Shared Environmental Effects Research Articles

Heritability of hoarding symptoms across adolescence and young adulthood: A longitudinal twin study.

BackgroundTwin studies of hoarding symptoms indicate low to moderate heritability during adolescence and considerably higher heritability in older samples, suggesting dynamic developmental etiological effects. The aim of the current study was to estimate the relative contribution of additive genetic and environmental effects to hoarding symptoms during adolescence and young adulthood and to estimate the sources of stability and change of hoarding symptoms during adolescence.MethodsUnivariate model-fitting was conducted in three cohorts of twins aged 15 (n = 7,905), 18 (n = 2,495) and 20–28 (n = 6,218). Longitudinal analyses were conducted in a subsample of twins for which data on hoarding symptoms was available at both age 15 and 18 (n = 1,701).ResultsHeritability estimates for hoarding symptoms at ages 15, 18 and 20–28 were 41% (95% confidence interval [CI]: 36–45%), 31% (95% CI: 22–39%) and 29% (95% CI: 24–34%) respectively. Quantitative sex-differences emerged in twins aged 15 at which point the heritability in boys was 33% (95% CI: 22–41%) and 17% (95% CI: 0–36%) in girls. Shared environmental effects played a negligible role across all samples with the exception of girls aged 15 where they accounted for a significant proportion of the variance (22%; 95% CI 6–36%). The longitudinal bivariate analyses revealed a significant phenotypic correlation of hoarding symptoms between ages 15 and 18 (0.40; 95% CI: 0.36–0.44) and a strong but imperfect genetic correlation (0.75; 95% CI: 0.57–0.94). The bivariate heritability was estimated to 65% (95% CI: 50–79%).ConclusionsHoarding symptoms are heritable from adolescence throughout young adulthood, although heritability appears to slightly decrease over time. Shared environmental effects contribute to hoarding symptoms only in girls at age 15. The stability of hoarding symptoms between ages 15 and 18 is largely explained by genetic factors, while non-shared environmental factors primarily have a time-specific effect. The findings indicate that dynamic developmental etiological effects may be operating across the life span.

Genetic and environmental influences on psychological traits and eating attitudes in a sample of Spanish schoolchildren

IntroductionThe heritability of eating disorders has been estimated to range from 22% to over 62%. The aim of this study is to determine the relative influence of genetics and environment that contribute to the drive for thinness, body dissatisfaction, perfectionism, and ineffectiveness, by evaluating sex differences in a sample of adolescent twins from Valencia, Spain. Material and methodsFive hundred eighty-four pairs of adolescent twins between 13 and 18 years of age completed the study. To determine zygosity, teachers responded to a questionnaire on physical similarity. Psychological traits of eating disorders were assessed with four sub-scales of the Eating Disorder Inventory (EDI); drive for thinness, body dissatisfaction, perfectionism, and ineffectiveness. Twin models were used to assess genetic and environmental (common and unique) factors affecting these four psychological traits. ResultsAll four traits showed significant genetic contributions among girls, with heritability estimates of 37.7% for ineffectiveness, 42.8% for perfectionism, 56.9% for drive for thinness, and 65.5% for body dissatisfaction. Among boys, body dissatisfaction showed no additive genetic contributions, indicating significant shared and individual specific environment effects. The three other traits in boys showed significant additive genetic contributions, but were lower than in girls. ConclusionsWith the exception of body dissatisfaction in boys, psychological traits of eating disorders show heritability patterns that differ according to sex.

Sequential recruitment of study participants may inflate genetic heritability estimates.

After the success of genome-wide association studies to uncover complex trait loci, attempts to explain the remaining genetic heritability (h 2) are mainly focused on unraveling rare variant associations and gene-gene or gene-environment interactions. Little attention is paid to the possibility that h 2 estimates are inflated as a consequence of the epidemiological study design. We studied the time series of 54 biochemical traits in 4373 individuals from the Cooperative Health Research In South Tyrol (CHRIS) study, a pedigree-based study enrolling ten participants/day over several years, with close relatives preferentially invited within the same day. We observed distributional changes of measured traits over time. We hypothesized that the combination of such changes with the pedigree structure might generate a shared-environment component with consequent h 2 inflation. We performed variance components (VC) h 2 estimation for all traits after accounting for the enrollment period in a linear mixed model (two-stage approach). Accounting for the enrollment period caused a median h 2 reduction of 4%. For 9 traits, the reduction was of >20%. Results were confirmed by a Bayesian Markov chain Monte Carlo analysis with all VCs included at the same time (one-stage approach). The electrolytes were the traits most affected by the enrollment period. The h 2 inflation was independent of the h 2 magnitude, laboratory protocol changes, and length of the enrollment period. The enrollment process may induce shared-environment effects even under very stringent and standardized operating procedures, causing h 2 inflation. Including the day of participation as a random effect is a sensitive way to avoid overestimation.

