African American emerging adults face unique contextual risks that place them at heightened risk for poor psychosocial outcomes. The purpose of this study was to identify profiles of contextual risks among rural African American emerging adults and determine how risk profiles relate to psychosocial outcomes. Our representative sample included 667 fifth graders who live in the rural South and were followed from preadolescence into emerging adulthood. Contextual risks were assessed at ages 19–21 years via six indicators: perceived stress, daily stress, community disadvantage, parent–child conflict, racial discrimination, and childhood trauma. Four psychosocial variables were also assessed at ages 19–21 years: self-regulation, racial identity, parent support, and friend support. Psychosocial outcomes were assessed at age 25 years: education, substance use, future orientation, depressive symptoms, and externalizing behaviors. Latent profile analysis results indicated that the sample could be characterized by three patterns of contextual risk: low contextual risk, high contextual risk, and high contextual risk–childhood trauma. Risk profiles were associated with psychosocial outcomes, with the childhood trauma and high-risk profiles faring worse than the low-risk profile. Further, childhood trauma was particularly predictive of worse outcomes for emerging adults. Findings highlight the need for research and prevention programs that mitigate the effects of contextual risks on psychosocial outcomes for African American emerging adults in rural areas.

Current adolescent substance use risk models have inadequately predicted use for African Americans, offering limited knowledge about differential predictability as a function of developmental period. Among a sample of 500 African American youth (ages 11–21), four risk indices (i.e., social risk, attitudinal risk, intrapersonal risk, and racial discrimination risk) were examined in the prediction of alcohol, marijuana, and cigarette initiation during early (ages 11–13), mid (ages 16–18), and late (ages 19–21) adolescence. Results showed that when developmental periods were combined, racial discrimination was the only index that predicted initiation for all three substances. However, when risk models were stratified based on developmental period, variation was found within and across substance types. Results highlight the importance of racial discrimination in understanding substance use initiation among African American youth and the need for tailored interventions based on developmental stage.

Parent–child relationships have long-term effects on health, particularly later inflammation and depression. We hypothesized that these effects would be mediated by later romantic partner relationships and elevated stressors in young adulthood, helping promote chronic, low grade, inflammation as well as depressive symptoms, and driving their covariation. It has been proposed recently that youth experiencing harsher parenting may also develop a stronger association between inflammation and depressive symptoms in adulthood and altered effects of stressors on outcomes. In the current investigation, we test these ideas using an 18-year longitudinal study of N = 413 African American youth that provides assessment of the parent–child relationship (at age 10), pro-inflammatory cytokine profile and depressive symptoms (at age 28), and potential mediators in early young adulthood (assessed at ages 21 and 24). As predicted, the effect of harsher parent–child relationships (age 10) on pro-inflammatory state and increased depressive symptoms at age 28 were fully mediated through young adult stress and romantic partner relationships. In addition, beyond these mediated effects, parent–child relationships at age 10 moderated the concurrent association between inflammation and depressive symptoms, as well as the prospective association between romantic partner relationships and inflammation, and resulted in substantially different patterns of indirect effects from young adult mediators to outcomes. The results support theorizing that the association of depression and inflammation in young adulthood is conditional on earlier parenting, and suggest incorporating this perspective into models predicting long-term health outcomes.

We examined two potentially interacting, connected pathways by which parental supportiveness during early adolescence (ages 1–13) may come to be associated with later African American young adult smoking. The first pathway is between parental supportiveness and young adult stress (age 19), with stress, in turn, predicting increased smoking at age 20. The second pathway is between supportive parenting and tumor necrosis factor (TNF) gene methylation (i.e., TNFm), a proinflammatory epitype, with low levels indicating greater inflammatory potential and forecasting increased risk for smoking in response to young adult stress. In a sample of 382 African American youth residing in rural Georgia, followed from early adolescence (age 10–11) to young adulthood (age 20), supportive parenting indirectly predicted smoking via associations with young adult stress, IE = –0.071, 95% confidence interval [–0.132, –0.010]. In addition, supportive parenting was associated with TNFm measured at age 20 (r = .177, p = .001). Further, lower TNFm was associated with a significantly steeper slope (b = 0.583, p = .003) of increased smoking in response to young adult stress compared to those with higher TNFm (b = 0.155, p = .291), indicating an indirect, amplifying role for supportive parenting via TNFm. The results suggest that supportive parenting in early adolescence may play a role in understanding the emergence of smoking in young adulthood.

