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Assortative mating (AM) is defined as the correlation between matting partners with respect to a phenotype. In humans, AM has been described for different types of anthropometric, socioeconomic, and behavioral traits including mental disorders. Partner's similarity with respect to a phenotype can be due to couples' attraction based on that phenotype (direct assortment), based on a secondary phenotype that is highly correlated to it (indirect assortment), or even as a consequence of phenotypic convergence among partners due to the environmental factors that partners share during their cohabitation. Disentangling the nature of the observed AM for a phenotype is essential to understand its genetic consequence. Assortative mating for heritable traits induces a correlation of genetic values among partners, whereas assortment on environmental factors (e.g. social homogamy) shared by partners does not. The correlation of the genetic values of the partners in turn affects the amount of genetic variance of the trait assorted on, which has implications on its heritability. To disentangle the underlying causes of AM in mental disorders, we use a population-wide analysis of the Danish population (XXX individuals or pairs). We will compare different types of correlation in pair of relations (e.g., spouses, in-laws, co-in-laws, etc.) to distinguish between assortative mating due to shared genetic factors and assortative mating driven by environmental and social factors in nine mental disorders: substance use, schizophrenia, depression, bipolar, ADHD, autism, phobia, anxiety, and anorexia. We observed different extend of correlation between pairs of relatives which is the key to distinguishing between assortative mating due to shared genetic factors and assortative mating driven by environmental and social factors. Our findings will provide valuable insights into the mechanisms underlying AM in mental disorders. [ABSTRACT FROM AUTHOR]

Twin-based heritability estimates for eating disorders range from 28% to 88% for anorexia nervosa (AN), 54% to 83% for bulimia nervosa, and 41% to 57% for binge-eating disorder (BE), underscoring their complex polygenic nature. Eating disorders are highly comorbid with both somatic diseases and other psychiatric disorders. Studies have shown that anorexia nervosa is positively genetically correlated with many psychiatric illnesses, such as obsessive-compulsive disorder, but negatively genetically correlated with a range of metabolic traits, including type 2 diabetes and obesity. Indeed, one possible mechanism for such comorbidities can be attributed to the pleiotropic nature of genetic variants, in that they can influence more than one phenotype. Investigating the pleiotropy of AN and BE genetics within a sample of mostly unaffected participants without an eating disorder presents a comprehensive picture of the clinical comorbidities linked to the genetics of these disorders. Using the PGC-ED (freeze 3) summary statistics from the largest genome-wide association study (GWAS) on AN to date and the first GWAS on BE, we generated polygenic risk scores (PRSs) via SBayesRC. Using AN and BE PRSs as our exposures, we conducted two phenome-wide association studies (pheWASs) in the UK Biobank (n = 488,377), in which our outcomes were diagnoses within the International Classification of Diseases, Tenth Revision (ICD-10) with at least 200 cases. We controlled for age, sex, genotype chip, ten genetic principal components, and assessment centre. Preliminary results indicate that, after Bonferroni correction for multiple testing, AN PRS was associated with greater odds of anxiety disorder (Odds ratio [OR] = 1.04, 95% Confidence intervals [95% CI] 1.03, 1.06, p = 8.96 × 10-9) and depressive episode (OR = 1.07, 95% CI 1.04, 1.1, p = 8.14 × 10-6), and with lower odds of coeliac disease (OR = 0.89, 95% CI 0.87, 0.93, p = 1.86 × 10-9), obesity (OR = 0.97, 95% CI 0.96, 0.98, p = 6.06 × 10-9), and non-insulin-dependent diabetes mellitus (OR = 0.96, 95% CI 0.95, 0.97, p = 2.09 × 10-13). BE PRS was associated with greater odds of a number of endocrine, metabolic, and nutritional diseases, including non-insulin-dependent diabetes mellitus (OR = 1.13, 95% CI 1.09, 1.21, p = 4.82 × 10-7) and obesity (OR = 1.12, 95% CI 1.10, 1.13, p = 2.98 × 10-91), circulatory diseases such as hypertension (OR = 1.03, 95% CI 1.02, 1.04, p = 4.39 × 10-22) and chronic ischaemic heart disease (OR = 1.03, 95% CI 1.02, 1.05, p = 5.44 × 10-7), and psychiatric illnesses such as depressive episode (OR = 1.03, 95% CI 1.02, 1.05, p = 1.44 × 10-8). This study is the first ever pheWAS of BE genetics and an updated pheWAS of AN genetics; we highlight the pleiotropic nature of the genetics of BE and AN. Moving forward, we must pay close attention to the metabolic component of both AN and BE. [ABSTRACT FROM AUTHOR]