Are people with chronic low back pain meeting the physical activity guidelines? A co-twin control study

BackgroundDespite a large amount of research investigating physical activity (PA) levels in people with chronic low back pain (LBP), no study has investigated whether people with chronic LBP are meeting the World Health Organization (WHO) PA guidelines. Furthermore, with genetics and the early shared environment substantially influencing the presence of LBP and PA engagement, these factors could confound the association between LBP and PA and need to be controlled for. PurposeThis study aimed to investigate the association between chronic LBP and meeting the PA guidelines, while controlling for the effects of genetics and early shared environment. DesignThis is a cross-sectional co-twin control study. Patient SampleA cross-sectional analysis was performed on 1,588 twins from the Murcia Twin Registry in Spain with available data on LBP and PA from the 2013 data collection wave. Outcome MeasuresThe exposure and outcome variables in our study were self-reported. Twins reporting a history of chronic LBP were asked follow-up questions to inform on the presence of recent LBP (within the past 4 weeks), previous LBP (no pain within the past 4 weeks), and persistent LBP (no pain-free month in the last 6 months). These were our exposure variables. Our outcome variable was meeting the WHO PA guidelines, which involved at least 75 minutes of vigorous-intensity PA, or at least 150 minutes of moderate-intensity PA per week. MethodsTo investigate the association between chronic LBP and meeting the PA guidelines, we first performed a multivariate logistic regression on the total sample of twins. Co-variables entered the model if the univariate association between the co-variable, and both the exposure and the outcome reached a significance of p<.2. Second, to adjust for the influence of genetics and early shared environment, we performed a conditional multivariate logistic regression on complete twin pairs discordant for LBP. The Murcia Twin Registry is supported by Fundación Séneca, Regional Agency for Science and Technology, Murcia, Spain (08633/PHCS/08 and 15302/PHCS/10) and the Ministry of Science and Innovation, Spain (PSI11560-2009). Funding for this project has also been received from Fundación MAPFRE (2012). The authors declare that there are no conflicts of interest. ResultsThere was a significant inverse association between recent LBP and meeting the PA guidelines (odds ratio [OR]=0.71, p=.034). When controlling for genetics and early shared environment, this association disappeared. There was no association between previous (OR=0.95, p=.779) or persistent LBP (OR=0.78, p=.192) and meeting the PA guidelines. ConclusionTwins with recent LBP are less likely to meet the PA guidelines than those with no history of chronic LBP, highlighting the importance of incorporating PA promotion in the treatment of these individuals. Genetics and early shared environment appear to be confounding the association between LBP and PA, although this needs to be further tested in larger twin samples.

Cardiorespiratory Fitness and Adiposity as Determinants of Metabolic Health-Pooled Analysis of Two Twin Cohorts.

The joint effects of cardiorespiratory fitness (CRF) and body composition on metabolic health are not well known. To examine the associations of CRF, fat-free mass index (FFMI), and fat mass index (FMI) with metabolic health in individual twins and controlling for genetic and shared environmental effects by studying monozygotic intrapair differences. Two cross-sectional samples of healthy adult monozygotic and dizygotic twins were drawn from population-based Danish and Finnish national twin registries (n = 996 and n = 309). CRF was defined as VO2max divided by fat-free mass. Insulin sensitivity and acute insulin response indices were derived from an oral glucose tolerance test. A continuous metabolic syndrome score was calculated. Visceral and liver fat were measured in the Finnish sample. Associations were analyzed separately in both cohorts with multivariate linear regression and aggregated with meta-analytic methods. Insulin sensitivity, acute insulin response, metabolic syndrome score, visceral, and liver fat amount had strong and statistically significant associations with FMI (|β| 0.53 to 0.79), whereas their associations with CRF and FFMI were at most weak (|β| 0.02 to 0.15). The results of the monozygotic intrapair differences analysis showed the same pattern. Although FMI is strongly associated with worsening of metabolic health traits, even after controlling for genetic and shared environmental factors, there was little evidence for the effects of CRF or FFMI on metabolic health. This suggests that changing FMI rather than CRF or FFMI may affect metabolic health irrespective of genetic or early environmental determinants.

