Racial discrimination during middle age predicts higher serum phosphorylated tau and neurofilament light chain levels a decade later: A study of aging black Americans.

INTRODUCTION: Recent evidence suggests that exposure to the stress of racism may increase the risk of dementia for Black Americans. METHODS: The present study used 17 years of data from a sample of 255 Black Americans to investigate the extent to which exposure to racial discrimination predicts subsequent changes in serum Alzheimer's Disease Research Center (ADRC) biomarkers: serum phosphorylated tau181(p-tau181), neurofilament light (NfL), and glial fibrillary acidic protein (GFAP). We hypothesized that racial discrimination assessed during middle age would predict increases in these serum biomarkers as the participants aged into their 60s. RESULTS: Our findings indicate that exposure to various forms of racial discrimination during a person's 40s and early 50s predicts an 11-year increase in both serum p-tau181 and NfL. Racial discrimination was not associated with subsequent levels of GFAP. DISCUSSION: These findings suggest that racial discrimination in midlife may contribute to increased AD pathology and neurodegeneration later in life. HIGHLIGHTS: A 17-year longitudinal study of Black Americans. Assessments of change in serum p-tau181, neurofilament light, and glial fibrillary acidic protein. Exposure to racial discrimination during middle age predicted increases in p-tau181 and neurofilament light. Education was positively related to both p-tau181 and exposure to racial discrimination.

Specifying the psychosocial pathways whereby child and adolescent adversity shape adult health outcomes.

BACKGROUND: Social scientists generally agree that health disparities are produced, at least in part, by adverse social experiences, especially during childhood and adolescence. Building on this research, we use an innovative method to measure early adversity while drawing upon a biopsychosocial perspective on health to formulate a model that specifies indirect pathways whereby childhood and adolescent adversity become biologically embedded and influence adult health. METHOD: Using nearly 20 years of longitudinal data from 382 Black Americans, we use repeated-measures latent class analysis (RMLCA) to construct measures of childhood/adolescent adversities and their trajectories. Then, we employ structural equation modeling to examine the direct and indirect effects of childhood/adolescent adversity on health outcomes in adulthood through psychosocial maladjustment. RESULTS: RMLCA identified two classes for each component of childhood/adolescent adversity across the ages of 10 to 18, suggesting that childhood/adolescent social adversities exhibit a prolonged heterogeneous developmental trajectory. The models controlled for early and adult mental health, sociodemographic and health-related covariates. Psychosocial maladjustment, measured by low self-esteem, depressive and anxiety symptoms, and lack of self-control, mediated the relationship between childhood/adolescent adversity, especially parental hostility, racial discrimination, and socioeconomic class, and both self-reported illness and blood-based accelerated biological aging (with proportion mediation ranging from 8.22% to 79.03%). CONCLUSION: The results support a biopsychosocial model of health and provide further evidence that, among Black Americans, early life social environmental experiences, especially parenting, financial stress, and racial discrimination, are associated with adult health profiles, and furthermore, psychosocial mechanisms mediate this association.

Neighborhood disadvantage is associated with biological aging: Intervention-induced enhancement of couple functioning confers resilience.

The accelerated pace of biological aging predicts mortality and morbidity later in life. The current study examines whether a change in supportive couple functioning buffers accelerated aging associated with stressful community environments among Black Americans who live in rural, Southern, disadvantaged neighborhoods. We examined 348 Black American middle-aged adults assigned randomly to receive the Protecting Strong African American Families (ProSAAF) intervention or a control condition. The program was designed to enhance supportive couple functioning among Black Americans. We used DunedinPoAm to quantify the methylation pace of aging and employed the Area Deprivation Index at the census block group level to measure neighborhood disadvantage. Neighborhood disadvantage was associated with the accelerated pace of aging. Further, participation in ProSAAF enhanced supportive couple functioning, and improvement in couple functioning protected participants from the harmful effects of neighborhood disadvantage on the accelerated pace of aging. These findings supported mediated moderation and suggested that family-based prevention programs that enhance couple support may decrease the erosive effects of neighborhood disadvantage and improve prospects for healthy aging among rural, Southern, Black Americans living in difficult circumstances. This may provide a supplemental strategy for decreasing health disparities due to neighborhood disadvantage by enhancing family systems.

