Individual-specific Environment Research Articles

Phenotypic and familial associations between childhood maltreatment and cannabis initiation and problems in young adult European-American and African-American women

BackgroundChildhood maltreatment is a known risk factor for cannabis initiation and problem use, but the extent to which this association is attributable to shared familial influences is unknown. We estimate the magnitude of associations between childhood maltreatment, timing of cannabis initiation, and cannabis-related problems, in European-American (EA) and African-American (AA) women, and parse the relative influence of additive genetic (A), shared environmental (C), and individual-specific environmental (E) factors on these constructs and their covariation. MethodsData were from diagnostic telephone interviews conducted with 3786 participants (14.6% AA) in a population-based study of female twins. Logistic regression analyses and twin modeling were used to test for associations, and estimate the relative contributions of genetic and environmental influences to childhood maltreatment and cannabis outcomes and their covariation. ResultsMaltreatment was significantly associated with increased likelihood of cannabis initiation before age 15 among EAs (OR=6.33) and AAs (OR=3.93), but with increased likelihood of later initiation among EAs only (OR=1.68). Maltreatment was associated with cannabis problems among both groups (EA OR=2.32; AA OR=2.03). Among EA women, the covariation between maltreatment and cannabis outcomes was primarily attributable to familial environment (rC=0.67–0.70); among AAs, only individual-specific environment contributed (rE=0.37–0.40). ConclusionChildhood maltreatment is a major contributor to early initiation of cannabis as well as progression to cannabis problems in both AA and EA women. Distinctions by race/ethnicity are not in the relative contribution of genetic factors, but rather in the type of environmental influences that contribute to stages of cannabis involvement.

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.

Prevalence, Incidence Proportion, and Heritability for Tinnitus: A Longitudinal Twin Study.

The purpose of this longitudinal twin study was to explore the effect of tinnitus on hearing thresholds and threshold shifts over two decades and to investigate the genetic contribution to tinnitus in a male twin cohort (n = 1114 at baseline and 583 at follow-up). The hypothesis was that participants with faster hearing deterioration had a higher risk for developing tinnitus and there is an underlying role of genetic influences on tinnitus. Male mono- and dizygotic twin pairs, born between 1914 and 1958 were included. Mixed models were used for comparison of hearing threshold shifts, adjusted for age. A co-twin comparison was made within pairs discordant for tinnitus. The relative influence of genetic and environmental factors was estimated by genetic modeling. The overall prevalence of tinnitus was 13.5% at baseline ((Equation is included in full-text article.)age 50) and 34.4% at follow-up ((Equation is included in full-text article.)age 67). The overall incidence proportion was 27.8%. Participants who reported tinnitus at baseline or at both time points were older. At baseline, the hearing thresholds differed between tinnitus cases and controls at all frequencies. New tinnitus cases at follow-up had the greatest hearing threshold shift at the high-frequency area compared with the control group. Within pairs, the tinnitus twin had poorer hearing than his unaffected co-twin, more so for dizygotic than monozygotic twin pairs. The relative proportion of additive genetic factors was approximately 0.40 at both time points, and the influence of individual-specific environment was 0.56 to 0.61. The influence of genetic factors on tinnitus was largely independent of genetic factors for hearing thresholds. Our hypotheses were confirmed: The fastest hearing deterioration occurred for new tinnitus cases. A moderate genetic influence for tinnitus was confirmed.

Differences between White and Black young women in the relationship between religious service attendance and alcohol involvement.

We examined the associations of religious attendance during childhood (C-RA) and adulthood (A-RA) with alcohol involvement (ever drinking, timing of first alcohol use, and alcohol use disorder [AUD]) in White and Black female twins. As genetic and environmental factors influence religious attendance and alcohol involvement, we examined the extent to which they contribute to their association. Data on 3,234 White and 553 Black female twins (18-29 years) from the Missouri Adolescent Female twin Study. Significant correlations between C-RA or A-RA and alcohol involvement were parsed into their additive genetic, shared environmental, and individual-specific environmental sources. C-RA was associated with ever drinking and timing of first alcohol use in Whites. A-RA was associated with ever drinking and AUD in both Whites and Blacks. Shared environmental influences did not contribute to alcohol or religiosity phenotypes in Blacks. In Whites, the association between C-RA and alcohol was due to shared environmental influences, whereas the association between A-RA and alcohol was attributable to additive genetic, shared environmental, and individual-specific environmental sources. Individual-specific environment and genetics contributed to associations between A-RA and ever drinking and AUD, respectively, in Blacks. Factors other than C-RA contribute to lower rates of alcohol involvement in Blacks. Shared environment does not contribute to links between A-RA and alcohol involvement in Blacks. The protective impact of childhood religiosity on alcohol use and misuse is important in Whites and is due to familial factors shared by religiosity and alcohol involvement. (Am J Addict 2017;26:437-445).