In the current manuscript, we provide an overview of a research program at the University of Georgia's Center for Family Research designed to expand upon rapid and ongoing developments in the fields of genetics and epigenetics. By placing those developments in the context of translational research on family and community determinants of health and well-being among rural African Americans, we hope to identify novel, modifiable environments and biological processes. In the first section of the article, we review our earlier work on genotypic variation effects on the association between family context and mental and physical health outcomes as well as differential responses to family-based intervention. We then transition to discuss our more recent research on the association of family and community environments with epigenetic processes. In this second section of the article, we begin by briefly reviewing terminology and basic considerations before describing evidence that early environments may influence epigenetic motifs that potentially serve as mediators of long-term effects of early family and community environments on longer term health outcomes. We also provide evidence that genotype may sometimes influence epigenetic outcomes. Finally, we describe our recent efforts to use genome-wide characterization of epigenetic patterns to better understand the biological impact of protective parenting on long-term shifts in inflammatory processes and its potential implications for young adult health. As will be clear, research on epigenetics as a mediator of the connections between family/community processes and a range of health outcomes is still in its infancy, but the potential to develop important insights regarding mechanisms linking modifiable environments to biological processes and long-term health outcomes already is coming into view.

For the past quarter century, scientists at the Center for Family Research at the University of Georgia have conducted research designed to promote understanding of normative developmental trajectories among low socioeconomic status African American children, youths, and young adults. In this paper, we describe a recent expansion of this research program using longitudinal, epidemiological studies and randomized prevention trials to test hypotheses about the origins of disease among rural African American youths. The contributions of economic hardship, downward mobility, neighborhood poverty, and racial discrimination to allostatic load and epigenetic aging are illustrated. The health benefits of supportive family relationships in protecting youths from these challenges are also illustrated. A cautionary set of studies is presented showing that some psychosocially resilient youths demonstrate high allostatic loads and accelerated epigenetic aging, suggesting that, for some, “resilience is just skin deep.” Finally, we end on an optimistic note by demonstrating that family-centered prevention programs can have health benefits by reducing inflammation, helping to preserve telomere length, and inhibiting epigenetic aging.

An association has been found between receipt of harsh parenting in childhood and adult health problems. However, this research has been principally retrospective, has treated children as passive recipients of parental behavior, and has overlooked individual differences in youth responsivity to harsh parenting. In a 10-year multiple-wave prospective study of African American families, we addressed these issues by focusing on the influence of polymorphisms in the oxytocin receptor gene (OXTR), variants of which appear to buffer or amplify responses to environmental stress. The participants were 303 youths, with a mean age of 11.2 at the first assessment, and their parents, all of whom were genotyped for variations in the rs53576 (A/G) polymorphism. Teachers rated preadolescent (ages 11 to 13) emotionally intense and distractible temperaments, and adolescents (ages 15 and 16) reported receipt of harsh parenting. Allostatic load was assessed during young adulthood (ages 20 and 21). Difficult preadolescent temperament forecast elevated receipt of harsh parenting in adolescence, and adolescents who experienced harsh parenting evinced high allostatic load during young adulthood. However, these associations emerged only among children and parents who carried A alleles of the OXTR genotype. The results suggest the oxytocin system operates along with temperament and parenting to forecast young adults’ allostatic load.

This study investigated the influences of neighborhood factors (residential stability and neighborhood disadvantage) and variants of the serotonin transporter linked polymorphic region (5-HTTLPR) genotype on the development of substance use among African American children aged 10–24 years. To accomplish this, a harmonized data set of five longitudinal studies was created via pooling overlapping age cohorts to establish a database with 2,689 children and 12,474 data points to span ages 10–24 years. A description of steps used in the development of the harmonized data set is provided, including how issues such as the measurement equivalence of constructs were addressed. A sequence of multilevel models was specified to evaluate Gene × Environment effects on growth of substance use across time. Findings indicated that residential instability was associated with higher levels and a steeper gradient of growth in substance use across time. The inclusion of the 5-HTTLPR genotype provided greater precision to the relationships in that higher residential instability, in conjunction with the risk variant of 5-HTTLPR (i.e., the short allele), was associated with the highest level and steepest gradient of growth in substance use across ages 10–24 years. The findings demonstrated how the creation of a harmonized data set increased statistical power to test Gene × Environment interactions for an under studied sample.

This study was designed to investigate a genetic moderation effect of dopamine receptor 4 gene (DRD4) alleles that have seven or more repeats (long alleles) on an intervention to deter drug use among rural African American adolescents in high-risk families. Adolescents (N = 291, M age = 17) were assigned randomly to the Adults in the Making (AIM) program or to a control condition and were followed for 27.5 months. Adolescents provided data on drug use and vulnerability cognitions three times after pretest. Pretest assessments of caregiver depressive symptoms, disruption in the home, and support toward the adolescent were used to construct a family risk index. Adolescents living in high-risk families who carried at least one DRD4 long allele and were assigned to the control condition evinced greater escalations in drug use than did (a) adolescents who lived in high-risk families, carried the DRD4 long allele, and were assigned to AIM, or (b) adolescents assigned to either condition who carried no DRD4 long alleles. AIM-induced reductions in vulnerability cognitions were responsible for the Family Risk × AIM × DRD4 status drug use prevention effects. These findings support differential susceptibility predictions and imply that prevention effects on genetically susceptible individuals may be underestimated.

