these two types of benefits. In the second example, we explored the genetic and environmental relationship between personality disorders and sick leave. In the third example, a co-twin control design was applied to explore whether there is a true protective relationship between moderate alcohol consumption and health. The fourth example shows to what degree anxiety and depression are associated with later sick leave granted for not only mental disorders, but also somatic disorders, adjusted for confounding by genetic and shared environmental factors. In the fifth example, we address the socioeconomic gradient in sick leave, adjusting for non-observed confounders associated with the family in a co-twin control design. Our examples illustrate some of the potentials obtainable by linking national registries with twin data. The efforts that have been made to create the NTR in Norway and the International Network of Twin Studies (INTR) internationally make these types of linkage studies easier to conduct and available to more researchers. As there are still many areas to explore, we encourage epidemiological researchers to make use of this possibility.

BACKGROUND:Mental disorders strongly influence work capability in young adults, but it is not clear which disorders that are most strongly associated with sick leave, and which diagnoses that are stated on the sick leave certificates. Better knowledge of the impairments associated with different mental disorders is needed for optimal planning of interventions and prioritization of health services. In the current study, we investigate the prospective associations between eight mood, anxiety, and alcohol use disorders, and later sick leave granted for mental, somatic, or any disorder.METHODS:Lifetime mental disorders were assessed by structured diagnostic interviews in 2,178 young adults followed for eight years with registry data on sick leave. Relative risk ratios were estimated for the associations between each mental disorder and the different forms of sick leave.RESULTS:All included diagnoses were associated with later sick leave. In adjusted analyses, major depressive disorder and generalized anxiety disorder were the strongest predictors of sick leave granted for mental disorders, whereas social anxiety disorder and specific phobia were the strongest predictors of sick leave granted for somatic disorders. Specific phobia and major depressive disorder had the highest attributable fractions for all-cause sick leave.CONCLUSIONS:Mood and anxiety disorders constituted independent risk factors for all cause sick leave, whereas alcohol use disorders seemed to be of less importance in young adulthood. Disorders characterised by distress were most strongly associated with sick leave granted for mental disorders, whereas disorders characterised by fear primarily predicted sick leave granted for somatic conditions. A large part of all sick leave is related to specific phobia, due to the high prevalence of this disorder. The impairment associated with this common disorder may be under-acknowledged, and it could decrease work capacity among individuals with somatic disorders. This disorder has good treatment response and may be overlooked as a target for interventions aimed at prevention of sick leave.

Background: Results from observational studies suggest that people who drink little or no alcohol are less healthy than medium drinkers. This has been demonstrated for many different measures of health, including sick leave. However, whether these associations are causal or due to confounding remains to be clarified. The aim of this study was to use a discordant twin design to determine whether the increased level of sick leave associated with a low level of alcohol consumption, as compared to those with a medium level of consumption, reflects a causal mechanism or is due to genetic or environmental confounding.Methods: Six thousand seven hundred thirty-four young adult twins from the Norwegian Institute of Public Health's twin panel were in 1998 assessed for frequency of alcohol use and binge drinking. Data were linked to the Norwegian National Insurance Administration's recordings of sick leave over a 10 year period. The associations between alcohol consumption and sick leave were first estimated in the total study population, and then within di-and monozygotic twin pairs discordant for alcohol use.Results: Compared to medium consumption, both low and high alcohol consumption was associated with increased risk of sick leave. When low level drinkers were compared to medium level drinkers in a discordant twin design, the results were consistent with the association being due to genetic confounding rather than a causal effect.Conclusions: The increased level of sick leave observed with low level drinkers seems to be mainly explained by confounding from genetic factors. In all observational studies of the relationship between alcohol consumption and health, one should be aware that important genetic confounders are likely to influence the results.