A novel sibling-based design to quantify genetic and shared environmental effects: application to drug abuse, alcohol use disorder and criminal behavior.

Twin studies have been criticized for upwardly biased estimates that might contribute to the missing heritability problem. We identified, from the general Swedish population born 1960-1990, informative sibships containing a proband, one reared-together full- or half-sibling and a full-, step- or half-sibling with varying degrees of childhood cohabitation with the proband. Estimates of genetic, shared and individual specific environment for drug abuse (DA), alcohol use disorder (AUD) and criminal behavior (CB), assessed from medical, legal or pharmacy registries, were obtained using Mplus. Aggregate estimates of additive genetic effects for DA, AUD and CB obtained separately in males and females varied from 0.46 to 0.73 and agreed with those obtained from monozygotic and dizygotic twins from the same population. Of 54 heritability estimates from individual classes of informative sibling trios (3 syndromes × 9 classes of trios × 2 sexes), heritability estimates from the siblings were lower, tied and higher than those from obtained from twins in 26, one and 27 comparisons, respectively. By contrast, of 54 shared environmental estimates, 33 were lower than those found in twins, one tied and 20 were higher. With adequate information, human populations can provide many methods for estimating genetic and shared environmental effects. For the three externalizing syndromes examined, concerns that heritability estimates from twin studies are upwardly biased or were not generalizable to more typical kinds of siblings were not supported. Overestimation of heritability from twin studies is not a likely explanation for the missing heritability problem.

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

The 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. Five 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. All 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. With the exception of body dissatisfaction in boys, psychological traits of eating disorders show heritability patterns that differ according to sex.

Suicide attempts in a national population of twins concordant for psychoses

Psychotic disorders are associated with an increased risk of suicide attempts, the etiology of which remains unknown across diagnoses. Thus it is relevant to understand how genetic and environmental factors contribute to the liability of suicide attempts in psychosis. The current study aims to examine the role of genetic and environmental factors in suicide attempts across psychotic disorders in twins concordant for psychosis. The study population consisted of all twin pairs in the Israeli National Psychiatric Case Registry hospitalized with a last discharge diagnosis of a psychotic disorder. Twin pairs (N=116) were born between 1900 and 1993 and hospitalized from 1964 to 2001. Competing genetic models were examined to decompose the variance in suicide attempts into: the individual-specific environment (unique), shared-family environment, and genetic effects. Across schizophrenia, psychosis and non-affective psychosis comparison of genetic models showed a model combining shared-family and unique environmental effects were superior to competing genetic models. Modeling estimates for attempted suicide were: in non-affective psychosis 60% to the shared-family and 40% to the unique environment; in schizophrenia 60% to the shared-family and 40% to the unique environment; and in psychosis 66% to the shared-family and 34% to the unique environment. Across psychosis, schizophrenia and non-affective psychosis vulnerability toward suicide attempts consists predominantly of substantial individual and familial environmental elements.

