Genetic and Environmental Influences on Sexual Orientation: Moderation by Childhood Gender Nonconformity and Early-Life Adversity.

Existing evidence indicates genetic and non-genetic influences on sexual orientation; however, the possibility of gene-environment interplay has not been previously formally tested despite theories indicating this. Using a Finnish twin cohort, this study investigated whether childhood gender nonconformity and early-life adversities independently moderated individual differences in sexual orientation and childhood gender nonconformity, the relationship between them, and the etiological bases of the proposed moderation effects. Sexual orientation, childhood gender nonconformity, and early-life adversities were assessed using standard questionnaires. Structural equation twin model fitting was carried out using OpenMx. Childhood gender nonconformity was significantly associated with reduced phenotypic variance in sexual orientation (ß = - 0.14, 95% CI - 0.27, - 0.01). A breakdown of the underlying influences of this moderation effect showed that this was mostly due to moderation of individual-specific environmental influences which significantly decreased as childhood gender nonconformity increased (ßE = - 0.38; 95% CI - 0.52, - 0.001) while additive genetic influences were not significantly moderated (ßA = 0.05; 95% CI - 0.30, 0.27). We also observed that the relationship between sexual orientation and childhood gender nonconformity was stronger at higher levels of childhood gender nonconformity (ß = 0.10, 95% CI 0.05, 0.14); however, significance of the underlying genetic and environmental influences on this relationship could not be established in this sample. The findings indicate that beyond a correlation of their genetic and individual-specific environmental influences, childhood gender nonconformity is further significantly associated with reduced individual-specific influences on sexual orientation.

Causal Influences of Same-Sex Attraction on Psychological Distress and Risky Sexual Behaviors: Evidence for Bidirectional Effects.

Although health disparities among same-sex attracted compared to heterosexual individuals are typically explained by minority stress, there is limited evidence for a causal effect. This study investigated whether same-sex attraction was causally associated with psychological distress and risky sexual behavior using sociosexual behavior as a proxy. The sample comprised monozygotic and dizygotic twins and their non-twin siblings (n = 2036, 3780 and 2356, respectively) genotyped and assessed for same-sex attraction, psychological distress (anxiety and depressive symptoms), and risky sexual behavior. Causal influences were investigated with same-sex attraction as the predictor and psychological distress and risky sexual behavior as the outcomes in two separate Mendelian Randomization-Direction of Causation (MRDoC) models using OpenMx in R. The MRDoC model improves on the Mendelian Randomization and Direction of Causation twin models by allowing analyses of variables with similar genetic architectures, incorporating polygenic scores as instrumental variables and specifying pleiotropy and residual covariance. There were significant causal influences flowing from same-sex attraction to psychological distress and risky sexual behavior (standardized coefficients = 0.13 and 0.16; 95% CIs 0.03-0.23 and 0.08-0.25, respectively). Further analyses also demonstrated causal influences flowing from psychological distress and risky sexual behavior toward same-sex attraction. Causal influences from same-sex attraction to psychological distress and risky sexual behavior may reflect minority stress, which reinforces ongoing measures to minimize social disparities. Causal influences flowing in the opposite direction may reflect rejection sensitivity, stigma-inducing outcomes of risky sexual behavior, and recall bias; however, further research is required to specifically investigate these processes.

Investigating the genetic and environmental aetiologies of non-suicidal and suicidal self-harm: a twin study.

BACKGROUND: Self-harm is a major health concern, not only as a signal of distress but also as a strong predictor of later suicide. Self-harm can be further refined into suicidal self-harm (SSH, i.e. suicide attempt) and non-suicidal self-harm (NSSH). Understanding the aetiologies of NSSH and SSH can help inform suicide prevention strategies. Using a twin design, we investigated the phenotypic and aetiological relationships between NSSH and SSH, and their aetiological overlap with mental health problems. METHODS: We analysed data from the Twins Early Development Study using structural equation modelling. At age 21 years, 9063 twins (62.4% female) answered questions related to self-harm. At age 16 years, 19 self- or parent-reported mental health measures were administered, including measures of internalising and externalising problems, psychotic-like experiences and substance abuse. RESULTS: Prevalences for NSSH and SSH were 21.9% and 10.5%, respectively. Additive genetic factors explained half of the variance in NSSH (55%) and SSH (50%), with the rest explained by non-shared environmental factors. Phenotypically, NSSH and SSH were strongly correlated (r = 0.87) with their correlation explained by genetic (57%) and non-shared environmental (43%) factors. We found no evidence that NSSH and SSH differed in their phenotypic and aetiological relationships with mental health measures. CONCLUSION: Our findings suggest no aetiological difference between NSSH and SSH. NSSH and SSH should be regarded as two different ends of a continuum, rather than as two distinct categories.

