This study was designed to examine the prospective relations of perceived racial discrimination with allostatic load (AL), along with a possible buffer of the association. A sample of 331 African Americans in the rural South provided assessments of perceived discrimination from ages 16 to 18 years. When youths were 18, caregivers reported parental emotional support, and youths assessed peer emotional support. AL and potential confounder variables were assessed when youths were 20. Latent Growth Mixture Modeling identified two perceived discrimination classes: high and stable and low and increasing. Adolescents in the high and stable class evinced heightened AL even with confounder variables controlled. The racial discrimination to AL link was not significant for young adults who received high emotional support.

BackgroundSmoking 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.ResultsConsistent with prior findings, smoking was associated with significant DNA demethylation at two distinct loci within AHRR (cg05575921 and cg21161138) with the degree of demethylation being greater than that observed in the prior cohort of 19-year-old smoking subjects. Additionally, methylation status at the AHRR residue interrogated by cg05575921 was highly correlated with serum cotinine levels (adjusted R2 = 0.42, P < 0.0001).ConclusionsWe conclude that AHRR DNA methylation status is a sensitive marker of smoking history and could serve as a biomarker of smoking that could supplement self-report or existing biomarker measures in clinical or epidemiological analyses of the effects of smoking. In addition, if properly configured as a clinical assay, the determination of AHRR methylation could also be used as a screening tool in efforts to target antismoking interventions to nascent smokers in the early phases of smoking.

Background 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. Objective Building upon this research, the present study investigates additional avenues whereby low income might accelerate biological aging. Methods 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. Results 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. Conclusions These findings support the view that chronic financial pressures associated with low income exerts a weathering effect that results in premature aging.

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A longitudinal, prospective design was used to investigate a moderation effect in the association between a genetic vulnerability factor, a variable nucleotide repeat polymorphism in the promoter region of 5HTT (5-HTTLPR) and increases in youths’ substance use. The primary study hypothesis predicted that involved-supportive parenting would attenuate the link between the 5-HTTLPR polymorphism and longitudinal increases in substance use. African American youths residing in rural Georgia (N = 253; M age = 11.5 years) provided four waves of data on their own substance use; the youths’ mothers provided data on their own parenting practices. Genetic data were obtained from youths via saliva samples. Latent growth curve modeling indicated that 5-HTTLPR status (presence of 1 or 2 copies of the s allele) was linked with increases in substance use over time; however, this association was greatly reduced when youths received high levels of involved-supportive parenting. This study demonstrates that parenting processes have the potential to ameliorate genetic risk.

The present study tests a developmental model designed to explain the romantic relationship difficulties and reluctance to marry often reported for African Americans. Using longitudinal data from a sample of approximately 400 African American young adults, we examine the manner in which race-related adverse experiences during late childhood and early adolescence give rise to the cynical view of romantic partners and marriage held by many young African Americans. Our results indicate that adverse circumstances disproportionately suffered by African American youth (viz., harsh parenting, family instability, discrimination, criminal victimization, and financial hardship) promote distrustful relational schemas that lead to troubled dating relationships, and that these negative relationship experiences, in turn, encourage a less positive view of marriage.

To test the differential susceptibility to parenting hypothesis, a 4-wave, randomized prevention design was used to examine the impact of the Strong African American Families (SAAF) program on past-month substance use across 29 months as a function of DRD4 genotype. Youths (N = 337; M age = 11.65 years) were assigned randomly to treatment condition. Those carrying a 7-repeat allele showed greater differential response to intervention vs. control than those with two 4-repeat alleles. Control youths but not treatment youths with a 7-repeat allele reported increases in past-month substance use across the 29-month study period, but this pattern did not emerge for those with the 4-repeat allele. Supporting the differential susceptibility to parenting hypothesis, the results suggest a greater preventive effect for youths carrying a 7-repeat allele, a role for DRD4 in the escalation of substance use during adolescence, and potential for an enhanced understanding of early-onset substance use. KeywordsDRD4; parenting; substance use; susceptibility Belsky & Pluess (2009) suggest that children with so-called "risk alleles," i.e., genetic variations thought to be associated with adverse outcomes, may be more sensitive to the impact of parenting behavior than are children who do not have these alleles. Preliminary evidence with young children has lent considerable support to the hypothesis that variability at DRD4, a well-studied 48-base pair (bp) repeat in the coding region of the dopamine D4 receptor, mayCorrespondence concerning this article should be directed to Steven R. H. Beach, 510 Boyd GSRC, Institute for Behavioral Research, University of Georgia, Athens, GA 30602. srhbeach@uga.edu. The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript version, any version derived from this manuscript by NIH, or other third parties. The published version is available at www.apa.org/pubs/journals/fam NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript indeed contribute to differential susceptibility to parenting (Bakermans-Kranenburg, van IJzendoorn, Pijlman, Mesman, & Juffer, 2008;Belsky, Bakermans-Kranenburg & van IJzendoorn, 2007). Variation at DRD4 also has been studied as a risk factor for certain problems in childhood, including ADHD (Gizer, Ficks, & Waldman, 2009) and risk for substance use (e.g., Conner, Hellemann, Ritchie, & Noble, 2010). Based on the hypotheses that DRD4 would confer differential susceptibility to parenting influences in adolescence and that substance use would escalate during adolescence, we predicted genetic moderation of a parenting-based prevention program on substance use outcomes would emerge.We used the Strong African Americ...