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Background: The distribution of fat and adipose tissue is an important predictor of disease risk. Variation in fat distribution during adolescence is correlated with fat distribution in adulthood. Objective: The objective was to gain insight into the relative contribution of genes and environment to the stability of subcutaneous fat distribution from early adolescence into young adulthood. Design: Ratio of trunk to extremity skinfold thickness (TER) data from the Leuven Longitudinal Twin Study (n = 105 Belgian twin pairs followed from 10 to 18 y of age) was entered into a longitudinal path analysis. Results: The best-fitting model included additive genetic sources of variance and nonshared environment. Heritabilities ranged between 84.3% (95% CI: 63.9-92.3%) and 88.6% (95% CI: 76.5-94.1%) in boys and between 78.4% (95% CI: 59.3-88.3%) and 88.3% (95% CI: 77.0-93.8%) in girls. The majority of the phenotypic tracking (boys: 0.40-0.78; girls: 0.38-0.72) could be attributed to the moderate-to-high genetic correlations (rG) (between 0.27-0.84 and 0.38-0.80 for the various age intervals in boys and girls, respectively). This rG could be attributed to both genetic sources of variance, which are the same throughout adolescence, as well as genetic sources of variance that are 'switched-on' at a certain age, the effect of which is then transmitted to subsequent observations. Environmental correlations (rE) in boys ranged between 0.51 and 0.70 but contributed relatively little to phenotypic tracking because the amount of variance explained by the environment was low (11.4-15.7%). In girls rE was low to moderate at best (0.09-0.48). Conclusion: Phenotypic tracking in subcutaneous fat distribution during adolescence is predominantly explained by additive genetic sources of variance. KEY WORDS Heritability, stability, subcutaneous adipose tissue distribution, growth, twins

Variation in liability to cannabis use disorder has a strong genetic component (estimated twin and family heritability about 50–70%) and is associated with negative outcomes, including increased risk of psychopathology. The aim of the study was to conduct a large genome-wide association study (GWAS) to identify novel genetic variants associated with cannabis use disorder.

To provide insights into the biology of opioid dependence (OD) and opioid use (i.e., exposure, OE), we completed a genome-wide analysis comparing 4503 OD cases, 4173 opioid-exposed controls, and 32,500 opioid-unexposed controls, including participants of European and African descent (EUR and AFR, respectively). Among the variants identified, rs9291211 was associated with OE (exposed vs. unexposed controls; EUR z= −5.39, p= 7.2 × 10–8). This variant regulates the transcriptomic profiles of SLC30A9and BEND4in multiple brain tissues and was previously associated with depression, alcohol consumption, and neuroticism. A phenome-wide scan of rs9291211 in the UK Biobank (N> 360,000) found association of this variant with propensity to use dietary supplements (p= 1.68 × 10–8). With respect to the same OE phenotype in the gene-based analysis, we identified SDCCAG8(EUR + AFR z= 4.69, p= 10–6), which was previously associated with educational attainment, risk-taking behaviors, and schizophrenia. In addition, rs201123820 showed a genome-wide significant difference between OD cases and unexposed controls (AFR z= 5.55, p= 2.9 × 10–8) and a significant association with musculoskeletal disorders in the UK Biobank (p= 4.88 × 10–7). A polygenic risk score (PRS) based on a GWAS of risk-tolerance (n= 466,571) was positively associated with OD (OD vs. unexposed controls, p= 8.1 × 10–5; OD cases vs. exposed controls, p= 0.054) and OE (exposed vs. unexposed controls, p= 3.6 × 10–5). A PRS based on a GWAS of neuroticism (n= 390,278) was positively associated with OD (OD vs. unexposed controls, p= 3.2 × 10–5; OD vs. exposed controls, p= 0.002) but not with OE (p= 0.67). Our analyses highlight the difference between dependence and exposure and the importance of considering the definition of controls in studies of addiction.