Genetic influences on hormonal markers of chronic hypothalamic-pituitary-adrenal function in human hair.

Cortisol is the primary output of the hypothalamic-pituitary-adrenal (HPA) axis and is central to the biological stress response, with wide-ranging effects on psychiatric health. Despite well-studied biological pathways of glucocorticoid function, little attention has been paid to the role of genetic variation. Conventional salivary, urinary and serum measures are strongly influenced by diurnal variation and transient reactivity. Recently developed technology can be used to measure cortisol accumulation over several months in hair, thus indexing chronic HPA function. In a socio-economically diverse sample of 1070 twins/multiples (ages 7.80-19.47 years) from the Texas Twin Project, we estimated effects of sex, age and socio-economic status (SES) on hair concentrations of cortisol and its inactive metabolite, cortisone, along with their interactions with genetic and environmental factors. This is the first genetic study of hair neuroendocrine concentrations and the largest twin study of neuroendocrine concentrations in any tissue type. Glucocorticoid concentrations increased with age for females, but not males. Genetic factors accounted for approximately half of the variation in cortisol and cortisone. Shared environmental effects dissipated over adolescence. Higher SES was related to shallower increases in cortisol with age. SES was unrelated to cortisone, and did not significantly moderate genetic effects on either cortisol or cortisone. Genetic factors account for sizable proportions of glucocorticoid variation across the entire age range examined, whereas shared environmental influences are modest, and only apparent at earlier ages. Chronic glucocorticoid output appears to be more consistently related to biological sex, age and genotype than to experiential factors that cluster within nuclear families.

Rethinking the transmission gap: What behavioral genetics and evolutionary psychology mean for attachment theory: A comment on Verhage et al. (2016).

Traditional attachment theory posits that attachment in infancy and early childhood is the result of intergenerational transmission of attachment from parents to offspring. Verhage et al. (2016) present meta-analytic evidence addressing the intergenerational transmission of attachment between caregivers and young children. In this commentary, we argue that their appraisal of the behavioral genetics literature is incomplete. The suggested research focus on shared environmental effects may dissuade the pursuit of profitable avenues of research and may hinder progress in attachment theory. Specifically, further research on the "transmission gap" will continue to limit our understanding of attachment etiology. We discuss recent theoretical developments from an evolutionary psychological perspective that can provide a valuable framework to account for the existing behavioral genetic data. (PsycINFO Database Record

Heritability of tic disorders: a twin-family study.

Genetic-epidemiological studies that estimate the contributions of genetic factors to variation in tic symptoms are scarce. We estimated the extent to which genetic and environmental influences contribute to tics, employing various phenotypic definitions ranging between mild and severe symptomatology, in a large population-based adult twin-family sample. In an extended twin-family design, we analysed lifetime tic data reported by adult mono- and dizygotic twins (n = 8323) and their family members (n = 7164; parents and siblings) from 7311 families in the Netherlands Twin Register. We measured tics by the abbreviated version of the Schedule for Tourette and Other Behavioral Syndromes. Heritability was estimated by genetic structural equation modeling for four tic disorder definitions: three dichotomous and one trichotomous phenotype, characterized by increasingly strictly defined criteria. Prevalence rates of the different tic disorders in our sample varied between 0.3 and 4.5% depending on tic disorder definition. Tic frequencies decreased with increasing age. Heritability estimates varied between 0.25 and 0.37, depending on phenotypic definitions. None of the phenotypes showed evidence of assortative mating, effects of shared environment or non-additive genetic effects. Heritabilities of mild and severe tic phenotypes were estimated to be moderate. Overlapping confidence intervals of the heritability estimates suggest overlapping genetic liabilities between the various tic phenotypes. The most lenient phenotype (defined only by tic characteristics, excluding criteria B, C and D of DSM-IV) rendered sufficiently reliable heritability estimates. These findings have implications in phenotypic definitions for future genetic studies.

