Genetic and environmental sources of familial resemblance in anxiety: a nuclear twin family design

Background A dominant feature of anxiety disorders is familial aggregation. However, the underlying mechanisms of between- and within-generational anxiety resemblance remain poorly understood. By disentangling the genetic v. environmental sources of familial resemblance in anxiety, we can help prevent within-family transmission of anxiety disorders. Therefore, data from both parents and twins are needed to obtain unbiased and detailed estimations of genetic and environmental sources of similarity between family members. Methods We examined data from 991 families with same-sex twins. Trait anxiety in twins was assessed via self-report and parent report, while parental trait anxiety was assessed via self-report. We established a nuclear twin family model and estimated genetic and environmental variances using two survey waves. Results The results suggested that additive genetic (A), dominant genetic (D), and non-shared environmental (E) influences significantly contributed to trait anxiety, whereas familial environmental influences (F) and passive gene–environment correlations (rGE) did not. Sibling environmental influences (S) were only found in self-report data, and increased when genetic influences decreased from Wave 1 to Wave 2. Conclusions Our study highlights the important role of broad heritability in intrafamilial trait anxiety similarity. Parent–child resemblance occurred primarily due to shared genetic makeup rather than direct environmental transmission. Sibling-specific environments, as the only source of shared environments, need further investigation. These findings have both theoretical and practical significance for anxiety disorders. Future research can expand our understanding by examining the gene–environment interplay and sex differences.

Familial resemblance in markers of testicular function in fathers and their young sons: a cross-sectional study

STUDY QUESTION Is testicular function associated within father–son pairs? SUMMARY ANSWER Familial resemblance in testis volume and serum markers of spermatogenesis was observed in father–son pairs. WHAT IS KNOWN ALREADY Studies suggest familial clustering of male subfertility and impaired spermatogenesis, but in men from the general population little is known about concordance in testicular function between fathers and sons. STUDY DESIGN, SIZE, DURATION This cross-sectional study with simultaneous collection of data in fathers and sons included 72 pairs (144 fathers and sons), unselected regarding testicular function were included. PARTICIPANTS/MATERIALS, SETTING, METHODS A subgroup of men from the background population and participating in a study on testicular function were asked permission to invite their fathers to participate in a similar setup. Fathers (median age of 53 years) and sons (median age of 19 years) participated in the same study setup including assessment of testis size, having a blood sample taken and analysed for serum levels of reproductive hormones (FSH, inhibin B, LH, testosterone, oestradiol, sex hormone-binding globulin (SHBG) and calculated free testosterone) and delivering a semen sample for assessment of traditional semen parameters. Mixed-effects models were fitted to estimate the familial resemblance as the proportion of variance in markers of testicular function due to shared factors for fathers and sons accounted for using random-effects. Variance components were calculated from both unadjusted and adjusted models. MAIN RESULTS AND THE ROLE OF CHANCE After adjustments, variance component analyses showed that familial resemblance between fathers and sons accounted for 48% (P < 0.001) of the variation in testicular volume, 32% (P = 0.009) of the variation in FSH, 31% (P = 0.009) of the variation in the inhibin B/FSH ratio, 33% (P = 0.007) and 45% (P < 0.001) of the variation in testosterone and free testosterone, respectively, and 31% (P = 0.009) of the variation in SHBG. None of the semen parameters were associated within father–son pairs. LIMITATIONS, REASONS FOR CAUTION The present study may have lacked power to detect associations for semen quality, as large intra- and inter-individual variation occur in semen parameters. WIDER IMPLICATIONS OF THE FINDINGS In this study, testis volume, serum testosterone and serum markers of spermatogenesis including FSH were associated in fathers and sons, suggesting an impact of paternal genetics for testicular function in the son. However, the estimated familial resemblance for spermatogenesis markers highlights that other factors, such as maternal genetics and prenatal as well as adult exposures, are also of major importance for testicular function. STUDY FUNDING/COMPETING INTEREST(S) The study has received funding from Danish Health Authority, Research Fund of the Capital Region of Denmark and Independent Research Fund Denmark (8020-00218B). None of the funders had any role in the study design, collection, analysis or interpretation of data, writing of the paper of publication decisions. The authors have nothing to disclose. TRIAL REGISTRATION NUMBER N/A.

Genetics and Not Shared Environment Explains Familial Resemblance in Adult Metabolomics Data

Metabolites are small molecules involved in cellular metabolism where they act as reaction substrates or products. The term ‘metabolomics’ refers to the comprehensive study of these molecules. The concentrations of metabolites in biological tissues are under genetic control, but this is limited by environmental factors such as diet. In adult mono- and dizygotic twin pairs, we estimated the contribution of genetic and shared environmental influences on metabolite levels by structural equation modeling and tested whether the familial resemblance for metabolite levels is mainly explained by genetic or by environmental factors that are shared by family members. Metabolites were measured across three platforms: two based on proton nuclear magnetic resonance techniques and one employing mass spectrometry. These three platforms comprised 237 single metabolic traits of several chemical classes. For the three platforms, metabolites were assessed in 1407, 1037 and 1116 twin pairs, respectively. We carried out power calculations to establish what percentage of shared environmental variance could be detected given these sample sizes. Our study did not find evidence for a systematic contribution of shared environment, defined as the influence of growing up together in the same household, on metabolites assessed in adulthood. Significant heritability was observed for nearly all 237 metabolites; significant contribution of the shared environment was limited to 6 metabolites. The top quartile of the heritability distribution was populated by 5 of the 11 investigated chemical classes. In this quartile, metabolites of the class lipoprotein were significantly overrepresented, whereas metabolites of classes glycerophospholipids and glycerolipids were significantly underrepresented.

Familial Resemblance in Body Shape and Composition, Metabolic Syndrome, Physical Activity and Physical Fitness: A Summary of Research in Portuguese Families and Siblings

We report a summary of Portuguese families and siblings research under the umbrella of the Portuguese Healthy Family Project. Families lived in mainland Portugal, as well as in the Azores and Madeira islands. All samples comprise children and adolescents (9–20 years) and their parents (27–57 years). Recruitment procedures and phenotypes were detailed. Familial resemblance in body shape and composition, metabolic syndrome, physical fitness, physical activity and sedentary behaviors are presented, as well as future research avenues.

Does Breastfeeding Behavior Run in Families? Evidence From Twins, Their Sisters and Their Mothers in the Netherlands

The aim of the present article was to study the prevalence and the heritability of the initiation of breastfeeding in the Netherlands. The study was carried out in 5,581 participants from the Netherlands Twin Register, and included female twins, their sisters and mothers. All of the participants were born between 1911 and 1991. Breastfeeding was self-reported by the participants, and its prevalence was estimated conditional on birth cohort (born before 1955, 1955–1964, 1965–1974, 1975, or later). To estimate the heritability, we conducted extended twin-family modeling using the SEM package OpenMx in R. Mothers of twins had lower prevalence to initiate breastfeeding and the prevalence of initiation of breastfeeding increased with birth cohort: among mothers of twins 66% in the oldest (pre-1955) to 74% in the youngest (post-1974) and among mothers, who were twins themselves or sisters of twins, 79% in the oldest (pre-1955) to 85% in the youngest (post-1974). When accounting for prevalence differences between mothers of twins and other women, heritability of initiation of breastfeeding was 70%. However, the familial resemblance for sister and mother-daughter pairs was clearly lower than for DZ twin pairs, but as the number of non-twin sisters was relatively low, this observation did not lead to a significant contribution of a special shared twin environment.