Liability to alcohol dependence (AD) is heritable, but little is known about its complex polygenic architecture or its genetic relationship with other disorders. To discover loci associated with AD and characterize the relationship between AD and other psychiatric and behavioral outcomes, we carried out the largest genome-wide association study to date of DSM-IV-diagnosed AD. Genome-wide data on 14,904 individuals with AD and 37,944 controls from 28 case–control and family-based studies were meta-analyzed, stratified by genetic ancestry (European, n= 46,568; African, n= 6,280). Independent, genome-wide significant effects of different ADH1Bvariants were identified in European (rs1229984; P= 9.8 × 10–13) and African ancestries (rs2066702; P= 2.2 × 10–9). Significant genetic correlations were observed with 17 phenotypes, including schizophrenia, attention deficit–hyperactivity disorder, depression, and use of cigarettes and cannabis. The genetic underpinnings of AD only partially overlap with those for alcohol consumption, underscoring the genetic distinction between pathological and nonpathological drinking behaviors.

Alcohol involvement has familial associations with bulimic symptoms (i.e., binge eating, inappropriate compensatory behaviors), with several studies indicating a genetic overlap between the two. It is unclear whether overlapping familial risk with alcohol involvement extends to other eating disorder symptoms. Understanding the genetic overlap between alcohol involvement and other eating disorder symptoms may aid in more targeted interventions for comorbid alcohol use‐eating disorder symptoms. Thus, we investigated associations between alcohol involvement and 2 core eating disorder symptoms: drive for thinness and body dissatisfaction in adolescent female and male twins. We assessed 3 levels of alcohol involvement: alcohol use in the last month, having ever been intoxicated, and alcohol intoxication frequency via self‐report. The Eating Disorder Inventory‐IIassessed drive for thinness and body dissatisfaction. Sex‐specific biometrical twin modeling examined the genetic overlap between alcohol involvement and eating disorder symptoms. Phenotypic associations between alcohol involvement, drive for thinness, and body dissatisfaction were significantly greater in girls compared with boys. A majority of the associations between alcohol involvement, drive for thinness, and body dissatisfaction in girls, but not boys, met our threshold for twin modeling (phenotypic r >0.20). Moderate genetic correlations were observed between the 3 aspects of alcohol involvement and drive for thinness. Moderate genetic correlations were observed between alcohol use and intoxication frequency and body dissatisfaction. Together with the literature on alcohol involvement and bulimic symptoms, these findings suggest a generalized association between alcohol involvement and eating disorder symptoms in girls, whereas this association may be symptom specific in boys. Genetic correlations indicate that the amount and direction of this genetic overlap differs across specific symptoms. When intervening on comorbid alcohol involvement and eating disorder symptoms, it may be important to target‐specific eating disorder symptoms. It is unclear whether alcohol involvement (AI) has familial associations with eating disorder symptoms beyond symptoms of bulimia nervosa. We investigated associations between alcohol involvement and drive for thinness (DT) and body dissatisfaction (BD) in adolescent twins using sex‐specific biometrical twin modeling. Moderate genetic correlations were observed between AIand DT. Findings suggest the amount and direction of the genetic overlap between AIand eating disorder symptoms differs across specific symptoms.

The authors sought to decompose the covariance between seven dimensions of religiosity and two internalizing psychiatric disorders (major depression and phobia) and two externalizing substance use disorders (alcohol dependence and nicotine dependence). Significant negative correlations, accounted for by shared additive genetic effects, were found between alcohol dependence and six of the seven religiosity factors. Additive genetic effects accounted for significant negative correlations between nicotine dependence and one religiosity factor, social religiosity, and between phobia and unvengefulness. Common environmental effects accounted for a significant positive correlation between phobia and the factor God as judge. No statistically significant covariance due to genetic or environmental effects was found for major depression and any of the seven religiosity factors. Overall, although several statistically significant bivariate relationships were found, the estimates of covariance due to additive genetic effects were modest.