Does educational attainment increase the risk of low back pain when genetics are considered? A population-based study of Spanish twins

Background ContextThere is limited research investigating educational attainment as a risk factor for low back pain (LBP), with the influence of gender commonly being neglected. Furthermore, genetics and early shared environment explain a substantial proportion of LBP cases and need to be controlled for when investigating risk factors for LBP. PurposeTo investigate whether educational attainment affects the prevalence and risk of LBP differently in men and women while controlling for the influence of genetics and early shared environment. Study DesignThis is a cross-sectional and prospective twin case-control study. Patient SampleAdult monozygotic (MZ) and dizygotic (DZ) twins from the Murcia Twin Registry, with available data on educational attainment, formed the base sample for this study. The prevalence analysis considered twins with available data on LBP in 2013 (n=1,580). The longitudinal analysis considered twins free of LBP at baseline (2009–2011), with available data on LBP at follow-up (2013) (n=1,077). Outcome MeasuresData on the lifetime prevalence of activity limiting LBP (outcome) and educational attainment (risk factor) were self-reported. MethodsThe prevalence analysis investigated the cross-sectional association between educational attainment and LBP, whereas the longitudinal analysis investigated whether educational attainment increased the risk of developing LBP. Both analyses were performed in the following sequence. First, a total sample analysis was performed on all twins (considering them as individuals), adjusting for confounding variables selected by the data. Second, to control for the influence of genetics and early shared environment, a within-pair case-control analysis (stratified by zygosity) was performed on complete twin pairs discordant for LBP (ie, one twin had LBP, whereas the co-twin did not). All analyses were stratified for gender where possible, with an interaction term determining whether gender was a significant moderator of the association between educational attainment and LBP. ResultsWomen with either general secondary or university education were less likely to experience (prevalence analysis) or to develop LBP (longitudinal analysis). Educational attainment did not affect the risk of LBP in men. When controlling for the effects of genetics and early shared environment, the relationship between educational status and LBP in women was no longer statistically significant. ConclusionsEducational attainment affects LBP differently in men and women, with higher levels of education only decreasing the risk of developing LBP in women. After adjusting for genetics and early shared environment, the relationship between educational attainment and LBP in women disappears. This suggests that genetics and early shared environment are confounding the relationship between educational attainment and LBP in women.

A sibling based design to quantify genetic and shared environmental effects of venous thromboembolism in Sweden

IntroductionFew large studies have examined the heritability of venous thromboembolism (VTE). Moreover, twin studies have been suggested to overestimate heritability. The aim of the present study was to determine the heritability nationwide in the general Swedish population using full siblings and half-siblings. MethodsVTE was defined using the Swedish patient register. Full sibling (FS) and half-sibling (HS) pairs born 1950–1990 were obtained from the Swedish Multi-generation Register. A maximum of 5years age difference was allowed. We also required that the individuals within the pair should reside in the same household for at least 8years or not at all (0years) before the youngest turned 16. Information about sibling pair residence within the same household, small residential area, and municipality was obtained from Statistics Sweden. We assumed three potential sources of liability to VTE: additive genetic (A), shared (or common/familial) environment (C), and unique environment (E) components. ResultsTotally 881,206 FS pairs and 95,198 HS pairs were included. The full model predicted heritability for VTE with 47% for males and 40% for females. Environmental factors shared by siblings contributed to 0% of the variance in liability for both sexes, and unique environment (E) components accounted for 53% in males and 60% in females. ConclusionThe high heritability of VTE risk indicates that genetic susceptibility plays a substantial role for VTE in the Swedish general population. Overestimation of heritability from twin studies is not likely. The proportion of the variance attributable to shared familial environment factors is small.Subject codes: Genetics, epidemiology, thrombosis, cardiovascular disease, embolism

Food fussiness and food neophobia share a common etiology in early childhood.

