Same-sex Dizygotic Twin Pairs Research Articles

Concurrent and longitudinal associations of developmental language disorder with peer victimization in adolescence: evidence from a co-twin study.

Children with developmental language disorder (DLD) experience higher levels of peer victimization than their peers. However, it is not known if such associations reflect genetic and environmental confounding. We used a co-twin control design to investigate the association of language difficulties (DLD and separately poor pragmatic language) with peer victimization and compare the developmental trajectories of peer victimization across adolescence for those with and without language difficulties. Participants were 3,400 pairs of twins in the Twins Early Development Study (TEDS), a UK-based population birth cohort. Language abilities were assessed via online tests at age 11 and peer victimization was self-reported at ages 11, 14 and 16. Language difficulties were defined as language abilities at least -1.25 SD below the mean of the TEDS sample. We performed linear regressions and latent growth curve modeling at a population level and within monozygotic and same-sex dizygotic twin pairs. At population level, youth with DLD experienced higher levels of peer victimization at ages 11 (β = 0.27, 95% Confidence Interval (CI) 0.20-0.35), 14 (β = 0.15, 95% CI 0.03-0.27) and 16 (β = 0.17, 95% CI 0.03-0.32) and a sharper decline in peer victimization between ages 11 and 16 compared to their peers without DLD. The associations between DLD and peer victimization were reduced in strength and not statistically significant in within-twin models. Moreover, there was no difference in the rate of change in peer victimization between twin pairs discordant for DLD. Results were similar for the association of poor pragmatic language with peer victimization. Associations between language difficulties (DLD and separately, poor pragmatic language) and peer victimization were confounded by genetic and shared environmental factors. Identifying specific factors underlying these associations is important for guiding future work to reduce peer victimization among adolescents with language difficulties.

Ocular and systemic associations and heritability of retinal arterial wall-to-lumen ratios in a twin cohort.

To investigate ocular and systemic factors associated with the retinal arterial wall-to-lumen ratio (WLR) and to determine the relative contribution of genetic and environmental variation to WLR in healthy adults. This cross-sectional twin study included 78 monozygotic and 67 dizygotic same-sex twin pairs aged 58.4 ± 9.8 (mean ± SD) years. Lumen diameter (LD) and outer diameter (OD) of a superotemporal retinal artery were measured using adaptive optics fundus photography, and the WLR was calculated. Linear mixed model regression analysis of associations with WLR comprised the descriptive variables ocular axial length (AL), intraocular pressure (IOP), height, weight, body mass index (BMI), smoking, blood pressure, high density (HDL), low density (LDL) and very low density (VLDL) lipoproteins, total cholesterol and triglycerides. The relative influence of genes and environment on WLR was calculated through polygenetic modelling. Increasing age and arterial blood pressure were associated with a higher WLR, while increasing retinal artery OD and ocular AL were associated with a lower WLR. Sex, smoking status, BMI, IOP, cholesterol levels or triglycerides had no detectable impact on the WLR. Broad-sense heritability of WLR was 21% (95% CI: 1-41%), while environmental factors accounted for the remaining 79% of the interindividual variance (95% CI: 59-99%). Retinal artery wall thickness was closely linked to increasing age and higher arterial blood pressure, the latter being mediated by the environment over genes.

Reconsidering the failure model: Using a genetically controlled design to assess the spread of problems from reactive aggression to internalizing symptoms through peer rejection across the primary school years.

According to the failure model (Patterson & Capaldi, 1990), peer rejection is the intermediary link between problem behaviors and internalizing symptoms. The present study tested the model with 464 monozygotic and same-sex dizygotic twin pairs (234 female, 230 male dyads). Teacher-reported reactive aggression and internalizing symptoms, and peer-reported peer rejection were collected at ages 6, 7, and 10 (from 2001 to 2008). Support for the failure model emerged in conventional non-genetically controlled analyses, but not twin-difference score analyses (which remove shared environmental and genetic contributions). Univariate biometric models attributed minimal variance in failure model variables to shared environmental factors, suggesting that genetic factors play an important unacknowledged role in developmental pathways historically ascribed to nonshared experiences in the failure model.