Childhood adversity predicts black young adults' DNA methylation-based accelerated aging: A dual pathway model.

We expand upon prior work (Gibbons et al., ) relating childhood stressor effects, particularly harsh childhood environments, to risky behavior and ultimately physical health by adding longer-term outcomes - deoxyribonucleic acid (DNA) methylation-based measures of accelerated aging (DNAm-aging). Further, following work on the effects of early exposure to danger (McLaughlin et al., ), we also identify an additional pathway from harsh childhood environments to DNAm-aging that we label the danger/FKBP5 pathway, which includes early exposure to dangerous community conditions that are thought to impact glucocorticoid regulation and pro-inflammatory mechanisms. Because different DNAm-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNAm-aging based on chronological age with later indices that focused on predicting biological outcomes. We utilize data from Family and Community Health Study participants (N = 449) from age 10 to 29. We find that harshness influences parenting, which, in turn, influences accelerated DNAm-aging through the risky cognitions and substance use (i.e., behavioral) pathway outlined by Gibbons et al. (). Harshness is also associated with increased exposure to threat/danger, which, in turn, leads to accelerated DNAm-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway).

Intervention effects on self-control decrease speed of biological aging mediated by changes in substance use: A longitudinal study of African American youth.

Biological aging is a common root for multiple diseases causing morbidity and mortality, and trajectories of aging may start early in life. This study was designed to examine whether a universal family-based substance use preventive intervention to enhance self-control and reduce substance use would also result in reductions in biological aging among Black youth from the rural South. The Adults in the Making (AIM) program is a randomized controlled trial with six 2-h sessions for Black youth. The 216 youths agreeing to provide blood at age 22 included 114 who had received the AIM intervention and 102 who assigned to the control group. We examined accelerated DNA methylation (DNAm)-based aging using a recently developed measure, "GrimAge," that has been shown to predict the risk of early mortality and that is known to be more strongly affected by substance use than other DNAm-based aging indices. Relative to those randomly assigned to the control group, those receiving the intervention demonstrated significantly enhanced self-control, slower increases in substance use, and reduced Grim aging at age 22. Using a bootstrapping method with 1000 replications, we found a significant indirect effect of AIM on reduced Grim aging through its effect on self-control and substance use. Sensitivity analyses examined effects using other indices of DNAm-based aging. These findings suggest that a family-based program designed to enhance rural Black youth's self-control can have beneficial effects on self-control, enhancing young adult health and health behavior, and ultimately decreased mortality risk.

El envejecimiento biológico es una causa común de varias enfermedades que causan morbilidad y mortalidad, y las trayectorias del envejecimiento pueden comenzar en las primeras etapas de la vida. Este estudio se diseñó para analizar si una intervención preventiva familiar y universal en el abuso de sustancias orientada a mejorar el autocontrol y a reducir el consumo de sustancias también tendría como resultado disminuciones del envejecimiento biológico entre jóvenes negros del sur rural. El programa Adults in the Making (AIM) es un ensayo controlado aleatorizado con seis sesiones de dos horas para jóvenes negros. Entre los 216 jóvenes que aceptaron dar sangre a los 22 años se encontraban 114 que habían recibido la intervención del AIM y 102 asignados al grupo de referencia. Analizamos el envejecimiento basado en la metilación acelerada del ADN (ADNm) usando un método de medición desarrollado recientemente que se llama "GrimAge", el cual, según se ha demostrado, predice el riesgo de mortalidad temprana y está más marcadamente afectado por el consumo de sustancias que otros índices de envejecimiento basados en el ADNm. En relación con las personas asignadas aleatoriamente al grupo de referencia, las que recibieron la intervención demostraron un autocontrol considerablemente mayor, aumentos más lentos de consumo de sustancias y un menor envejecimiento Grim a los 22 años. Utilizando un método de muestreo con reemplazamiento con 1000 reproducciones, hallamos un efecto indirecto significativo del AIM en un menor envejecimiento Grim mediante su efecto en el autocontrol y el consumo de sustancias. Los análisis de sensibilidad examinaron los efectos utilizando otros índices de envejecimiento basados en el ADNm. Estos resultados indican que un programa familiar diseñado para aumentar el autocontrol de los jóvenes negros de zonas rurales puede tener efectos beneficiosos en el autocontrol, mejorar la salud de los adultos jóvenes y su conducta con respecto a la salud y, finalmente, disminuir el riesgo de mortalidad.