We hypothesized that presence of the short allele in the promoter region of the serotonin transporter would moderate the effect of early cumulative socioeconomic status (SES) risk on epigenetic change among African American youth. Contrasting hypotheses regarding the shape of the interaction effect were generated using vulnerability and susceptibility frameworks and applied to data from a sample of 388 African American youth. Early cumulative SES risk assessed at 11–13 years based on parent report interacted with presence of the short allele to predict differential methylation assessed at age 19. Across multiple tests, a differential susceptibility perspective rather than a diathesis–stress framework best fit the data for genes associated with depression, consistently demonstrating greater epigenetic response to early cumulative SES risk among short allele carriers. A pattern consistent with greater impact among short allele carriers also was observed using all cytosine nucleotide–phosphate–guanine nucleotide sites across the genome that were differentially affected by early cumulative SES risk. We conclude that the short allele is associated with increased responsiveness to early cumulative SES risk among African American youth, leading to epigenetic divergence for depression-related genes in response to exposure to heightened SES risk among short allele carriers in a “for better” or “for worse” pattern.

This study was designed to examine the prospective relations of life stress and genetic status with increases in drug use. African Americans (N = 399) in rural Georgia (Wave 1 mean age = 17 years) provided three waves of data across 27.5 months and a saliva sample from which the dopamine receptor D4 (DRD4) gene was genotyped. Multilevel growth curve modeling analysis indicated that emerging adults manifested the highest escalations in drug use when they reported high life stress and carried an allele of DRD4 with 7 or more repeats (7 + R allele). In addition, emerging adults who reported high life stress and carried the 7 + R allele evinced the largest increases in two proximal risk factors for drug use: affiliations with drug-using companions and drug use vulnerability cognitions. Furthermore, when the Gene × Environment interaction effects on the increases in affiliations with drug-using companions and vulnerability cognitions were entered into the model forecasting drug use, the Life Stress × DRD4 Status interaction on drug use became nonsignificant in the presence of the risk mechanisms. This finding provides an example of “second generation” Gene × Environment interaction research in which the interaction's effects on proximal risk mechanisms account for its effects on outcomes.

This study examined the prospective relations of adolescents' perceptions of discrimination and their genetic status with increases in conduct problems. Participants were 461 African American youths residing in rural Georgia (Wave 1 mean age = 15.5 years) who provided three waves of data and a saliva sample from which a polymorphism in the SCL6A4 (serotonin transporter [5-HTT]) gene polymorphism known as the 5-HTT linked promoter region (5-HTTLPR) was genotyped. Data analyses using growth curve modeling indicated that perceived discrimination was significantly related to the slope of conduct problems. As hypothesized, interactions between perceived discrimination and genetic status emerged for male but not female youths. Compared with those carrying two copies of the long allele variant of 5-HTTLPR, male youths carrying one or two copies of its short allele variant evinced higher rates of conduct problems over time when they perceived high levels of racial discrimination. These findings are consistent with resilience and differential susceptibility propositions stating that genes can both foster sensitivity to adverse events and confer protection from those events.

A three-wave cascade model linking life stress to increases in risk behavior was tested with 347 African American emerging adults living in the rural South. Data analyses using structural equation modeling and latent growth curve modeling demonstrated that life stress was linked to increases in risk behavior as African Americans transitioned out of secondary school. The cascade model indicated that life stress fostered increases in negative emotions. Negative emotions, in turn, were linked to increases in affiliations with deviant peers and romantic partners; this forecast increases in risk behavior. The findings supported a stress proliferation framework, in which primary stressors affect increases in secondary stressors that carry forward to influence changes in risk behaviors that can potentially compromise mental health.

A longitudinal model that linked involved–supportive parenting and siblings' ability-camouflaging self-presentations to peers with the development of externalizing and internalizing symptoms was tested with 152 pairs of first- and second-born African American siblings (mean ages 12.7 years and 10.2 years at the first wave of data collection). Three waves of data were collected at 1-year intervals. Teachers assessed siblings' externalizing symptoms, internalizing symptoms, and academic competence; siblings reported their own self-presentations and desire for peer acceptance; and mothers and siblings provided multiinformant assessments of involved–supportive parenting. Involved–supportive parenting at Wave 1 was linked with peer-directed self-presentations at Wave 2. Wave 2 self-presentations were linked indirectly with changes from Wave 1 to Wave 3 in externalizing and internalizing symptoms through their association with academic competence.This study was supported by a grant (2 R01 HD30588) from the National Institute of Child Health and Human Development.