The sleep homeostatic response to sleep deprivation in humans is heritable.

Following sleep deprivation, increases in delta power have historically been used to index increases in sleep pressure. Research in mice has demonstrated that the homeostatic delta power response to sleep deprivation is heritable. Whether this is true in humans is unknown. In the present study, we used delta power and ORP, a novel measure of sleep depth, to investigate the effects of acute sleep deprivation on sleep depth and to assess the heritability of sleep homeostasis in humans. ORP and delta power were examined during baseline and recovery sleep following 38 h of sleep deprivation in 57 monozygotic and 38 dizygotic same-sex twin pairs. Two complementary methods were used to estimate the trait heritability of sleep homeostasis. During recovery sleep, ORP was lower and delta power was higher than at baseline, indicating deeper sleep. However, at the end of the recovery night, delta power reached baseline levels but ORP demonstrated incomplete recovery. Both ORP and delta power showed a broad sense heritability of sleep homeostasis following sleep deprivation. The classical approach demonstrated an h2 estimate of 0.43 for ORP and 0.73 for delta power. Mixed-effect multilevel models showed that the proportion of variance attributable to additive genetic transmission was 0.499 (95% CI = 0.316-0.682; p < .0001) for ORP and 0.565 (95% CI = 0.403-0.726; p < .0001 for delta power. These results demonstrate that the homeostatic response to sleep deprivation is a heritable trait in humans and confirm ORP as a robust measure of sleep depth.

Heritability of REM sleep neurophysiology in adolescence

Alterations of rapid eye movement (REM) sleep have long been observed in patients with psychiatric disorders and proposed as an endophenotype—a link between behavior and genes. Recent experimental work has shown that REM sleep plays an important role in the emotional processing of memories, emotion regulation, and is altered in the presence of stress, suggesting a mechanism by which REM sleep may impact psychiatric illness. REM sleep shows a developmental progression and increases during adolescence—a period of rapid maturation of the emotional centers of the brain. This study uses a behavioral genetics approach to understand the relative contribution of genes, shared environmental and unique environmental factors to REM sleep neurophysiology in adolescents. Eighteen monozygotic (MZ; n = 36; 18 females) and 12 dizygotic (DZ; n = 24; 12 females) same-sex twin pairs (mean age = 12.46; SD = 1.36) underwent whole-night high-density sleep EEG recordings. We find a significant genetic contribution to REM sleep EEG power across frequency bands, explaining, on average, between 75 to 88% of the variance in power, dependent on the frequency band. In the lower frequency bands between delta and sigma, however, we find an additional impact of shared environmental factors over prescribed regions. We hypothesize that these regions may reflect the contribution of familial and environmental stress shared amongst the twins. The observed strong genetic contribution to REM sleep EEG power in early adolescence establish REM sleep neurophysiology as a potentially strong endophenotype, even in adolescence—a period marked by significant brain maturation.

Smoking remains associated with education after controlling for social background and genetic factors in a study of 18 twin cohorts

We tested the causality between education and smoking using the natural experiment of discordant twin pairs allowing to optimally control for background genetic and childhood social factors. Data from 18 cohorts including 10,527 monozygotic (MZ) and same-sex dizygotic (DZ) twin pairs discordant for education and smoking were analyzed by linear fixed effects regression models. Within twin pairs, education levels were lower among the currently smoking than among the never smoking co-twins and this education difference was larger within DZ than MZ pairs. Similarly, education levels were higher among former smoking than among currently smoking co-twins, and this difference was larger within DZ pairs. Our results support the hypothesis of a causal effect of education on both current smoking status and smoking cessation. However, the even greater intra-pair differences within DZ pairs, who share only 50% of their segregating genes, provide evidence that shared genetic factors also contribute to these associations.