Effects of physical driving experience on body movement and motion sickness among passengers in a virtual vehicle.

Virtual vehicles (e.g., driving video games) can give rise to visually induced motion sickness. Typically, people drive virtual vehicles. In the present study, we investigated motion sickness among participants who were exposed to virtual vehicles as passengers; that is, they observed vehicle motion, but did not control it. We also asked how motion sickness and the postural precursors of motion sickness might be influenced by participants' previous experience of driving physical vehicles. Participants viewed a recording of a virtual automobile in a driving video game. Drivers were young adults with several years of experience driving physical automobiles, while non-drivers were individuals in the same age group who did not have a driver's license and had never driven an automobile. During exposure to the virtual vehicle, we monitored movement of the head and torso. The independent measures included the incidence and severity of motion sickness. After exposure to the virtual vehicle, the incidence and severity of motion sickness did not differ between Drivers and Non-Drivers. By contrast, postural movement differed between participants who later became motion sick and those who did not. In addition, during exposure to the virtual vehicle, physical driving experience was related to patterns of postural activity that preceded motion sickness. The results are consistent with the postural instability theory of motion sickness, and illuminate relations between the control of physical and virtual vehicles.

Childhood adversity is linked to adult health among African Americans via adolescent weight gain and effects are genetically moderated.

Identifying the mechanisms linking early experiences, genetic risk factors, and their interaction with later health consequences is central to the development of preventive interventions and identifying potential boundary conditions for their efficacy. In the current investigation of 412 African American adolescents followed across a 20-year period, we examined change in body mass index (BMI) across adolescence as one possible mechanism linking childhood adversity and adult health. We found associations of childhood adversity with objective indicators of young adult health, including a cardiometabolic risk index, a methylomic aging index, and a count of chronic health conditions. Childhood adversities were associated with objective indicators indirectly through their association with gains in BMI across adolescence and early adulthood. We also found evidence of an association of genetic risk with weight gain across adolescence and young adult health, as well as genetic moderation of childhood adversity's effect on gains in BMI, resulting in moderated mediation. These patterns indicated that genetic risk moderated the indirect pathways from childhood adversity to young adult health outcomes and childhood adversity moderated the indirect pathways from genetic risk to young adult health outcomes through effects on weight gain during adolescence and early adulthood.

Can We Uncouple Neighborhood Disadvantage and Delinquent Behaviors? An Experimental Test of Family Resilience Guided by the Social Disorganization Theory of Delinquent Behaviors.

Although the influence of neighborhood disadvantage on youth development of delinquent behavior is well established, findings from this research have yet to inform the development of family-centered prevention programming to protect youth from these erosive effects. The current paper examines the role of family integration in buffering the impact of social disadvantage in a sample of N = 298 families randomly assigned either to a control condition or to a family-based prevention program previously shown to enhance marriage and parenting. We first confirmed that neighborhood concentrated disadvantage predicted change in delinquent behaviors across the course of the study. Additionally, replicating prior work, parents participating in the Protecting Strong African American Families (ProSAAF) program, relative to those randomly assigned to the control group, significantly improved their use of effective communication strategies with each other and reduced ineffective conflict in front of youth. This resulted in a significant indirect effect of ProSAAF on change in youth delinquent behaviors. Furthermore, using mediated moderation analysis, the study tested the buffering effect of greater family integration, showing that experimentally produced change in interparental communication skills and the resulting reduction in youth exposure to parental conflict buffered the effect of neighborhood disadvantage on change in youth delinquent behaviors, supporting a mediated moderation model in which family environments buffer neighborhood effects.