Background‘Food fussiness’ (FF) is the tendency to be highly selective about which foods one is willing to eat, and emerges in early childhood; ‘food neophobia’ (FN) is a closely related characteristic but specifically refers to rejection of unfamiliar food. These behaviors are associated, but the extent to which their etiological architecture overlaps is unknown. The objective of this study was to quantify the relative contribution of genetic and environmental influences to variation in FF and FN in early childhood; and to establish the extent to which they share common genetic and environmental influences.MethodParticipants were 1,921 families with 16‐month‐old twins from the Gemini birth cohort. Parents completed the Child Eating Behaviour Questionnaire which included three FF items and four FN items. Bivariate quantitative genetic modeling was used to quantify: (a) genetic and environmental contributions to variation in FF and FN; and (b) the extent to which genetic or environmental influences on FF and FN are shared across the traits.ResultsFood fussiness and FN were strongly correlated (r = .72, p < .001). Proportions of variation in FF were equally explained by genetic (.46; 95% CI: 0.41–0.52) and shared environmental influences (.46; 95% CI: 0.41–0.51). Shared environmental effects accounted for a significantly lower proportion of variation in FN (.22; 95% CI: 0.14–0.30), but genetic influences were not significantly different from those on FF (.58, 95% CI: 0.50–0.67). FF and FN largely shared a common etiology, indicated by high genetic (.73; 95% CI: 0.67–0.78) and shared environmental correlations (.78; 95% CI: 0.69–0.86) across the two traits.ConclusionsFood fussiness and FN both show considerable heritability at 16 months but shared environmental factors, for example the home environment, influenced more interindividual differences in the expression of FF than in FN. FF and FN largely share a common etiology.

Longitudinal Effects on Early Adolescent Language: A Twin Study.

We evaluated genetic and environmental contributions to individual differences in language skills during early adolescence, measured by both language sampling and standardized tests, and examined the extent to which these genetic and environmental effects are stable across time. We used structural equation modeling on latent factors to estimate additive genetic, shared environmental, and nonshared environmental effects on variance in standardized language skills (i.e., Formal Language) and productive language-sample measures (i.e., Productive Language) in a sample of 527 twins across 3 time points (mean ages 10-12 years). Individual differences in the Formal Language factor were influenced primarily by genetic factors at each age, whereas individual differences in the Productive Language factor were primarily due to nonshared environmental influences. For the Formal Language factor, the stability of genetic effects was high across all 3 time points. For the Productive Language factor, nonshared environmental effects showed low but statistically significant stability across adjacent time points. The etiology of language outcomes may differ substantially depending on assessment context. In addition, the potential mechanisms for nonshared environmental influences on language development warrant further investigation.

Genetic and environmental components of female depression as a function of the severity of the disorder.

BackgroundBoth clinical care and genome‐wide studies need to account for levels of severity in the etiology of depression. The purpose of the study is to estimate the genetic and environmental components of female depression as a function of the severity of the disorder.MethodsA genetic and environmental model analysis of depression incidence was made using the IOP Depression Severity Measure (IDSM). Details of lifetime depression incidence were obtained by questionnaire from twins on the DTR registry. Data from 1449 matched female twin pairs in the age range 19–85 years in four ordinal categories of increasing severity were employed in the analysis.ResultsEstimates of additive and dominance genetic components of 27% and 25% were found when all three levels of depression were included, and near zero and 33% when the recurrent/severe level was excluded. Shared environmental effects were not significant in either case, but the estimate for random environmental effects was greater when the severe level was excluded.ConclusionsThese results suggest that the incidence of severe depression is associated with homozygotic alleles and the less severe with heterozygotic alleles. This is in accord with the finding that the hereditary component of severe depression is relatively high and that milder forms are more dependent on life‐time environmental factors. Such conclusions have clinical implications for the diagnosis and treatment of the disorder by practicing psychiatrists. They also lead to the importance of focusing future genome‐wide and linkage studies on those females with severe levels of depression if progress in identifying genetic risk loci is to be made.

A National Swedish Twin-Sibling Study of Alcohol Use Disorders.