Initial reactions to tobacco and cannabis smoking: a twin study

AbstractBackground and AimsInitial subjective reactions to cannabis and tobacco, broadly classified as positive or negative, have previously been explored for their associations with onset and maintenance of subsequent abuse/dependence. We examine (i) the factorial architecture of self‐reported initial reactions to cannabis and tobacco; (ii) whether these factors associate with concurrently reported age at onset of DSM‐IV diagnosis of nicotine dependence and cannabis abuse/dependence; and (iii) estimate heritable variation in and covariation between the factors.DesignFactorial and exploratory structural equation modeling was conducted to examine the factor structure of initial reactions. Cox proportional hazards modeling was employed to examine their association with time to onset of diagnosis of DSM‐IV nicotine dependence and cannabis abuse/dependence. Classical twin modeling, using univariate and multivariate models, was used to parse variance in each factor (and the covariance between factors) to their additive genetic, shared environmental and non‐shared environmental sources.Setting and ParticipantsGeneral population sample of Caucasian female twins aged 18–32 years, with a life‐time history of tobacco [n = 2393] and cannabis [n = 1445] use.MeasurementSelf‐report of initial subjective reactions to tobacco (cigarettes) and cannabis the first time they were used and time to onset of life‐time history of DSM‐IV diagnosis of abuse (cannabis) and dependence (cannabis or nicotine).FindingsFactors representing putatively positive and negative reactions to cannabis and tobacco emerged. Initial reactions to tobacco were associated with onset of DSM‐IV diagnosis of nicotine dependence and cannabis abuse/dependence while initial reactions to cannabis were associated with onset of DSM‐IV diagnosis of cannabis abuse/dependence alone. Genetic factors played a moderate role in each factor (heritability of 27–35%, P < 0.05), with the remaining variance attributed to individual–specific environment. Covariation across the factors indexing positive and negative initial reactions was attributable to genetic sources (0.18–0.58, P < 0.05) and to overlapping individual‐specific environmental factors (−0.16 to 0.36, P < 0.05).ConclusionsInitial subjective reactions to tobacco are associated with onset of DSM‐IV diagnosis of nicotine dependence and cannabis abuse/dependence while initial subjective reactions to cannabis are only associated with onset of diagnosis of DSM‐IV cannabis abuse/dependence. Genetic and environmental factors underpin the overlap across the factors representing initial reactions, both positive and negative.

Three-and-a-Half-Factor Model? The Genetic and Environmental Structure of the CBCL/6–18 Internalizing Grouping

In the present article, multivariate genetic item analyses were employed to address questions regarding the ontology and the genetic and environmental etiology of the Anxious/Depressed, Withdrawn, and Somatic Complaints syndrome dimensions of the Internalizing grouping of the Child Behavior Checklist/6-18 (CBCL/6-18). Using common and independent pathway genetic factor modeling, it was examined whether these syndrome dimensions can be ascribed a realist ontology. Subsequently, the structures of the genetic and environmental influences giving rise to the observed symptom covariation were examined. Maternal ratings of a population-based sample of 17,511 Dutch twins of mean age 7.4 (SD = 0.4) on the items of the Internalizing grouping of the Dutch CBCL/6-18 were analyzed. Applications of common and independent pathway modeling demonstrated that the Internalizing syndrome dimensions may be better understood as a composite of unconstrained genetic and environmental influences than as causally relevant entities generating the observed symptom covariation. Furthermore, the results indicate a common genetic basis for anxiety, depression, and withdrawn behavior, with the distinction between these syndromes being driven by the individual-specific environment. Implications for the substantive interpretation of these syndrome dimensions are discussed.

Stable genes and changing environments: body mass index across adolescence and young adulthood.

The transition between adolescence and young adulthood is a developmentally sensitive time where children are at an increased risk for becoming overweight and developing obesity. Twin studies have reported that body mass index [BMI] is highly heritable, however, it remains unclear whether the genetic influences are sex-limited and whether non-additive genetic influences contribute to body mass index [BMI] during these ages. In the current report, we examined self-reported data on BMI in same [n = 2,744] and opposite-sex [n = 1,178] siblings participating in the National Longitudinal Study on Adolescent Health [Add Health]. To investigate whether the same or different genes contributed to BMI for both sexes, we fit quantitative sex-limited genetic models to three waves of data collection. At each of the three Waves of assessment, models that included additive genetic, individual-specific environment, and no sex-limited genetic influences fit the data most parsimoniously. Heritable effects on BMI at each of the three Waves were large for both sexes and ranged between .75 and .86. While genetic contributions across the ages were highly correlated, longitudinal analyses indicated that the relevant individual-specific environmental influences on BMI in adolescence and young adulthood change sizably. These results underscore the importance of understanding early genetic influences on BMI and highlight the role environmental experiences have at later ages when new genetic influences appear to make a small contribution to individual variation in BMI.