Aunque la influencia de los barrios desfavorecidos en el desarrollo de conductas delictivas en los jóvenes está firmemente consolidada, los hallazgos de esta investigación contribuirán al desarrollo de un programa de prevención centrado en la familia para proteger a los jóvenes de estos efectos erosivos. El presente artículo analiza el papel de la integración familiar en la moderación del efecto de las desventajas sociales en una muestra de N = 298 familias asignadas aleatoriamente a una condición de control o a un programa de prevención basado en la familia que anteriormente ha demostrado mejorar el matrimonio y la crianza. Primero confirmamos que la desventaja concentrada de los barrios predijo el cambio de conductas delictivas a lo largo del transcurso del estudio. Además, replicando trabajos anteriores, los padres que participaron en el programa "Protección de Familias Afroamericanas Fuertes" (Protecting Strong African American Families, ProSAAF), en comparación con aquellos asignados aleatoriamente al grupo de control, mejoraron considerablemente su uso de estrategias de comunicación eficaz entre ellos y redujeron el conflicto ineficaz en frente de los jóvenes. Esto resultó en un efecto indirecto considerable del ProSAAF en el cambio de las conductas delictivas en los jóvenes. Además, mediante el uso del análisis de moderación mediada, el estudio evaluó el efecto moderador de una mayor integración familiar, lo cual demostró que el cambio producido experimentalmente en las habilidades de comunicación interparental y la reducción resultante de la exposición de los jóvenes al conflicto parental moderaron el efecto de la desventaja del barrio en el cambio de las conductas delictivas de los jóvenes. Todo esto respaldó un modelo de moderación mediada en el cual los entornos familiares moderan los efectos del barrio.

Childhood Adversities as Determinants of Cardiovascular Disease Risk and Perceived Illness Burden in Adulthood: Comparing Retrospective and Prospective Self-Report Measures in a Longitudinal Sample of African Americans.

A large body of evidence suggests that exposure to childhood adversities increases risk for poor quality physical health in adulthood. Much of this evidence is based on retrospective measures which are believed to be contaminated by the limitations and biases of autobiographical memory. Using longitudinal data on 454 African Americans (61 percent female) this study examines the corroboration between prospective and retrospective measures of childhood adversities gathered approximately two decades apart, and the relative ability of the measures to predict self-reported illnesses and a biomarker of 30-year cardiovascular disease risk. Comparisons indicated that the retrospective and prospective measures demonstrated weak convergence and did not provide completely equivalent information about self-reported adverse childhood experiences. A series of regression models indicated that the two measures of adversities exhibited similar associations with the cardiovascular disease biomarker but divergent associations with self-reported illnesses. Furthermore, both the prospective and retrospective measures simultaneously predicted cardiovascular disease risk in adulthood. That the prospective measure did not significantly predict perceived illnesses after adjusting for the retrospective measure is evidence that childhood adversities predict self-reported health burden insofar as respondents remember those adversities as adults. The findings provide evidence that retrospective self-report measures of childhood adversities do not closely converge with prospective measures, and that retrospective measures may not provide valid estimates of the association between childhood adversities and perceived illnesses in adulthood.

Youth Adversities Amplify the Association between Adult Stressors and Chronic Inflammation in a Domain Specific Manner: Nuancing the Early Life Sensitivity Model.

There is strong evidence that chronic, systemic inflammation hastens onset of the diseases of old age that ultimately lead to death. Importantly, several studies suggest that childhood adversity predicts chronic inflammation. Unfortunately, this research has been plagued by retrospective reports of childhood adversity, an absence of controls for adult stressors, and a failure to investigate various competing models of the link between childhood adversity and chronic inflammation. The present study was designed to address these limitations. Using 18 years of data collected from 413 African Americans (58% female) included in the Family and Community Health Study, hierarchical regression analyses provided support for a nuanced early life sensitivity explanation for the link between early adversity and adult chronic inflammation. Controlling for health risk behaviors and adult SES, late childhood (ages 10-12) adversity amplified the association between adult adversity (age 29) and chronic inflammation. This interaction operated in a domain-specific fashion. Harsh parenting amplified the relation between intimate partner hostility and inflammation, whereas early discrimination amplified the relation between adult discrimination and inflammation. These findings suggest that individuals may be primed to respond physiologically to adverse adult circumstances that resemble those experienced earlier in life.

Biological embedding of neighborhood disadvantage and collective efficacy: Influences on chronic illness via accelerated cardiometabolic age.