In recent years there has been a renewed scientific interest in the study of religiosity, including research on genetic and environmental contributions to religiosity. In this article, we investigate genetic and environmental effects on 7 religiosity factors and explore how genetic and environmental effects covary across these factors. Seven religiosity factors estimated from 78 items were examined in a sample of adult male and female twins. The 7 religiosity factors were largely influenced by additive genetic and unique environmental effects, with relatively little influence from common environmental effects. Multivariate genetic analyses found the 7 religiosity factors were influenced by 1 common additive genetic factor, 3 common unique environmental factors, and unique environmental effects specific to each religiosity factor. The results suggest that for the population studied, additive genetic and unique environmental effects largely account for the variance across the religiosity construct.

Hearing loss is a common neurosensory deficit; nearly 50 of children with hearing loss have a genetic etiology. With the discovery of 40 genes and more than 100 loci involved in hearing loss, genetic testing is becoming more widely available. The information obtained through genetic testing can be perceived and used in different ways by parents of deaf children and deaf adults, based on their prior knowledge and understanding of these advances. It is therefore important to clarify the feelings of these potential consumers towards genetic services for hearing loss and understand their goals for genetic testing. The present study evaluates the feelings of consumers towards the advances in the genetics of hearing loss, the motivations for pursuing testing, and the perceived impact testing may have on their lives. We surveyed 808 parents of children with hearing loss nationally and 156 young deaf adults at Gallaudet University. In this study, learning the etiology of the hearing loss was the most commonly cited motivation for pursuing genetic testing and for parents was the most commonly cited outcome that genetic testing may have on their childrens lives. Culturally Deaf respondents were less likely to believe that genetic testing will impact their lives or their childrens lives and were less likely to report positive feelings about advances in the genetics of hearing loss. Cultural affiliation and genetic testing status, rather than hearing status, contributed more to the participants responses. © 2009 WileyLiss, Inc.

AbstractThe children of twins (COT) design has been proposed as an alternative to the adoption study to resolve the direct effects of parental treatment from secondary parent?child association due to genetic factors. The basic analytical approach compares the parent?offspring correlation with the correlation between children and the monozygotic (MZ) twins of their parents. We show that a significant difference between these correlations does not imply direct environmental causality when the measured parental treatment in question is dyadic, that is, influenced by both parents even when mating is random. Nongenetic causal effects yield very similar patterns of correlation to secondary genetic effects on dyadic treatment variables. The fact that many candidate environments, such as parental divorce, are dyadic gives reason to question the interpretation of their correlations with behavior in the children of twins.

We examined longitudinally the psychometric properties of the Twin Inventory of Relationships and Experiences (TIRE), an instrument designed to assess non‐shared and shared environmental experiences in twins and siblings. A community sample of 1,117 pairs of like‐sex monozygotic and dizygotic twins, aged eight to 16, and their parents, was used. Results indicated that the TIRE provided constructs that are consistent across informants, gender and time. These dimensions showed good longitudinal stability within raters, and low to moderate inter‐rater agreement; the results are consistent with those of other studies using different instruments to assess family environment. It is concluded that the TIRE may be used to assess dimensions of the non‐shared environment of twins and siblings and their influence on children's development. Copyright © 2001 Whurr Publishers Ltd.

Background:The role of genetics in the etiology of peanut allergy is unknown. For complex genetic traits, twin studies can provide information on the relative contribution of genetic factors to a disease, as the relative confounding effects of environmental factors are markedly decreased. Objective:This study was performed to search for evidence that genetic factors influence peanut allergy by comparing the concordance rate for this allergy among monozygotic and dizygotic twins. Methods:Twin pairs with at least one member with peanut allergy were ascertained through the Food Allergy Network by advertisements in the organization’s newsletters and Web site. Individuals with peanut allergy or parental surrogates were interviewed by telephone. A full atopic history was obtained, and peanut allergy and zygosity were determined using previously validated questionnaires. Heritability of peanut allergy was determined using univariate genetic model fitting by maximum likelihood with the Mx statistical modeling software package. Results:Seventy-five twin pairs were recruited. Seventeen pairs were excluded because of unconvincing peanut allergy histories (9 pairs, including 4 of uncertain zygosity) or because one twin had reportedly never ingested peanut (8 pairs). The median age of the 58 remaining twin pairs was 5 years (range 1 to 58 years). Seventy individuals had peanut allergy. In addition to convincing histories of peanut allergy, 52 (74%) had been tested (skin prick testing with or without radioallergosorbent assay) and all had positive reactions to peanut. Twenty-nine of the 70 had experienced 1 reaction to peanut; 29 of 70 had multisystem reactions. Among the monozygotic pairs (n = 14), 9 were concordant for peanut allergy (pairwise concordance, 64.3%) and among dizygotic pairs (n = 44), 3 were concordant for peanut allergy (pairwise concordance, 6.8%; χ2= 21.38, P< .0001). Heritability of peanut allergy was estimated at 81.6% (95% confidence interval 41.6% to 99.7%) with model fitting using a population prevalence of peanut allergy of 0.4%. Conclusions:The significantly higher concordance rate of peanut allergy among monozygotic twins suggests strongly that there is a significant genetic influence on peanut allergy. (J Allergy Clin Immunol 2000;106:53-6.)