The relationship between the genetic and environmental risk factors for alcohol use disorders (AUD) detected in Swedish medical, pharmacy, and criminal registries has not been hitherto examined. Prior twin studies have varied with regard to the detection of shared environmental effects and sex differences in the etiology of AUD. In this report, structural equation modeling in OpenMx was applied to (1) the three types of alcohol registration in a population-based sample of male-male twins and reared-together full and half siblings (total 208,810 pairs), and (2) AUD, as a single diagnosis, in male-male, female-female, and opposite-sex (OS) twins and reared-together full and half siblings (total 787,916 pairs). An independent pathway model fit best to the three forms of registration and indicated that between 70% and 92% of the genetic and 63% and 98% of the shared environmental effects were shared in common with the remainder unique to each form of AUD registration. Criminal registration had the largest proportion of unique genetic and environmental factors. The best fit model for AUD estimated the heritability to be 22% and 57%, respectively, in females and males. Both shared (12% vs. 6%) and special twin environment (29% vs. 2%) were substantially more important in females versus males. In conclusion, AUD ascertained from medical, pharmacy, and criminal Swedish registries largely share the same genetic and environmental risk factors. Large sex differences in the etiology of AUD were seen in this sample, with substantially stronger familial environmental and weaker genetic effects in females versus males.

Genetic and environmental effects on body mass index from infancy to the onset of adulthood: an individual-based pooled analysis of 45 twin cohorts participating in the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins) study1–3

Both genetic and environmental factors are known to affect body mass index (BMI), but detailed understanding of how their effects differ during childhood and adolescence is lacking. We analyzed the genetic and environmental contributions to BMI variation from infancy to early adulthood and the ways they differ by sex and geographic regions representing high (North America and Australia), moderate (Europe), and low levels (East Asia) of obesogenic environments. Data were available for 87,782 complete twin pairs from 0.5 to 19.5 y of age from 45 cohorts. Analyses were based on 383,092 BMI measurements. Variation in BMI was decomposed into genetic and environmental components through genetic structural equation modeling. The variance of BMI increased from 5 y of age along with increasing mean BMI. The proportion of BMI variation explained by additive genetic factors was lowest at 4 y of age in boys (a(2) = 0.42) and girls (a(2) = 0.41) and then generally increased to 0.75 in both sexes at 19 y of age. This was because of a stronger influence of environmental factors shared by co-twins in midchildhood. After 15 y of age, the effect of shared environment was not observed. The sex-specific expression of genetic factors was seen in infancy but was most prominent at 13 y of age and older. The variance of BMI was highest in North America and Australia and lowest in East Asia, but the relative proportion of genetic variation to total variation remained roughly similar across different regions. Environmental factors shared by co-twins affect BMI in childhood, but little evidence for their contribution was found in late adolescence. Our results suggest that genetic factors play a major role in the variation of BMI in adolescence among populations of different ethnicities exposed to different environmental factors related to obesity.

Neighborhood Disadvantage and Parenting: Behavioral Genetics Evidence of Child Effects.

The criminological literature has a long tradition of emphasizing the socialization effects that parents have on children. By contrast, evidence from behavioral genetics research gives precedence to child effects on parental management techniques over parental effects on children's outcomes. Considering these diverging lines of scholarship and literature, the current study explores a novel hypothesis that child effects on parenting may be conditioned by the level of the disadvantage of the neighborhood in which the child's family resides. By using measures of perceived parenting as dependent variables, the researchers analyze data on 733 same-sex sibling pairs derived from the Add Health study by taking advantage of the DeFries-Fulker analytical technique. The results show that in adequate neighborhoods, between 43% and 55% of the variance in the measures of perceived parenting is due to genetic factors, whereas shared environmental effects are negligible. In disadvantaged neighborhoods, genetic effects are negligible, whereas shared environmental influences account for between 34% and 57% of the variance in perceived parenting. These results offer partial support for the contextualized gene-environment correlation, which provides initial evidence that although both parental socialization effects and child effects exist, these effects can be modified by the context.

The Genetic and Environmental Association Between Parental Monitoring and Risk of Cannabis, Stimulants, and Cocaine Initiation in a Sample of Male Twins: Does Parenting Matter?

Our aim was to test the direction of causation between self-report parental monitoring (PM) and the liability to illicit drug initiation (DI) as indicated by cannabis, cocaine, and stimulants. We fitted a multiple indicator model to test causal and non-causal models based on a large, genetically informative cross-sectional sample of male twins. The sample comprised 1,778 males aged 24-62 years from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. Data came from self-report measures of lifetime cannabis, stimulants, and cocaine initiation, and retrospective assessment of PM between ages 8-17 years. Multivariate modeling showed that familial aggregation in PM and DI were both explained by a combination of additive genetic and shared environmental effects. Moreover, the significant association between PM and DI was best explained by a correlated liability model versus causal models. PM has typically been assumed to be an environmental, causal risk factor for drug use and has been shown to be among the more salient environmental risk factors for illicit DI. Our data were not consistent with this causal hypothesis. Instead, a correlated liability model in which PM and risk of DI share common genetic and environmental risks provided a better fit to the data.