Parenting styles in relation to childhood obesity, smoking and drinking: A gene-environment interaction study.

The present study assessed gene-environment interactions linking maternal parenting styles to childhood obesity and alcohol and tobacco use. Data were retrieved from the first wave of the German Twin Family Panel. Participants comprised three birth cohorts, aged 5, 11 and 17 years, with approximately 500 pairs of same-sex monozygotic twins and 500 pairs of same-sex dizygotic twins per cohort. Self-reported parenting styles were measured in five dimensions: emotional warmth, psychological control, negative communication, monitoring and inconsistent parenting. Outcome variables included children's body mass index z-score (BMIz) and smoking and alcohol drinking frequency. Gene-environment interaction models were used to assess how parenting styles might moderate genetic and environmental influences on BMIz and smoking and drinking behaviours. A positive interaction of genetic effects with psychological control was found for BMIz at age 5 years, indicating that genetic influences on BMIz increased with psychological control. No interaction effect was found for BMIz at ages 11 and 17 years. Regarding adolescent smoking, positive interaction between genetic effects and negative communication was found, indicating that genetic influences on smoking increased with negative communication. There was no significant moderating effect of parenting styles on adolescent drinking. The present study found preliminary evidence indicating that parenting styles moderated genetic and environmental impacts on body weight status and smoking. Moderation effects of parenting on BMIz were observed only at a very young age. The moderating effects of parenting influenced adolescent smoking but not drinking.

Visual search: Heritability and association with general intelligence.

Visual search guides goal-directed action in humans and many other species, and it has been studied extensively in the past. Yet, no study has investigated the relative contributions of genes and environments to individual differences in visual search performance, or to which extent etiologies are shared with broader cognitive phenotypes. To address this gap, we studied visual search and general intelligence in 156 monozygotic (MZ) and 158 same-sex dizygotic (DZ) twin pairs. We found that different indexes of visual search performance (response latency and visual search efficiency) were moderately heritable. Phenotypic correlations between visual search and intelligence were small-to-moderate, and only a small proportion of the genetic variance in visual search was shared with genetic variance in intelligence. We discuss these findings in the context of the "generalist genes hypothesis" stating that different cognitive functions have a common genetic basis.

What Matters and What Matters Most for Survival After age 80? A Multidisciplinary Exploration Based on Twin Data.

Given research and public interest for conditions related to an extended lifespan, we addressed the questions of what matters and what matters most for subsequent survival past age 80. The data was drawn from the population-based and multidisciplinary Swedish OCTO Twin Study, in which a sample (N = 699) consisting of identical and same-sex fraternal twin pairs, followed from age 80 until death, provided detailed data on health, physical functioning, life style, personality, and sociodemographic conditions. Information concerning date of birth and death were obtained from population census register. We estimated heritability using an ACE model and evaluated the role of multiple predictors for the mortality-related hazard rate using Cox regression. Our findings confirmed a low heritability of 12%. As expected, longer survival was associated with being a female, an apolipoprotein E (APOE) e4 allele non-carrier, and a non-smoker. Several diseases were found to be associated with shorter survival (cerebrovascular, dementia, Parkinson’s, and diabetes) as well as certain health conditions (high diastolic blood pressure, low body mass index, and hip fracture). Stronger grip and better lung function, as well as better vision (but not hearing), and better cognitive function (self-evaluated and measured) was related to longer survival. Social embeddedness, better self-evaluated health, and life-satisfaction were also significantly associated with longer survival. After controlling for the impact of comorbidity, functional markers, and personality-related predictors, we found that sex, cerebrovascular diseases, compromised cognitive functioning, self-related health, and life-satisfaction remained as strong predictors. Cancer was only associated with the mortality hazard when accounting for other co-morbidities. The survival estimates were mostly in anticipated directions and contained effect sizes within the expected range. Noteworthy, we found that some of the so-called “soft-markers” remained strong predictors, despite a control for other factors. For example, self-evaluation of health and ratings of life-satisfaction provide additional and valuable information.