Social welfare support runs in families. Recent studies using Nordic registry data have found individualdifferences in genetic factors to be of substantial importance for medical benefits. However, to date there hasbeen no genetically informative studies on receiving social welfare support. To prevent young adults to notdrop out of the work life and become recipients of social welfare support, it is of substantial interest toclarify to what extent the familiarity of social welfare support is due to genetic or social differences betweenfamilies. We used data from the Historical-Event Database on 7,698 Norwegian twins born 1967-1979 toestimate the relative contribution of genetic factors, the effective familial environment (i.e. the “sharedenvironment”), and individual-specific environmental factors. We found that the two forms of familial risk,genetic and shared environmental, explained 39% and 45%, respectively, of the risk for receiving socialwelfare support among young Norwegian twins. Only 17% of the variance in risk factors could be explainedby individual-specific risk factors. It appears that risk for receiving social welfare support can to a greatextent be explained by environmental differences between families. Therefore prevention strategies targetingsocial inequalities between families would indeed be effective. Furthermore, genetic risk factors are alsoimportant in explaining risk for receiving social welfare support. These effects could be mediated throughheritable traits related to substance abuse, psychiatric disorders, and personality. Individual-specific risk factorswere of very little importance. Hence, with regard to receiving social welfare support, family matters.

Objective: To explore and quantify the relative strengths of the genetic contribution vs the contribution of modifiable environmental factors to severe osteoarthritis (OA) having progressed to total joint arthroplasty.Design: Incident data from the Norwegian Arthroplasty Registry were linked with the Norwegian Twin Registry on the National ID-number in 2014 in a population-based prospective cohort study of same-sex twins born 1915-60 (53.4% females). Education level and height/weight were self-reported and Body Mass Index (BMI) calculated. The total follow-up time was 27 years for hip arthroplasty (1987-2014, 424,914 person-years) and 20 years for knee arthroplasty (1994-2014, 306,207 person-years). We estimated concordances and the genetic contribution to arthroplasty due to OA in separate analyses for the hip and knee joint.Results: The population comprised N = 9058 twin pairs (N = 3803 monozygotic (MZ), N = 5226 dizygotic (DZ)). In total, 73% (95% confidence intervals (CI) = 66-78%) and 45% (95% CI = 30-58%) of the respective variation in hip and knee arthroplasty could be explained by genetic factors. Zygosity (as a proxy for genetic factors) was associated with hip arthroplasty concordance over time when adjusted for sex, age, education and BMI (HR = 2.98, 95% CI = 1.90-4.67 for MZ compared to DZ twins). Knee arthroplasty was to a greater extent dependent on BMI when adjusted for zygosity and the other covariates (HR = 1.15, 95% CI = 1.02-1.29).Conclusion: Hip arthroplasty was strongly influenced by genetic factors whereas knee arthroplasty to a greater extent depended on a high BMI. The study may imply there is a greater potential for preventing progression of knee OA to arthroplasty in comparison with hip OA. (C) 2016 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.

Monozygotic (MZ) twinning is considered to be a random event whereas spontaneous dizygotic (DZ)twinning is influenced by several factors. Thus, secular changes in twinning rates are usually explained bychanges in DZ twinning alone. Maternal body mass index (BMI) before pregnancy and maternal height arebelieved to be significant drivers of twinning. Our aim in this study was to explore to what degree maternalbody composition influences twinning. Data on births and maternal height and BMI from the Medical BirthRegistry Norway (MBRN) was analyzed applying multivariate logistic regression analysis. The resultsshowed that increasing maternal BMI and height has a positive association with twinning. There is anincreased risk of DZ twinning for a maternal BMI > 25, OR 1.31-1.43 and for maternal height ≥ 173 cm,OR 1.28. In explaining secula

