Social Science Genetics

Despite advancements in genomics, misconceptions about the extent to which genetics contributes to observable differences across racial groups persist. These misconceptions are often rooted in genetic essentialism, a social-cognitive bias that leads individuals to believe that most complex traits are primarily determined by genetics. This scientifically inaccurate belief overlooks the environmental and social influences on complex human outcomes, reinforcing deterministic views about human diversity. Our study examines how and for whom genetics education can reduce genetic essentialist beliefs using targeted interventions. We use data from a randomized control trial collected at a large US west coast public university in 2023, including 2,061 undergraduate students. Participants were randomly assigned to one of four curriculum-based interventions, ensuring balanced characteristics across conditions. Three interventions were compared: population thinking (PT); multifactorial causation (MC); and a curriculum where we combined both approaches, which we call full Humane Genetics Curriculum (HGC). Results are reported relative to a control group that taught students about climate change. Using structural equation modeling, we explore the effectiveness of these interventions with our data. We find that all three interventions reduce genetic essentialist beliefs by decreasing the perception of between-group racial variation and by reducing genetic attributions for complex human traits. We also find that the three intervention curricula are highly effective across sociodemographic group characteristics such as self-reported gender, self-reported race, and cultural/political belief systems. Yet the interventions were more effective among students who possessed greater baseline genetics knowledge. Using these findings, we offer evidence-based strategies for curriculum development.

Genetic essentialism is a social-cognitive prejudice involving the belief that people of the same race share genes that make them behaviorally, physically, and cognitively uniform and also genetically distinct from other other races. It can be exacerbated by a basic, Mendelian-based genetics and biology education in the United States. To combat this phenomenon, the Humane Genomics Literacy curriculum was developed. Shown to be highly effective in several randomized control trials to date, HGL aims to both increase students’ understanding of population genetics and multifactorial inheritance and to reduce beliefs in genetic essentialism using evidence from scientific studies. HGL instruction is specifically focused on  using science to help students gain a less gene-centric understanding of racial group differences. In this article, we carefully describe the original HGL curriculum in terms of content and the unique pedagogical practices that the curriculum includes. Next, we discuss how to adapt the curriculum for the college classroom. We aim to provide a guide for genetics educators who are interested in using HGL in their own college classrooms.

Adolescent depression is a heritable psychiatric condition with rising global prevalence and severe long-term outcomes, yet its biological underpinnings remain poorly understood. We conducted the first genome-wide association study of adolescent-onset depression, comprising 102,428 cases (diagnosis or clinical symptom thresholds) and 286,911 controls, including diverse ancestries. Cross-ancestry meta-analysis identified 52 independent variants across 17 loci; European-only analysis found 61 variants at 29 loci, with a SNP-based heritability of 9.8%. Comparative analyses revealed two genes unique to adolescent-onset versus lifetime depression, enriched in neuronal subtypes, and two genes as potential drug repurposing targets. Polygenic scores were associated with adolescent-onset depression across ancestries, persistent depression trajectories, more severe outcomes, as well as reduced cortical volume, surface area and white matter integrity. Genetic correlation and Mendelian randomisation analyses support shared genetic liability and causal links with early puberty and modifiable health and behavioural risk factors. These findings uncover novel genetic loci and refine biological pathways underlying adolescent-onset depression, revealing age-specific mechanisms and early intervention opportunities.

A thorough understanding of depression susceptibility requires research to comprehensively assimilate a vast and complex array of risk factors. We leverage data from the National Longitudinal Study of Adolescent to Adult Health to integrate factors spanning biological (genetic data), psychological (health, personality, positive cognition, and self-worth), social (family, peers, school, and neighbourhood experiences), built (geo-coded healthcare, education, labour force, religion, crime, poverty, political climate), and natural (geo-coded population density, rainfall, and urban distances) systems and their contribution to depression symptoms in adolescence and adulthood using relatedness-based linear mixed models (N= 5,030). First, a subset of 81 individual-level factors explained 83-86% of the variance in adolescence and 14% in adulthood symptoms. Positive cognition (feeling accepted and loved) contributed the most in adolescence (15%, SE= 4%), and factors contributed relatively equally in adulthood. Second, all 162 factors capturing interconnected genetic, psychological, social, built, and natural systems explained 82-86% of the variance in adolescence and 32% in adulthood. The psychological system (adolescence 41-42% SE= 5%, adulthood 6% SE= 1%), psychological-genetic interaction (adolescence 26-28% SE= 5%, adulthood 15% SE= 3%), social-genetic interaction (adolescence 6-8% SE= 2%) contributed most to depression symptoms. We provide a holistic understanding of depression risk and emphasise feeling supported and accepted as crucial for early detection.