Genetic and Environmental Effects on Same-sex Sexual Behavior: A Population Study of Twins in Sweden

There is still uncertainty about the relative importance of genes and environments on human sexual orientation. One reason is that previous studies employed self-selected, opportunistic, or small population-based samples. We used data from a truly population-based 2005-2006 survey of all adult twins (20-47 years) in Sweden to conduct the largest twin study of same-sex sexual behavior attempted so far. We performed biometric modeling with data on any and total number of lifetime same-sex sexual partners, respectively. The analyses were conducted separately by sex. Twin resemblance was moderate for the 3,826 studied monozygotic and dizygotic same-sex twin pairs. Biometric modeling revealed that, in men, genetic effects explained .34-.39 of the variance, the shared environment .00, and the individual-specific environment .61-.66 of the variance. Corresponding estimates among women were .18-.19 for genetic factors, .16-.17 for shared environmental, and 64-.66 for unique environmental factors. Although wide confidence intervals suggest cautious interpretation, the results are consistent with moderate, primarily genetic, familial effects, and moderate to large effects of the nonshared environment (social and biological) on same-sex sexual behavior.

The heritability of hedonic capacity and perceived stress: a twin study evaluation of candidate depressive phenotypes

Anhedonia and stress sensitivity have been identified as promising depressive phenotypes. Research suggests that stress-induced anhedonia is a possible mechanism underlying the association between stress and depression. The present proof-of-concept study assessed whether hedonic capacity and stress perception are heritable and whether their genetic and environmental contributions are shared. Twenty monozygotic (MZ) and 15 dizygotic (DZ) twin pairs completed a probabilistic reward task that provides an objective behavioral measure of hedonic capacity (reward responsiveness) and completed several questionnaires including the Perceived Stress Scale (PSS). Bivariate Cholesky models were used to investigate whether covariation between (1) depressive symptoms and hedonic capacity, (2) depressive symptoms and perceived stress, and (3) perceived stress and hedonic capacity resulted from shared or residual genetic and environmental factors. Additive genetic (A) and individual-specific environment (E) factors contributed to 46% and 54% of the variance in hedonic capacity, respectively. For perceived stress, 44% and 56% of the variance was accounted for by A and E factors, respectively. The genetic correlation between depression and hedonic capacity was moderate (ra=0.29), whereas the correlation between depression and stress perception was large (ra=0.67). Genetic and environmental correlations between hedonic capacity and stress perception were large (ra=0.72 and re=-0.43). The present study provides initial feasibility for using a twin approach to investigate genetic contributions of a laboratory-based anhedonic phenotype. Although these preliminary findings indicate that hedonic capacity and perceived stress are heritable, with substantial shared additive genetic contributions, replications in larger samples will be needed.

Heritability of flow-mediated dilation: a twin study.

Endothelial dysfunction assessed by brachial artery flow-mediated dilation (FMD) is a marker for early atherosclerotic vascular disease and future cardiovascular events. To estimate the heritability of brachial artery FMD using a twin design. We estimated the heritability of FMD using 94 middle-aged male twin pairs. FMD was measured by ultrasound, and traditional coronary heart disease risk factors were measured. Genetic modeling techniques were used to determine the relative contributions of genes and environment to the variation in FMD. The mean age of the twin participants was 54.9 +/- 2.8 years. The mean FMD was 0.047 +/- 0.030. The intraclass correlation coefficient was higher in MZ twins [0.38, 95% confidence interval (CI) 0.32-0.43] than in DZ twins (0.19, 95% CI 0.11-0.26), suggesting a role of genetic influence in FMD variation. Structural equation modeling showed that both genetic and unique environmental factors contributed significantly to the variation in FMD. The crude FMD heritability was 0.37 (95% CI 0.15-0.54). After adjustment for traditional cardiovascular risk factors, including age, total cholesterol, blood pressure, and body mass index, the heritability of FMD was 39% (95% CI 0.18-0.56). The remaining variation in FMD could be explained by individual-specific environment. This is the first study using twins to estimate the relative contributions of genetics and environment to the variation in FMD in a US population. Our results demonstrate a moderate genetic effect on brachial artery FMD, independent of traditional coronary risk factors. Our data also highlight the importance of unique environment on the variability in FMD.