The present study extends prior research on the link between neighborhood disadvantage and chronic illness by testing an integrated model in which neighborhood characteristics exert effects on health conditions through accelerated cardiometabolic aging. Hypotheses were tested using a sample of 408 African Americans from the Family and Community Health Study. Using four waves of data spanning young adulthood (ages 18-29), we first found durable effects of neighborhood disadvantage on accelerated cardiometabolic aging and chronic illness. Then, we used marginal structural modeling to adjust for potential neighborhood selection effects. As expected, accelerated cardiometabolic aging was the biopsychosocial mechanism that mediated much of the association between neighborhood disadvantage and chronic illness. This finding provides additional support for the view that neighborhood disadvantage can influence morbidity and mortality by creating social contexts that becomes biologically embedded. Perceived neighborhood collective efficacy served to buffer the relationship between neighborhood disadvantage and biological aging, identifying neighborhood-level resilience factor. Overall, our results indicate that neighborhood context serves as a fundamental cause of weathering and accelerated biological aging. Residing in a disadvantaged neighborhood increases biological wear and tear that ultimately leads to onset of chronic illness, but access to perceived collective efficacy buffers the impact of these neighborhood effects. From an intervention standpoint, identifying such an integrated model may help inform future health-promoting interventions.

Prevention of Early Substance Use Mediates, and Variation at SLC6A4 Moderates, SAAF Intervention Effects on OXTR Methylation.

The Strong African American Family (SAAF) program has been shown to have a variety of short and long-term benefits for participating youth and families. However, biological mechanisms potentially influencing long-term effects on resilience in young adulthood have not been examined. In the current investigation, we examine the effects of SAAF on methylation of the OXTR gene in young adulthood, focusing on a regulatory region previously identified to be both responsive to stress and implicated in resilience. Using the subsample of participants from the original study for whom methylation data was available (N = 388), we replicated the previously reported G × E effect on prevention of early substance use and then examined whether there would also be a moderated effect on OXTR methylation in early adulthood, with "s" allele carriers, but not "LL" participants, showing a significant indirect effect of SAAF on OXTR methylation. Results suggest that for susceptible youth (i.e., "s" allele carriers), preventive intervention may "get under the skin," in a manner potentially beneficial for long-term outcomes. Implications for examination of OXTR methylation in future prevention research are discussed.

Methylation of the oxytocin receptor gene mediates the effect of adversity on negative schemas and depression.

Building upon various lines of research, we posited that methylation of the oxytocin receptor gene (OXTR) would mediate the effect of adult adversity on increased commitment to negative schemas and in turn the development of depression. We tested our model using structural equation modeling and longitudinal data from a sample of 100 middle-aged, African American women. The results provided strong support for the model. Analysis of the 12 CpG sites available for the promoter region of the OXTR gene identified four factors. One of these factors was related to the study variables, whereas the others were not. This factor mediated the effect of adult adversity on schemas relating to pessimism and distrust, and these schemas, in turn, mediated the impact of OXTR methylation on depression. All indirect effects were statistically significant, and they remained significant after controlling for childhood trauma, age, romantic relationship status, individual differences in cell types, and average level of genome-wide methylation. These finding suggest that epigenetic regulation of the oxytocin system may be a mechanism whereby the negative cognitions central to depression become biologically embedded.

When inflammation and depression go together: The longitudinal effects of parent-child relationships.

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.

Smoking in young adulthood among African Americans: Interconnected effects of supportive parenting in early adolescence, proinflammatory epitype, and young adult stress.

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.

A pilot investigation of the impact of smoking cessation on biological age.

BACKGROUND AND OBJECTIVES: Smoking is known to increase biological age. However, whether this process is reversible through smoking cessation is not known. In this pilot study, we attempt to determine whether smoking cessation reduces biological age. METHODS: We conducted regression analyses of methylation data from 22 subjects, as they entered and exited inpatient substance use treatment, to determine change in biological age, as indicated by the deviation of their methylomic age from chronological age across two time points. RESULTS: We found that, as compared to those subjects who did not stop smoking, subjects who significantly decreased their smoking consumption over a 1 month time period exhibited a marked reduction in methylomic age. CONCLUSION: The rapid and substantial reversal of accelerated aging associated with successful smoking cessation suggests that it can reverse well-known smoking effects on methylomic aging. This preliminary finding can be readily examined in other, larger data sets, and if replicated, this observation may provide smokers with yet another good reason to quit smoking. SCIENTIFIC SIGNIFICANCE: Successful smoking cessation makes patients appear biologically younger than they were at baseline, and to do so quite rapidly. In today's youth driven society, our observations may serve as a powerful impetus for some to quit smoking. (Am J Addict 2017;26:129-135).