The familial and genetic contribution to the association between depression and cardiovascular disease: a twin cohort study

Depression and cardiovascular disease (ischemic heart disease and stroke) are associated in a bidirectional manner. Their relatively high heritability has led to the hypothesis that this co-occurrence is related to shared familial and genetic factors; this study aims to test this hypothesis. We included 23,498 monozygotic and 39,540 same-sex dizygotic twins from the Danish Twin Registry followed from January 1977 until December 2011 in nationwide Danish registries. We used survival analyses accounting for censoring and competing risk of death to estimate cumulative incidence, casewise concordance, relative recurrence risk, and heritability of the co-occurrence of depression and cardiovascular disease by age using monozygotic and same-sex dizygotic twin pairs. The casewise concordance of ischemic heart disease or stroke in twins whose co-twin was diagnosed with depression was at all ages similar for the monozygotic and dizygotic twin pairs and to the cumulative incidence of ischemic heart disease or stroke, respectively, in the entire twin population. A similar pattern was seen in analyses of depression risk given the co-twin being diagnosed with ischemic heart disease or stroke. Relative recurrence risk and heritability estimates were also of modest size and with confidence intervals including unity. Results were similar after stratification by gender as well as when redefining depression to include the use of antidepressant medication from 1995. Our findings do not support that co-occurrence between depression and cardiovascular disease is explainable by shared genetic factors, nor did we find strong evidence of a familial effect.

Spindles are highly heritable as identified by different spindle detectors.

Sleep spindles, a defining feature of stage N2 sleep, are maximal at central electrodes and are found in the frequency range of the electroencephalogram (EEG) (sigma 11-16 Hz) that is known to be heritable. However, relatively little is known about the heritability of spindles. Two recent studies investigating the heritability of spindles reported moderate heritability, but with conflicting results depending on scalp location and spindle type. The present study aimed to definitively assess the heritability of sleep spindle characteristics. We utilized the polysomnography data of 58 monozygotic and 40 dizygotic same-sex twin pairs to identify heritable characteristics of spindles at C3/C4 in stage N2 sleep including density, duration, peak-to-peak amplitude, and oscillation frequency. We implemented and tested a variety of spindle detection algorithms and used two complementary methods of estimating trait heritability. We found robust evidence to support strong heritability of spindles regardless of detector method (h2 > 0.8). However not all spindle characteristics were equally heritable, and each spindle detection method produced a different pattern of results. The sleep spindle in stage N2 sleep is highly heritable, but the heritability differs for individual spindle characteristics and depends on the spindle detector used for analysis.

Familial risk and heritability of depression by age at first diagnosis in Danish twins.

Familial and genetic factors seem to contribute to the development of depression but whether this varies with age at diagnosis remains unclear. We examined the influence of familial factors on the risk of depression by age at first diagnosis. We included 23498 monozygotic and 39540 same-sex dizygotic twins from the population-based Danish Twin Registry, followed from 1977 through 2011 in nationwide registers. We used time-to-event analyses accounting for censoring and competing risk of death to estimate cumulative incidence, casewise concordance, relative recurrence risk, and heritability of first depression by age using monozygotic and same-sex dizygotic twin pairs. During follow-up, a total of 1545 twins were diagnosed with depression. For twins at age 35 or younger at first depression, heritability was estimated to be 24.8% (95% confidence interval [CI], 4.6-43.1%), whereas at age 90 it was 14.7% (95% CI, 3.1-26.3%). The relative recurrence risk was higher at younger ages: At age 35, the risk was 27.7-fold (95% CI, 20.0-35.5) and 6.9-fold (95% CI, 3.9-9.8) higher than the population risk for monozygotic and same-sex dizygotic twins, respectively, while the corresponding numbers were 3.0 (95% CI, 2.3-3.6) and 1.8 (95% CI, 1.3-2.2) at age 90. Heritability seemed similar for male and female twins. Familial risk of depression, caused either by genes or shared environment, seemed to slightly decrease with age at diagnosis and an elevated concordance risk for monozygotic over same-sex dizygotic pairs suggested a genetic contribution to the development of depression.