AbstractThis study explores the use of an individual's genetic (IGFS) and environmental factor score (IEFS), constructed using genetic model fitting of a multivariate strength phenotype. Maximal isometric and dynamic strength measures, one maximal repetition load (1RM) and muscle cross-sectional area (MCSA) were measured in 25 monozygotic and 16 dizygotic twin pairs. The use of IGFS and IEFS in predicting the sensitivity to environmental stress was evaluated by the association of the scores with strength training gains after a 10-week high resistance strength training programme. Results show a high contribution of genetic factors to the covariation between maximal strength and muscle cross-sectional area (84?97%) at pre-training evaluation. Individual factor scores explained the largest part of the variation in 1RM and other strength measures at pre-training and post-training evaluation respectively. Genes that are switched on due to training stress (gene?environment interaction) could explain the decrease in explained variation over time. A negative correlation was found between IGFS and strength training gains (?0.24 to ?0.51, P < 0.05); individuals with a high IGFS tend to gain less strength than individuals with low IGFS. Individual environmental factor scores have lower differential power. The predictive value of the IGFS has potential utility in identifying an individual's susceptibility to environmental stress in a variety of multifactorial characteristics, eg diseases and impairments, and for selection of sib pairs for QTL analyses. Twin Research (2000) 3, 99?108.

AbstractReligious attendance has been shown to correlate negatively with alcohol use. We investigated whether this relationship is driven by genetic or environmental factors. Data on frequency of church attendance and frequency of alcohol use were obtained from twins and their families in the Virginia 30 000 study. A comprehensive bivariate model of family resemblance was fitted to the data using Mx. This model is described in detail. Results indicate that genetic factors primarily account for the relationship between alcohol and church attendance in males, whilst shared environmental factors, including cultural transmission and genotype-environment covariance, are stronger determinants of this association in females.

AbstractResearch has consistently shown that religiousness is associated with lower levels of alcohol and drug use, but little is known about the nature of adolescent religiousness or the mechanisms through which it influences problem behavior in this age group. This paper presents preliminary results from the Mid-Atlantic School Age Twin Study, a prospective, population-based study of 6?18-year-old twins and their mothers. Factor analysis of a scale developed to characterize adolescent religiousness, the Religious Attitudes and Practices Inventory (RAPI), revealed three factors: theism, religious/spiritual practices, and peer religiousness. Twin correlations and univariate behavior-genetic models for these factors and a measure of belief that drug use is sinful reveal in 357 twin pairs that common environmental factors significantly influence these traits, but a minor influence of genetic factors could not be discounted. Correlations between the multiple factors of adolescent religiousness and substance use, comorbid problem behavior, mood disorders, and selected risk factors for substance involvement are also presented. Structural equation modeling illustrates that specific religious beliefs about the sinfulness of drugs and level of peer religiousness mediate the relationship between theistic beliefs and religious/spiritual practices on substance use. Limitations and future analyses are discussed.

This study focuses on the quantification of genetic and environmental factors in arm strength after high-resistance strength training.

