Past research has linked low socio-economic status (SES) to inflammation, metabolic dysregulation, and various chronic and age-related diseases such as type 2 diabetes, coronary heart disease, stroke, and dementia. These studies suggest that the challenges and adversities associated with low SES may result in premature aging and increased risk of morbidity and mortality. Building upon this research, the present study investigates various avenues whereby low income might accelerate biological aging. Structural equation modeling and longitudinal data from a sample of 100 Black, middle-aged women residing in the United States was used to investigate the effect of income on a recently developed epigenetic measure of biological aging. This measure can be used as a "biological clock" to assess, at any point during adulthood, the extent to which an individual is experiencing accelerated or decelerated biological aging. Low income displayed a robust association with accelerated aging that was unaffected after controlling for other SES-related factors such as education, marital status, and childhood adversity. Further, our analyses indicated that the association between income and biological aging was not explained by health-related behaviors such as diet, exercise, smoking, alcohol consumption, or having health insurance. Rather, in large measure, it was financial pressure (difficulty paying bills, buying necessities, or meeting daily expenses) that accounted for the association between low income and accelerated aging. These findings support the view that chronic financial pressures associated with low income exert a weathering effect that results in premature aging.

Smoking is the largest preventable cause of morbidity and mortality in the United States. In previous work, we demonstrated that altered DNA methylation at the aryl hydrocarbon receptor repressor (AHRR) is correlated with self-reported smoking in 19-year-old African Americans with relatively low levels of smoking. However, one limitation of the prior work is that it was based on self-reported data only. Therefore, the relationship of AHRR methylation to smoking in older subjects and to indicators such as serum cotinine levels remains unknown. To address this question, we examined the relationship between genome- wide DNA methylation and smoking status as indicated by serum cotinine levels in a cohort of 22-year-old African American men.

Several studies have reported a relation between race-related stressors and the poor health of Black Americans. Such findings raise questions regarding the mediating biological mechanisms that might account for this link. The present study investigated elevated systemic inflammation, a factor shown to be a strong predictor of chronic illness and mortality in all ethnic populations, as a possible factor. Using 7 waves of data from the Family and Community Health Study, collected over a 20-year period from over 400 Black Americans, we investigated the extent to which exposure to discrimination and segregation at various points in the life course predicted adult inflammation at age 28. Our analyses examined whether cumulative stress, stress generation, or predictive adaptive response (PAR) models best accounted for any associations that existed between these race-related stressors and adult inflammation. At every wave of data collection, assessments of discrimination and segregation were related to adult inflammation. However, multivariate analyses using structure equation modeling indicated that the PAR model best explained the effect of these race-related stressors on inflammation. Exposure to discrimination and segregation during the juvenile years predicted adult inflammation and amplified the inflammatory effect of adult exposure to these race-related stressors. These effects were considerably more robust than that of traditional health risk factors such as diet, exercise, smoking, and low SES. Implications of these findings are discussed, including the limitations of the widely accepted risk factor approach to increasing the health of Black Americans. (PsycINFO Database Record

Although gene by environment studies are typically based on the assumption that some individuals possess genetic variants that enhance their vulnerability to environmental adversity, the differential susceptibility perspective posits that these individuals are simply more susceptible to environmental influence than others. An important implication of this perspective is that individuals most vulnerable to adverse social environments are the same ones who reap the most benefit from environmental support. Using longitudinal data from a sample of several hundred African Americans, we found that relatively common variants of the dopamine receptor gene and the serotonin transporter gene interact with social conditions to predict aggression in a manner consonant with the differential susceptibility perspective. When social conditions were adverse, individuals with these genetic variants manifested more aggression than other genotypes, whereas when the environment was favorable they demonstrated less aggression than other genotypes. Furthermore, we found that these genetic variants interact with environmental conditions to foster schemas and emotions consistent with the differential susceptibility perspective and that a latent construct formed by these schemas and emotions mediates the gene by environment interaction on aggression.