Higher aggression is related to poorer academic performance in compulsory education.

To conduct a comprehensive assessment of the association between aggression and academic performance in compulsory education. We studied aggression and academic performance in over 27,000 individuals from four European twin cohorts participating in the ACTION consortium (Aggression in Children: Unraveling gene-environment interplay to inform Treatment and InterventiON strategies). Individual level data on aggression at ages 7-16 were assessed by three instruments (Achenbach System of Empirically Based Assessment, Multidimensional Peer Nomination Inventory, Strengths and Difficulties Questionnaire) including parental, teacher and self-reports. Academic performance was measured with teacher-rated grade point averages (ages 12-14) or standardized test scores (ages 12-16). Random effect meta-analytical correlations with academic performance were estimated for parental ratings (in all four cohorts) and self-ratings (in three cohorts). All between-family analyses indicated significant negative aggression-academic performance associations with correlations ranging from -.06 to -.33. Results were similar across different ages, instruments and raters and either with teacher-rated grade point averages or standardized test scores as measures of academic performance. Meta-analytical r's were -.20 and -.23 for parental and self-ratings, respectively. In within-family analyses of all twin pairs, the negative aggression-academic performance associations were statistically significant in 14 out of 17 analyses (r=-.17 for parental- and r=-.16 for self-ratings). Separate analyses in monozygotic (r=-.07 for parental and self-ratings), same-sex dizygotic (r's=-.16 and -.17 for parental and self-ratings) and opposite-sex dizygotic (r's=-.21 and -.19 for parental and self-ratings) twin pairs suggested partial confounding by genetic effects. There is a robust negative association between aggression and academic performance in compulsory education. Part of these associations were explained by shared genetic effects, but some evidence of a negative association between aggression and academic performance remained even in within-family analyses of monozygotic twin pairs.

The German Twin Family Panel (TwinLife).

The German Twin Family Panel (TwinLife) is a German longitudinal study of monozygotic and dizygotic same-sex twin pairs and their families that was designed to investigate the development of social inequalities over the life course. The study covers an observation period from approximately 2014 to 2023. The target population of the sample are reared-together twins of four different age cohorts that were born in 2009/2010 (cohort 1), in 2003/2004 (cohort 2), in 1997/1998 (cohort 3) and between 1990 and 1993 (cohort 4). In the first wave, the study included data on 4097 twin families. Families were recruited in all parts of Germany so that the sample comprises the whole range of the educational, occupational and income structure. As of 2019, two face-to-face, at-home interviews and two telephone interviews have been conducted. Data from the first home and telephone interviews are already available free of charge as a scientific use-file from the GESIS data archive. This report aims to provide an overview of the study sample and design as well as constructs that are unique in TwinLife in comparison with previous twin studies - such as an assessment of cognitive abilities or information based on the children's medical records and report cards. In addition, major findings based on the data already released are displayed, and future directions of the study are presented and discussed.

Heritability of Type 2 Diabetes in the Washington State Twin Registry.