Creating a Social World

Peer-group deviance is strongly associated with externalizing behaviors. We have limited knowledge of the sources of individual differences in peer-group deviance. To clarify genetic and environmental contributions to peer-group deviance in twins from midchildhood through early adulthood. Retrospective assessments using a life-history calendar. Analysis by biometric growth curves. General community. Members of male-male pairs from the population-based Virginia Twin Registry personally interviewed in 1998-2004 (n = 1802). Self-reported peer-group deviance at ages 8 to 11, 12 to 14, 15 to 17, 18 to 21, and 22 to 25 years. Mean and variance of peer-group deviance increased substantially with age. Genetic effects on peer-group deviance showed a strong and steady increase over time. Family environment generally declined in importance over time. Individual-specific environmental influences on peer-group deviance levels were stable in the first 3 age periods and then increased as most twins left home. When standardized, the heritability of peer-group deviance is approximately 30% at ages 8 to 11 years and rises to approximately 50% across the last 3 time periods. Both genes and shared environment contributed to individual differences in the developmental trajectory of peer-group deviance. However, while the correlation between childhood peer-group deviance levels and the subsequent slope of peer-group deviance over time resulting from genetic factors was positive, the same relationship resulting from shared environmental factors was negative. As male twins mature and create their own social worlds, genetic factors play an increasingly important role in their choice of peers, while shared environment becomes less influential. The individual-specific environment increases in importance when individuals leave home. Individuals who have deviant peers in childhood, as a result of genetic vs shared environmental influences, have distinct developmental trajectories. Understanding the risk factors for peer-group deviance will help clarify the etiology of a range of externalizing psychopathology.

Sex differences in genetic and environmental determinants of pulse pressure

Pulse pressure (PP) is an independent risk factor for cardiovascular disease. PP rises with age, more so in women. We examined sex differences in the correlations and variance components of PP in adult subjects from 767 nuclear families, enriched with those containing twins, from the Victorian Family Heart Study. After adjusting for age, we found no significant differences in the means or variances of PP in males and females. Under the assumption of no sex differences, the proportions of variance due to shared genes, shared environment, and individual-specific environment were 20%, 23% and 57%, respectively. However, same-sex relative pairs had significantly higher correlations than opposite-sex pairs (P = 0.005), implying the existence of sex-dependent effects. Extensions to the simple variance components model suggested three possible explanations for these differences: smaller genetic correlation between opposite-sex pairs (rhoG,MF = 0.45, P = 0.007); smaller environmental correlation between opposite-sex pairs (P = 0.0003); or different environmental and genetic correlations obtained by estimating genetic, environmental, and individual variance components separately for males and females (not nested, Akaike's Information Criterion (AIC) smaller by 6.69). Under the last model, the genetic component of PP variance is greater for males (1.62 vs 0.33) while the environmental component is greater for females (1.84 vs 0), which would have implications for the planning of gene discovery studies, since heritability would be higher in males. However, the second (environmental) approach best fits the data according to the AIC. Genetic explanations for sex differences in phenotypic correlations may be misleading unless shared environmental factors are also considered. PP illustrates a phenotype in which sex dependency represents an important component of phenotypic determination that can be revealed by detailed variance components modelling.

Genetic and Environmental Influences on Temperament in the First Year of Life: The Puerto Rico Infant Twin Study (PRINTS)

AbstractThree dimensions of temperament — difficult temperament, unadaptablility and unsociability — were assessed in the first year of life by maternal interview in twins born in Puerto Rico during 2001 and 2002. Eight hundred and sixty-five eligible mothers (80%) were traced and interviewed. Model- fitting results showed that additive genetic factors and the individual specific environment contributed to variation in all three dimensions. In addition, the pattern of variances and correlations suggested that sibling contrast effects influence ratings of difficult temperament. Moderate effects of the shared environment contributed to ratings of adaptability and sociability. There was a significant genetic correlation between difficult temperament and unadaptability. Genetic and environmental effects do not differ significantly between boys and girls. The study is the first population-based study of Puerto Rican twins and one of few to attempt the assessment of behavior in the first year. Preliminary results for difficult temperament and sociability were consistent with those in other populations and ages. In contrast, a significant effect of the shared environment on the temperamental trait of unadaptability has not been reported previously.

