Deaths due to hypertension in the US are highest among African Americans, who have a higher prevalence of hypertension and more severe hypertensive symptoms. Research indicates that there are both genetic and sociocultural risk factors for hypertension. Racial disparities in hypertension also likely involve genetic and sociocultural factors, but the factors may interact and manifest differently across racial groups. Here we use a biocultural approach to integrate genetic and social network data to better understand variation in blood pressure. We assay genetic variation at the angiotensin I converting enzyme gene (ACE) and analyze social network composition and structure in African Americans living in Tallahassee, FL (n = 138). We demonstrate that models including both genetic and social network data explain significantly more variation in blood pressure and have better model diagnostics than do models including only one datatype. Specifically, optimal models for systolic and diastolic blood pressure explain a notable 35% and 21%, respectively, of blood pressure variation. Analysis of the social networks reveals that individuals whose networks are dominated by family connections and are more fragmented have higher blood pressure. Historically, family support has been associated with better mental and physical health, but our results suggest that those family connections can also take a toll on health. These findings raise compelling questions regarding the roles of genetics, family, and social environment in hypertension in the African American community and suggest that interactions among these factors may help explain racial disparities in hypertension more accurately than any of the factors alone.

Objectives: The World Health Organization estimates that almost 300 million people suffer from depression worldwide. African Americans are understudied for depression-related phenotypes despite widespread racial disparities. In our study of African Americans, we integrated information on psychosocial stressors with genetic variation in order to better understand how these factors associated with depressive symptoms.Methods: Our research strategy combined information on financial strain and social networks with genetic data to investigate variation in symptoms of depression (CES-D scores). We collected self-report data on depressive symptoms, financial strain (difficulty paying bills) and personal social networks (a model of an individual's social environment), and we genotyped genetic variants in five genes previously implicated in depressive disorders (HTR1a, BDNF, GNB3, SLC6A4, and FKBP5) in 128 African Americans residing in Tallahassee, Florida. We tested for direct and gene-environment interactive effects of the psychosocial stressors and genetic variants on depressive symptoms.Results: Significant associations were identified between high CES-D scores and a stressful social environment (i.e., a high percentage of people in participants' social network who were a source of stress) and high financial strain. Only one genetic variant (rs1360780 in FKBP5) was significantly associated with CES-D scores and only when psychosocial stressors were included in the model; the T allele had an additive effect on depressive symptoms. Sex was also significantly associated with CES-D score in the model with psychosocial stressors and genetic variants; males had higher CES-D scores. No significant interactive effects were detected.Conclusions: A stressful social environment and material disadvantage increase depressive symptoms in the study population. Additional associations with FKBP5 and male sex were revealed in models that included both psychosocial and genetic data. Our results suggest that incorporating psychosocial stressors may empower

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The World Health Organization estimates that almost 300 million people suffer from depression worldwide. Depression is the most common mental health disorder and shows racial disparities in disease prevalence, age of onset, severity of symptoms, frequency of diagnosis, and treatment utilization across the United States. Since depression has both social and genetic risk factors, we propose a conceptual model wherein social stressors are primary risk factors for depression, but genetic variants increase or decrease individual susceptibility to the effects of the social stressors. Our research strategy incorporates both social and genetic data to investigate variation in symptoms of depression (CES-D scores). We collected data on financial strain (difficulty paying bills) and personal social networks (a model of an individual’s social environment), and we genotyped genetic variants in five genes involved in stress reactivity (HTR1a, BDNF, GNB3, SLC6A4, and FKBP5) in 135 African Americans residing in Tallahassee, Florida. We found that high financial strain and a high percentage of people in one’s social network who are a source of stress or worry were significantly associated with higher CES-D scores and explained more variation in CES-D scores than did genetic factors. Only one genetic variant (rs1360780 in FKBP5) was significantly associated with CES-D scores and only when the social stressors were included in the model. Interestingly, the effect of FKPB5 appeared to be strongest in individuals with high financial strain such that participants with a T allele at rs1360780 in FKBP5 and high financial strain had the highest mean CES-D scores in our study population. These results suggest that material disadvantage and a stressful social environment increases the risk of depression, but that individual-level genetic variation may increase susceptibility to the adverse health consequences of social stressors.