This study focuses on the quantification of genetic and environmental sources of variation in physical fitness components in 105 10-yr-old twin pairs and their parents. Nine motor tests and six skinfold measures were administered. Motor tests can be divided into those that are performance-related: static strength, explosive strength, running speed, speed of limb movement, and balance; and those that are health-related: trunk strength, functional strength, maximum oxygen uptake, and flexibility. The significance and contribution of genetic and environmental factors to variation in physical fitness were tested with model fitting. Performance-related fitness characteristics were moderately to highly heritable. The heritability estimates were slightly higher for health-related fitness characteristics. For most variables a simple model including genetic and specific environmental factors fitted the observed phenotypic variance well. Common environmental factors explained a significant part of the variation in speed components and flexibility. Assortative mating was significant and positive for speed components, balance, trunk strength, and cardiorespiratory fitness, but negative for adiposity. Static strength, explosive strength, functional strength, and cardiorespiratory fitness showed evidence for reduced genetic transmission or dominance. The hypothesis that performance-related fitness characteristics are more determined by genetic factors than health-related fitness was not supported. At this prepubertal age, genetic factors have the predominant effect on fitness.

Thomis, Martine A., Marc Van Leemputte, Hermine H. Maes, Cameron J. R. Blimkie, Albrecht L. Claessens, Guy Marchal, Eustachius Willems, Robert F. Vlietinck, and Gaston P. Beunen. Multivariate genetic analysis of maximal isometric muscle force at different elbow angles. J. Appl. Physiol.82(3): 959–967, 1997.—The maximal isometric moment at five different elbow joint angles was measured in 25 monozygotic and 16 dizygotic male adult twin pairs (22.4 ± 3.7 yr). Genetic model fitting was used to quantify the genetic and environmental contributions to individual differences in isometric strength. Additive genetic factors explained 66–78% of the variance in maximal torque at 170–140–110 and 80° flexion (extension = 180°). At 50° flexion, common and subject-specific environmental factors contributed equally to the variation. The contribution of unique environmental factors concurs with the level of variability in muscle activation and (dis)-comfort of torque production in the specific angle. The relative contribution of lever arm and force-length relationship in torque varies according to the angle. Because these factors might be genetic, this variability is reflected in the genetic contribution at the extreme angles of 170 and 50°. Multivariate analyses suggested a general set of genes that control muscle area and isometric strength, together with a more specific strength factor. Genetic correlations were high (0.82–0.99). Genes responsible for arm-segment lengths did not contribute to muscle area nor to isometric strength.

BACKGROUND: The Virginia Twin Study of Adolescent Behavioral Development is a cohort-longitudinal epidemiological study that uses the genetic twin design to study the development and maintenance of child psychiatric disorders. We determined the rates of DSM-III-R disorders, disorders with impairment, and age, sex, and co-morbidity effects. METHODS: Families of 2762 white twins aged 8 to 16 years participated. Twins and their parents were asked systematically about risk factors and current psychiatric symptoms by means of investigator-based psychiatric interviews and questionnaires. The DSM-III-R diagnoses were made for major depressive disorder, separation anxiety, overanxious disorder, simple phobia, social phobia, agoraphobia, oppositional defiant disorder, conduct disorder, and attention deficit hyperactivity disorder. RESULTS: The 3-month point prevalence for any DSM-III-R disorders was 413 per 1000, and that for disorders with associated impairment was 142 per 1000. Emotionnal disorders with impairment occurred in 89 per 1000, with girls being more commonly affected; behavioral disorders had a prevalence of 71 per 1000, with boys being more frequently affected. The proportion with disorder who also had functional impairment varied across disorders; anxiety and phobic disorders were particularly likely not to be accompanied by impairment. Rates of emotional and behavioral disorders increased over the age range. There was extensive comorbidity among disorders. CONCLUSIONS: The prevalence rates and patterns of findings from this study of twins are consistent with those of other epidemiological studies, supporting previous findings of few differences in rates of psychiatric disorder between twins and singletons. The importance of including measures of functional impairment is evident by its effect on rates of disorder and patterns of comorbidity.