Genetic and Environmental Influences on Temperament in the First Year of Life: The Puerto Rico Infant Twin Study (PRINTS)

Three dimensions of temperament -- difficult temperament, unadaptablility and unsociability -- were assessed in the first year of life by maternal interview in twins born in Puerto Rico during 2001 and 2002. Eight hundred and sixty-five eligible mothers (80%) were traced and interviewed. Model-fitting results showed that additive genetic factors and the individual specific environment contributed to variation in all three dimensions. In addition, the pattern of variances and correlations suggested that sibling contrast effects influence ratings of difficult temperament. Moderate effects of the shared environment contributed to ratings of adaptability and sociability. There was a significant genetic correlation between difficult temperament and unadaptability. Genetic and environmental effects do not differ significantly between boys and girls. The study is the first population-based study of Puerto Rican twins and one of few to attempt the assessment of behavior in the first year. Preliminary results for difficult temperament and sociability were consistent with those in other populations and ages. In contrast, a significant effect of the shared environment on the temperamental trait of unadaptability has not been reported previously.

Brain MRI abnormalities in schizophrenia: same genes or same environment?

Structural brain volume abnormalities are among the most extensively studied endophenotypes in schizophrenia. Bivariate genetic model fitting (adjusted to account for selection) was used to quantify the genetic relationship between schizophrenia and brain volumes and to estimate the heritability of these volumes. We demonstrated by simulation that the adjusted genetic model produced unbiased estimates for endophenotype heritability and the genetic and environmental correlations. The model was applied to brain volumes (whole brain, hippocampus, third and lateral ventricles) in a sample of 14 monozygotic (MZ) twin pairs concordant for schizophrenia, 10 MZ discordant pairs, 17 MZ control pairs, 22 discordant sibling pairs, three concordant sibling pairs, and 114 healthy control subjects. Whole brain showed a substantial heritability (88%) and lateral ventricles substantial common environmental effects (67%). Whole brain showed a significant genetic correlation with schizophrenia, whereas lateral ventricles showed a significant individual specific correlation with schizophrenia. There were significant familial effects for hippocampus and third ventricle, but the analyses could not resolve whether these were genetic or environmental in origin (around 30%each). Using genetic model fitting on twin and sibling data we have demonstrated differential sources of covariation between schizophrenia and brain volumes, genetic in the case of whole brain volume and individual specific environment in the case of lateral ventricles.

A twin study of genetic and environmental influences on psychological traits of eating disorders in a Japanese female sample.

The purpose of the present study was to clarify genetic and environmental origins of psychological traits of eating disorders using a Japanese female twin sample. Participants were 162 pairs of female twins consisting of 116 pairs of monozygotic (MZ) twins and 46 pairs of dizygotic (DZ) twins in their adolescence. Psychological traits of eating disorders were assessed with five subscales of the Eating Disorder Inventory (EDI). As a result of using univariate twin analyses, among five subscales of EDI (maturity fears, ineffectiveness, interpersonal distrust, interoceptive awareness, and perfectionism), perfectionism showed significant additive genetic contributions and individual specific environmental effects. On the other hand, maturity fears, ineffectiveness, interoceptive awareness, and interpersonal distrust indicated significant shared environment contributions and individual specific environment effects. The results suggest the importance of both genetic and shared environmental influences on psychological traits of eating disorders in the present study.

A Twin Study of Genetic and Environmental Influences on Psychological Traits of Eating Disorders in a Japanese Female Sample

The purpose of the present study was to clarify genetic and environmental origins of psychological traits of eating disorders using a Japanese female twin sample. Participants were 162 pairs of female twins consisting of 116 pairs of monozygotic (MZ) twins and 46 pairs of dizygotic (DZ) twins in their adolescence. Psychological traits of eating disorders were assessed with five subscales of the Eating Disorder Inventory (EDI). As a result of using univariate twin analyses, among five subscales of EDI (maturity fears, ineffectiveness, interpersonal distrust, interoceptive awareness, and perfectionism), perfectionism showed significant additive genetic contributions and individual specific environmental effects. On the other hand, maturity fears, ineffectiveness, interoceptive awareness, and interpersonal distrust indicated significant shared environment contributions and individual specific environment effects. The results suggest the importance of both genetic and shared environmental influences on psychological traits of eating disorders in the present study.