Multi-ancestral genome-wide association study of clinically defined nicotine dependence reveals strong genetic correlations with other substance use disorders and health-related traits.

Genetic research on nicotine dependence has utilized multiple assessments that are in weak agreement. We conducted a genome-wide association study of nicotine dependence defined using the Diagnostic and Statistical Manual of Mental Disorders (DSM-NicDep) in 61,861 individuals (47,884 of European ancestry, 10,231 of African ancestry, 3,746 of East Asian ancestry) and compared the results to other nicotine-related phenotypes. We replicated the well-known association at the locus (lead SNP: rs147144681, p =1.

Maternal Smoking during Pregnancy Interacts with Genetic Factors to Increase Risk for Low Birth Weight but not Harmful Offspring Smoking Behaviors in Europeans.

Introduction: Pregnant individuals who smoke face increased health risks because smoking harms both the mother and their developing offspring.

Methods: Using 307 417 Europeans from the UK Biobank, we examined whether exposure to maternal smoking during pregnancy (MSP) interacts with genetic risk to predict offspring birth weight (BW) and smoking behaviors. We investigated interactions between MSP and genetic risk at multiple levels: single variant, gene-level, and polygenic score.

Associations between prenatal caffeine exposure and child development: Longitudinal results from the Adolescent Brain Cognitive Development (ABCD) Study.

Objective: Though caffeine use during pregnancy is common, its longitudinal associations with child behavioral and physical health outcomes remain poorly understood. Here, we estimated associations between prenatal caffeine exposure, body mass index (BMI), and behavior as children enter adolescence.

Method: Longitudinal data and caregiver-reported prenatal caffeine exposure were obtained from the ongoing Adolescent Brain and Cognitive Development (ABCD) Study, which recruited 11,875 children aged 9-11 years at baseline from 21 sites across the United States starting June 1, 2016.

Examining the causal genetic effects of substance use on aging.

Substance use shortens lifespan, impedes health, and accelerates the biological aging process. We found widespread genetic correlations between alcohol, tobacco, cannabis, and opioid use and use disorders with indices of aging across the lifespan. There was evidence of tobacco and alcohol use and use disorders causally impacting physical, cognitive, and biological aging, with the effects of alcohol being more dependent on quantity of consumption; evidence of reverse causality was scant.

Evidence of correlations between human partners based on systematic reviews and meta-analyses of 22 traits and UK Biobank analysis of 133 traits.

Positive correlations between mates can increase trait variation and prevalence, as well as bias estimates from genetically informed study designs. While past studies of similarity between human mating partners have largely found evidence of positive correlations, to our knowledge, no formal meta-analysis has examined human partner correlations across multiple categories of traits. Thus, we conducted systematic reviews and random-effects meta-analyses of human male-female partner correlations across 22 traits commonly studied by psychologists, economists, sociologists, anthropologists, epidemiologists and geneticists.

The estimation of environmental and genetic parental influences.

Parents share half of their genes with their children, but they also share background social factors and actively help shape their child's environment - making it difficult to disentangle genetic and environmental causes of parent-offspring similarity. While adoption and extended twin family designs have been extremely useful for distinguishing genetic and nongenetic parental influences, these designs entail stringent assumptions about phenotypic similarity between relatives and require samples that are difficult to collect and therefore are typically small and not publicly shared. Here, we describe these traditional designs, as well as modern approaches that use large, publicly available genome-wide data sets to estimate parental effects.

Within-sibship genome-wide association analyses decrease bias in estimates of direct genetic effects.

Estimates from genome-wide association studies (GWAS) of unrelated individuals capture effects of inherited variation (direct effects), demography (population stratification, assortative mating) and relatives (indirect genetic effects). Family-based GWAS designs can control for demographic and indirect genetic effects, but large-scale family datasets have been lacking. We combined data from 178,086 siblings from 19 cohorts to generate population (between-family) and within-sibship (within-family) GWAS estimates for 25 phenotypes.

Neuroticism and reward-related ventral striatum activity: Probing vulnerability to stress-related depression.

Elevated neuroticism may confer vulnerability to the depressogenic effects of stressful life events (SLEs). However, the mechanisms underlying this susceptibility remain poorly understood. Accumulating evidence suggests that stress-related disruptions in neural reward processing might undergird links between stress and depression.

Estimation of Parental Effects Using Polygenic Scores.

Offspring resemble their parents for both genetic and environmental reasons. Understanding the relative magnitude of these alternatives has long been a core interest in behavioral genetics research, but traditional designs, which compare phenotypic covariances to make inferences about unmeasured genetic and environmental factors, have struggled to disentangle them. Recently, Kong et al.