Mental Health Disparities Mediating Increased Risky Sexual Behavior in Sexual Minorities: A Twin Approach.

Increased risky sexual behavior in sexual minorities relative to heterosexual individuals may be partly explained by mental health disparities, and both factors may be further jointly influenced by common genetic and environmental factors. However, these relationships have not been previously investigated. The objectives of the present study were to investigate mental health disparities as a mediator of the relationship between sexual orientation and risky sexual behavior, controlling for genetic and environmental effects in this relationship and testing for sex differences. Participants included 5814 twins from a Finnish twin cohort. Specified latent factors included sexual orientation, mental health indicators, and risky sexual behavior. Twin models were fitted to the factor structure of the data whereby a Cholesky decomposition on the factors was compared to a mediation submodel using OpenMx. Sex differences were tested in the final model. Phenotypically, mental health disparities partially mediated the relationship between sexual orientation and increased risky sexual behavior, with comparable effects in males and females. However, while this indirect route from sexual orientation to risky sexual behavior mainly contained transmitted genetic effects in males, there was a significant proportion of transmitted shared environmental effects in females. This is the first study to demonstrate that the mediation relationships between sexual orientation, mental health disparities, and risky sexual behavior are not confounded by genetic and environmental factors. The significant sex differences need to be recognized in future research and intervention design to improve sexual health in sexual minorities.

Do psychosocial factors mediate sexual minorities' risky sexual behaviour? A twin study.

OBJECTIVES: Risky sexual behavior among sexual minorities (lesbian, gay, and bisexual individuals) are partly attributed to mental health and other social disparities; but this may be confounded by correlated genetic and environmental influences. As preregistered, the present study investigated indirect associations between sexual minority status and increased lifetime sexual partners through increased psychosocial adversity (depressive and anxiety symptoms, intimate partner violence, and early life adversities) and substance use (alcohol, cannabis, and other illicit drugs), confounding by correlated genetic and environmental influences, and sex differences in these relationships. METHOD: The sample comprised sexual minority and heterosexual twins who participated in the first and second phases of the latest wave of data collection in the U.K. population-based Twins Early Development study cohort (June 2017 through February 2019; n = 9,697 and 8,718, respectively, Mage = 22.3 ± .92 years). Structural equation modeling was used to specify psychosocial adversity and substance use as mediators while genetic and environmental confounding was further determined by biometrical genetic analyses in which similarities in identical and nonidentical twins were compared. RESULTS: Increased psychosocial adversity and substance use fully mediated increased lifetime sexual partners in sexual minority women while this effect was partial (31.1%) in men. The best-fitting genetic models indicated that these relationships were not confounded by correlated genetic and environmental influences. CONCLUSIONS: The relationships between sexual minority status, psychosocial adversity, substance use, and sexual health disparities appeared independent of genetic and environmental influences. Individual and systemic interventions to reduce psychosocial disadvantage and substance use can also decrease sexual health disparities among sexual minorities. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Increased depressive and anxiety symptoms in non-heterosexual individuals: Moderation by childhood factors using a twin design.

BACKGROUND: Evidence indicates that minority stress does not sufficiently explain mental health disparities in non-heterosexual compared to heterosexual individuals. We investigated alternative mechanisms whereby childhood factors (childhood gender nonconformity, early-life adversities and parent-child interactions) moderate the relationships between sexual orientation and depressive and anxiety symptoms. METHODS: The sample comprised twin pairs from the Finnish Genetics of Sexuality and Aggression cohort (n = 3166 individuals, mean age = 37.5 ± 2.93 years). Twin analyses using structural equation modelling was performed in OpenMx. Specifically, we tested whether childhood factors differentially moderated the underlying genetic and environmental influences on the relationships between sexual orientation, and depressive and anxiety symptoms. RESULTS: The associations between non-heterosexuality, and depressive and anxiety symptoms (r = 0.09, 0.10 respectively) were significantly influenced by both genetic and environmental factors. The genetic influences explaining the relationships of sexual orientation with depressive and anxiety symptoms were maximal at high levels of childhood gender nonconformity (ßA = 0.09 and 0.11 respectively) whereas the individual-specific environmental influences on these relationships were maximal at lower levels of childhood gender nonconformity (ßE = -0.10). LIMITATIONS: Childhood factors were assessed retrospectively in a cross-sectional design. CONCLUSIONS: Childhood gender nonconformity is associated with increased genetic and decreased individual-specific environmental influences on mental health among non-heterosexual individuals. Childhood gender nonconformity may, thus, enhance genetic risk and non-genetic protective processes for depressive and anxiety symptoms among non-heterosexual individuals.