Musculoskeletal pain and work absence – a 10 year follow-up study of Norwegian young adult twins

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.

Individual Differences in Exercise Behavior: Stability and Change in Genetic and Environmental Determinants From Age 7 to 18

Exercise behavior during leisure time is a major source of health-promoting physical activity and moderately tracks across childhood and adolescence. This study aims to investigate the absolute and relative contribution of genes and the environment to variance in exercise behavior from age 7 to 18, and to elucidate the stability and change of genetic and shared environmental factors that underlie this behavior. The Netherlands Twin Register collected data on exercise behavior in twins aged approximately 7, 10, 12, 14, 16 and 18years (N=27,332 twins; 48% males; 47% with longitudinal assessments). Three exercise categories (low, middle, high) were analyzed by means of liability threshold models. First, a univariate model was fitted using the largest available cross-sectional dataset with linear and quadratic effects of age as modifiers on the means and variance components. Second, a simplex model was fitted on the longitudinal dataset. Heritability was low in 7-year-olds (14% in males and 12% in females), but gradually increased up to age 18 (79% in males and 49% in females), whereas the initially substantial relative influence of the shared environment decreased with age (from 80 to 4% in males and from 80 to 19% in females). This decrease was due to a large increase in the genetic variance. The longitudinal model showed the genetic effects in males to be largely stable and to accumulate from childhood to late adolescence, whereas in females, they were marked by both transmission and innovation at all ages. The shared environmental effects tended to be less stable in both males and females. In sum, the clear age-moderation of exercise behavior implies that family-based interventions might be useful to increase this behavior in children, whereas individual-based interventions might be better suited for adolescents. We showed that some determinants of individual differences in exercise behavior are stable across childhood and youth, whereas others come into play at specific ages. In view of the many benefits of regular exercise, identifying these determinants at specific ages should be a public health priority.

Longitudinal Stability of Genetic and Environmental Influences on the Association between Diurnal Preference and Sleep Quality in Young Adult Twins and Siblings.

Overlapping genetic influences have been implicated in diurnal preference and subjective sleep quality. Our overall aim was to examine overlapping concurrent and longitudinal genetic and environmental effects on diurnal preference and sleep quality over ~5 years. Behavioral genetic analyses were performed on data from the longitudinal British G1219 study of young adult twins and nontwin siblings. A total of 1556 twins and siblings provided data on diurnal preference (Morningness-Eveningness Questionnaire) and sleep quality (Pittsburgh Sleep Quality Index) at time 1 (mean age = 20.30 years, SD = 1.76; 62% female), and 862 participated at time 2 (mean age = 25.30 years, SD = 1.81; 66% female). Preference for eveningness was associated with poorer sleep quality at both time points (r = 0.25 [95% confidence intervals {CIs} = 0.20-0.30] and r = 0.21 [CI = 0.15-0.28]). There was substantial overlap in the genetic influences on diurnal preference and sleep quality individually, across time (genetic correlations [rAs]: 0.64 [95% CI = 0.59-0.67] and 0.48 [95% CI = 0.42-.053]). There were moderate genetic correlations between diurnal preference and sleep quality concurrently and longitudinally (rAs = 0.29-0.60). Nonshared environmental overlap was substantially smaller for all cross-phenotype associations (nonshared environmental correlations (rEs) = -0.02 to 0.08). All concurrent and longitudinal associations within and between phenotypes were largely accounted for by genetic factors (explaining between 60% and 100% of the associations). All shared environmental effects were nonsignificant. Nonshared environmental influences played a smaller role on the associations between phenotypes (explaining between -0.06% and 40% of the associations). These results suggest that to some extent, similar genes contribute to the stability of diurnal preference and sleep quality throughout young adulthood but also that different genes play a part over this relatively short time frame. While there was evidence of genetic overlap between phenotypes concurrently and longitudinally, the possible emergence of new genetic factors (or decline of previously associated factors) suggests that molecular genetic studies focusing on young adults should consider more tightly specified age groups, given that genetic effects may be time specific.