Background and aims: Sickness absence (SA) and disability pension (DP) are increasingly recognized asmajor public problems. Musculoskeletal disorders are among the most common diagnoses set by physiciansgranting SA and DP. Results from recent twin studies have established that SA and DP are influencednot only by environmental and social factors, but also moderately to substantially by genes. The aim of thecurrent study was to examine to what degree musculoskeletal complaints in young adults predict SA andDP, including SA granted for other diagnoses. As the participants were twins, we were able to performwithin pair analyses, to see if the associations between musculoskeletal pain and later DP or SA were confoundedby unmeasured genetic and shared environmental factors.Materials and methods: The Norwegian twin registry includes a questionnaire conducted in 1998. Fromthis, we included three measures of recurrent pain (lower back, neck/shoulders and muscular) as well assymptoms of anxiety and depression (measured by the Symptom Checklist-5 (SCL-5)). The questionnairehas been linked to highly reliable official registries on SA and DP, as well as a range of sociodemographicvariables, for a ten-year follow up period. We applied logistic (DP as dependent variable) and binomialregression (SA as dependent variable) analyses to explore the relationship between musculoskeletal painand DP and SA. In the final models, we adjusted for sociodemographic factors and symptoms of anxietyand depression. Differences between twins in a pair were explored by applying fixed effect models. Allanalyses were conducted using STATA version 13.1.Results: The final sample of 7,626 twins included 3,055 complete pairs (488 monozygotic (MZ) male, 349dizygotic (DZ) male, 747 MZ female, 589 DZ female, and 882 opposite sex twin pairs) and 1,516 singletons.By the end of follow up, 181 subjects (44 men and 137 women) received DP, and 63.7% of the sample(47.4% of males and 76.0% of females) had at least one period of SA extending 16 days. Pain at any sitewas significantly associated with DP in both sexes. Any increase in the number of pain sites reported wasassociated with about a 60% increased risk for receiving DP (OR 1.6, 95% CI 1.4-1.9), and the strength ofthe association was only marginally reduced when adjusted for symptoms of mental disorders (1.4, 1.2-1.7). In the within pair analyses the effect was no longer significant, indicating possible confounding fromgenetic and shared environmental effects. As for all cause SA, musculoskeletal pain predicted SA independentlyof all measured confounders, and the results remained significant in the within pair analyses (IncidenceRate Ratio (IRR) 1.12, 95% CI 1.03-1.23).Conclusion: In young adults, musculoskeletal pain strongly predicted SA and DP for a 10 year follow-upperiod. Musculoskeletal pain was associated with higher levels of all cause SA, even within discordant MZtwin pairs. Our results indicate that interventions to prevent musculoskeletal pain in young adults canreduce levels of SA and DP.

Background Low socioeconomic status (SES), indicated by low income and education, has consistently been found to be a strong predictor of sick leave. Several possible pathways from SES to sick leave have been described in previous literature, but there are also evidence indicating that the association can be confounded by common underlying factors. This study utilizes a population-based sample of employed young adult twins to estimate (i) the degree to which education and income are prospectively related to sick leave granted for mental, somatic, and any disorder, and (ii) whether these associations are confounded by familial factors. Methods Registry data on educational attainment and income at age 30 and subsequent sick leave were available for 6,103 employed young adult twins, among which there were 2,024 complete twin pairs. The average follow-up time was 6.57 years. Individual-level associations and fixed effects within twin pairs were estimated. Results Low education and income were associated with sick leave granted for both mental and somatic disorders, and with sick leave granted for any disorder. Associations were attenuated within dizygotic twin pairs and reduced to non-significance within monozygotic twin pairs, suggesting influence of familial factors on the associations between SES and sick leave. Conclusions Low SES is associated with a higher level of sick leave granted for both mental and somatic disorders among young adults, but these associations are confounded by factors that are common to co-twins. Education and income are therefore not likely to strongly affect sick leave in young adulthood.

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 (r(g)) 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 While cluster A personality disorders (PDs) have been shown to be moderately heritable, we know little about the temporal stability of these genetic risk factors. Method Paranoid PD (PPD) and schizotypal PD (STPD) were assessed using the Structured Interview for DSM-IV Personality in 2793 young adult twins from the Norwegian Institute of Public Health Twin Panel at wave 1 and 2282 twins on average 10 years later at wave 2. Using the program Mx, we fitted a longitudinal latent factor model using the number of endorsed criteria for PPD and STPD. Results The stability over time of the criteria counts for PPD and STPD, estimated as polychoric correlations, were +0.34 and +0.40, respectively. The best-fit longitudinal model included only additive genetic and individual-specific environmental factors with parameter estimates constrained to equality across the two waves. The cross-wave genetic and individual-specific environmental correlations for a latent cluster A factor were estimated to equal +1.00 and +0.13, respectively. The cross-time correlations for genetic and environmental effects specific to the individual PDs were estimated at +1.00 and +0.16–0.20, respectively. We found that 68% and 71% of the temporal stability of PPD and STPD derived, respectively, from the effect of genetic factors. Conclusion Shared genetic risk factors for two of the cluster A PDs are highly stable in adults over a 10-year period while environmental risk factors are relatively transient. Over two-thirds of the long-term stability of the common cluster A PD liability can be attributed to genetic influences.