MTHFR methylation moderates the impact of smoking on DNA methylation at AHRR for African American young adults.

Smoking has been shown to have a large, reliable, and rapid effect on demethylation of AHRR, particularly at cg05575921, suggesting that methylation may be used as an index of cigarette consumption. Because the availability of methyl donors may also influence the degree of demethylation in response to smoking, factors that affect the activity of methylene tetrahydrofolate reductase (MTHFR), a key regulator of methyl group availability, may be of interest. In the current investigation, we examined the extent to which individual differences in methylation of MTHFR moderated the association between smoking and demethylation at cg05575921 as well as at other loci on AHRR associated with a main effect of smoking. Using a discovery sample (AIM, N = 293), and a confirmatory sample (SHAPE, N = 368) of young adult African Americans, degree of methylation of loci in the first exon of MTHFR was associated with amplification of the association between smoking and AHRR demethylation at cg05575921. However, genetic variation at a commonly studied MTHFR variant, C677T, did not influence cg05575921 methylation. The significant interaction between MTHFR methylation and the smoking-induced response at cg05575921 suggests a role for individual differences in methyl cycle regulation in understanding the effects of cigarette consumption on genome wide DNA methylation.

Parenting, Socioeconomic Status Risk, and Later Young Adult Health: Exploration of Opposing Indirect Effects via DNA Methylation.

A sample of 398 African American youth, residing in rural counties with high poverty and unemployment, were followed from ages 11 to 19. Protective parenting was associated with better health, whereas elevated socioeconomic status (SES) risk was associated with poorer health at age 19. Genome-wide epigenetic variation assessed in young adulthood (age 19), was associated with both SES risk and protective parenting. Three categories of genes were identified whose methylation was associated with parenting, SES risk, and young adult health. Methylation was a significant mediator of the impact of parenting and SES risk on young adult health. Variation in mononuclear white blood cell types was also examined and controlled, showing that it did not account for observed effects of parenting and SES risk on health.

Implementing Family-Centered Prevention in Rural African American Communities: a Randomized Effectiveness Trial of the Strong African American Families Program.

Efforts to disseminate evidence-based prevention programs are hampered by a lack of real-world effectiveness trials undertaken with community providers. The Strong African American Families (SAAF) program is an empirically validated intervention designed to prevent problem behavior among rural African American youth. To evaluate the effectiveness of SAAF and its implementation protocols when delivered by a community provider, we conducted a randomized, wait-list-controlled trial with outcome measurements assessed longitudinally at baseline and 6 months after baseline. A total of 465 African American youth and their parents were recruited randomly from public school lists of fifth- and sixth-grade students in eight rural counties in south Georgia. Youth and parents assessed targeted outcomes in their homes. The main outcome, problem behavior vulnerability, was operationalized as a latent construct comprising three indicators: tolerance for deviance, intentions to engage in risky behavior, and affiliations with risk-taking peers. SAAF was implemented with uniformly high levels of adherence (85.5%; SD = 10.8) and attendance (M = 4.1, SD = 2.9, range = 0-7). Intent-to-treat and complier average causal effect analyses revealed significant program effects on intervention-targeted parenting practices, youth self-regulatory processes, and problem behavior vulnerability. SAAF influenced problem behavior vulnerability indirectly via effects on targeted parenting and youth processes. This study supported the effectiveness of SAAF in a community setting when a systematic implementation model supports participant engagement and intervention adherence.

Decreasing Substance use Risk among African American Youth: Parent-based Mechanisms of Change.

African American couples (N = 139; 67.7 % married; with children between the ages of 9 and 14) were randomly assigned to (a) a culturally sensitive, couple- and parenting-focused program designed to prevent stress-spillover (n = 70) or (b) an information-only control condition in which couples received self-help materials (n = 69). Eight months after baseline, youth whose parents participated in the program, compared with control youth, reported increased parental monitoring, positive racial socialization, and positive self-concept, as well as decreased conduct problems and self-reported substance use. Changes in youth-reported parenting behavior partially mediated the effect of the intervention on conduct problems and fully mediated its impact on positive self-concept, but did not mediate effects on lifetime substance use initiation. Results suggest the potential for a culturally sensitive family-based intervention targeting adults' couple and parenting processes to enhance multiple parenting behaviors as well as decrease youths' substance use onset and vulnerability.