Approximately 12% of U.S. adults have type 2 diabetes (T2D). Diagnosed T2D is caused by a combination of genetic and environmental factors including age and lifestyle. In adults 45 years and older, the Discordant Twin (DISCOTWIN) consortium of twin registries from Europe and Australia showed a moderate-to-high contribution of genetic factors of T2D with a pooled heritability of 72%. The purpose of this study was to investigate the contributions of genetic and environmental factors of T2D in twins 45 years and older in a U.S. twin cohort (Washington State Twin Registry, WSTR) and compare the estimates to the DISCOTWIN consortium. We also compared these estimates with twins under the age of 45. Data were obtained from 2692 monozygotic (MZ) and same-sex dizygotic (DZ) twin pairs over 45 and 4217 twin pairs under 45 who responded to the question 'Has a doctor ever diagnosed you with (type 2) diabetes?' Twin similarity was analyzed using both tetrachoric correlations and structural equation modeling. Overall, 9.4% of MZ and 14.7% of DZ twins over the age of 45 were discordant for T2D in the WSTR, compared to 5.1% of MZ and 8% of DZ twins in the DISCOTWIN consortium. Unlike the DISCOTWIN consortium in which heritability was 72%, heritability was only 52% in the WSTR. In twins under the age of 45, heritability did not contribute to the variance in T2D. In a U.S. sample of adult twins, environmental factors appear to be increasingly important in the development of T2D.

Characterizing genetic and environmental influences on variable DNA methylation using monozygotic and dizygotic twins.

Variation in DNA methylation is being increasingly associated with health and disease outcomes. Although DNA methylation is hypothesized to be a mechanism by which both genetic and non-genetic factors can influence the regulation of gene expression, little is known about the extent to which DNA methylation at specific sites is influenced by heritable as well as environmental factors. We quantified DNA methylation in whole blood at age 18 in a birth cohort of 1,464 individuals comprising 426 monozygotic (MZ) and 306 same-sex dizygotic (DZ) twin pairs. Site-specific levels of DNA methylation were more strongly correlated across the genome between MZ than DZ twins. Structural equation models revealed that although the average contribution of additive genetic influences on DNA methylation across the genome was relatively low, it was notably elevated at the highly variable sites characterized by intermediate levels of DNAm that are most relevant for epigenetic epidemiology. Sites at which variable DNA methylation was most influenced by genetic factors were significantly enriched for DNA methylation quantitative trait loci (mQTL) effects, and overlapped with sites where inter-individual variation correlates across tissues. Finally, we show that DNA methylation at sites robustly associated with environmental exposures such as tobacco smoking and obesity is also influenced by additive genetic effects, highlighting the need to control for genetic background in analyses of exposure-associated DNA methylation differences. Estimates of the contribution of genetic and environmental influences to DNA methylation at all sites profiled in this study are available as a resource for the research community (http://www.epigenomicslab.com/online-data-resources).

Links Between the Mother–Adolescent and Father–Adolescent Relationships and Adolescent Depression: A Genetically Informed Study

This study examined the unique roles of support and conflict in the relationship with the mother and the father in predicting changes in adolescents’ depressive symptoms over a 1-year period. Potential moderating effects of genetic factors (Gene × Environment interaction) and sex were also investigated. This study utilized a design of twins raised in the same family, based on a sample of 121 monozygotic and 88 dizygotic same-sex twin pairs (418 individuals; 52.2% girls) assessed in Grade 8 (M = 14.09, SD = .29) and in Grade 9 (M = 15.07, SD = .26). Depressive symptoms and the parent–adolescent relationship quality were measured with self-report questionnaires. Multilevel regressions revealed that a lack of support in the father–adolescent relationship predicted increased depressive symptoms among all adolescents, whereas conflict in the father–adolescent relationship predicted increased depressive symptoms more strongly as adolescents’ genetic vulnerability for depressive symptoms increased. Moreover, a high level of support in the relationship with the mother predicted increased depressive symptoms in boys—but not girls—with a high genetic risk for such problems. In line with a diathesis-stress model of psychopathology, these findings suggest that relationship quality with both parents might impact girls’ and boys’ depressive symptoms but that these associations depend to some extent on adolescents’ genetic vulnerabilities.

The etiology of autistic traits in preschoolers: a population-based twin study.

Autism Spectrum Disorders (ASD) are highly heritable, but the exact etiological mechanisms underlying the condition are still unclear. Using a multiple rater twin design in a large sample of general population preschool twins, this study aimed to (a) estimate the contribution of genetic and environmental factors to autistic traits, controlling for the possible effects of rater bias, (b) to explore possible sex differences in etiology and (c) to investigate the discordance in autistic traits in monozygotic and same-sex dizygotic twin pairs. The Netherlands Twin Register collected maternal and paternal ratings on autistic traits from a general population of 38,798 three-year-old twins. Autistic traits were assessed with the DSM-oriented Pervasive Developmental Problems scale of the Child Behavior Check List for preschoolers (1½-5years). Mother and fathers showed high agreement in their assessment of autistic traits (r=.60-.66). Differences between children in autistic traits were largely accounted for by genetic effects (boys: 78% and girls: 83%). Environmental effects that are unique to a child also played a modest role. Environmental effects shared by children growing up in the same family were negligible, once rater bias was controlled for. While the prevalence for clinical ASD is higher in boys than in girls, this study did not find evidence for striking differences in the etiology of autistic traits across the sexes. Even though the heritability was high, 29% of MZ twin pairs were discordant for high autistic traits (clinical range vs. normal development), suggesting that despite high genetic risk, environmental factors might lead to resilience, unaffected status in the context of genetic risk, in some children. It is important to focus future research on risk factors that might interplay with a genetic disposition for ASD, but also on protective factors that make a difference in the lives of children at genetic risk.

Genetic and environmental etiology of speech and word reading in Chinese

The present study examined the genetic and environmental etiology of the connection between speech and word reading in Chinese. A total of 371 pairs of Chinese twins (278 pairs of monozygotic twins and 93 pairs of same-sex dizygotic twins) were tested on speech discrimination and production, phonological skills, semantic skills, and Chinese word reading at the mean age 7.4years. Results of univariate genetic analyses showed moderate genetic influences on speech, semantic skills, and Chinese word reading, while moderate shared environmental influences on phonological skills. The genetic correlations among all the variables were significant. Results of testing several models on the link between speech and word reading supported a common genetic factor underlying speech, phonological skills, semantic skills, and word reading in Chinese. The present findings suggest that around 50% to 60% of individual differences of speech, semantic skills, and word reading in Chinese are due to genetic factors. Individual differences of phonological skills appear to be relatively less heritable than those in English. This may be partly due to the fact that the Chinese script does not map directly on any segmental phonological information. A single common genetic etiology for speech, phonological skills, semantic skills, and word reading suggests that development of these skills is highly connected.

Does the sex of one\u2019s co-twin affect height and BMI in adulthood? A study of dizygotic adult twins from 31 cohorts

BackgroundThe comparison of traits in twins from opposite-sex (OS) and same-sex (SS) dizygotic twin pairs is considered a proxy measure of prenatal hormone exposure. To examine possible prenatal hormonal influences on anthropometric traits, we compared mean height, body mass index (BMI), and the prevalence of being overweight or obese between men and women from OS and SS dizygotic twin pairs.MethodsThe data were derived from the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins) database, and included 68,494 SS and 53,808 OS dizygotic twin individuals above the age of 20 years from 31 twin cohorts representing 19 countries. Zygosity was determined by questionnaires or DNA genotyping depending on the study. Multiple regression and logistic regression models adjusted for cohort, age, and birth year with the twin type as a predictor were carried out to compare height and BMI in twins from OS pairs with those from SS pairs and to calculate the adjusted odds ratios and 95% confidence intervals for being overweight or obese.ResultsOS females were, on average, 0.31 cm (95% confidence interval (CI) 0.20, 0.41) taller than SS females. OS males were also, on average, taller than SS males, but this difference was only 0.14 cm (95% CI 0.02, 0.27). Mean BMI and the prevalence of overweight or obesity did not differ between males and females from SS and OS twin pairs. The statistically significant differences between OS and SS twins for height were small and appeared to reflect our large sample size rather than meaningful differences of public health relevance.ConclusionsWe found no evidence to support the hypothesis that prenatal hormonal exposure or postnatal socialization (i.e., having grown up with a twin of the opposite sex) has a major impact on height and BMI in adulthood.