Association of racial discrimination in health care settings and use of electronic cigarettes to quit smoking among Black adults.

INTRODUCTION: Black people are disproportionately burdened by tobacco-related diseases and are less successful at cigarette cessation with current treatments. We know little about the effectiveness of e-cigarettes as a smoking cessation method compared to currently approved methods in Black adults who smoke. Many Black adults report experiencing racial discrimination in health care, but if discrimination is related to utilization of smoking cessation aids including e-cigarettes and success with smoking cessation in this population is unclear. Therefore, this exploratory study aimed to understand how negative experiences and racial discrimination in health care influence use of e-cigarettes for cigarette cessation and success with cigarette cessation among Black adults. METHODS: The study interviewed 201 Black adults who used cigarettes and tried to quit in their lifetime from the Family and Community Health Study in 2016. The study asked if they had tried and successfully quit cigarettes with e-cigarettes vs. other methods (support groups, medications, nicotine replacement therapies, call-in help lines, cold turkey [quit on their own], counseling) and asked about their negative experiences and racial discrimination in health care. We performed separate logistic regressions that evaluated the association of negative experiences and racial discrimination in health care with 1) use of e-cigarettes for cigarette cessation vs. other quitting methods and 2) success with cigarette cessation using any method among Black adults while controlling for age, sex, socioeconomic status, health insurance status, and age of onset of cigarette use. RESULTS: More reported negative experiences and racial discrimination in health care were associated with ever trying to quit with e-cigarettes compared to other methods (OR:1.75, 95 % CI [1.05-2.91]), but negative experiences and racial discrimination in health care were not associated with cigarette quitting success. Interestingly, trying e-cigarettes was associated with being less successful at quitting compared to using other methods to quit smoking (OR: 0.40, 95 % CI [0.20, 0.81]). CONCLUSIONS: These results suggest that educating health care professionals that anticipated discrimination in health care settings may be driving Black adults who smoke to engage in non-evidence-based smoking cessation practices, such as e-cigarettes instead of those that are evidence-based, and may be more effective in this population.

Racial centrality mediates the association between adolescent racial discrimination and adult cigarette smoking outcomes among Black Americans.

OBJECTIVE: The objective of this study was to investigate racial centrality as a mediator of the association between Black adolescents' racial discrimination experiences and their cigarette use in early adulthood. METHODS: The data were drawn from the Family and Community Health Study, which is a longitudinal study of Black American families that began in 1996. Families with a child in 5th grade who identified as Black or African American were recruited from Iowa and Georgia. At baseline, there were 838 Black American children. Hierarchical regressions and bootstrap tests of the indirect effects were used to investigate whether racial centrality at Wave 5 (mean age = 21.6 years) mediated the association between adolescent discrimination at Waves 1-4 (mean ages = 10.5-18.8 years) and adult cigarette use at wave 6 (mean age = 23.5 years). RESULTS: Bivariate associations indicated racial discrimination was significantly associated positively with racial centrality and adult use of cigarettes. Racial centrality indirectly affected the association between racial discrimination and cigarette use such that greater racial centrality was associated with less cigarette use. Further, racial centrality predicted cessation among those who had smoked. Finally, racial centrality was higher among those who never smoked and those who had smoked and quit, relative to those who currently smoke. CONCLUSIONS: These findings suggest that having strong Black racial centrality is a mediator that reduces the risk of cigarette use among young adults who experience racial discrimination in adolescence. In addition, racial centrality also predicts smoking cessation among young Black Americans who smoke. Translational implications of these findings are discussed.

Association of Non-Cigarette Tobacco Advertisements and Racial Discrimination With Non-Cigarette Tobacco Product Use Among Black Adults.

INTRODUCTION: Black communities are targeted by more cigarette advertisements than White communities and racial discrimination among Black people is related to cigarette use. However, little is known about these factors with non-cigarette tobacco product use among Black adults. Therefore, this study assessed the association of non-cigarette advertisement exposure and racial discrimination with use of non-cigarette tobacco products among Black adults. AIMS AND METHODS: Black adults (n = 533) from The Family and Community Health Study in 2016 were asked if they had seen advertisements for e-cigarettes, snus pouches, filtered cigars, large cigars, cigarillos, dissolvable tobacco, smokeless tobacco, hookah, and tobacco pipe and if they used these in the past month. For products with the highest past month use and significant correlations with advertisement exposure, separate logistic regression models were performed that evaluated the association between advertisement exposure, racial discrimination, and non-cigarette tobacco product use while controlling for cigarette use, sex, socioeconomic status, and age. RESULTS: Use of cigarillos, large cigars, and hookah were higher than other non-cigarette tobacco products assessed. Logistic regressions revealed that more advertisement exposure in the past month was associated with higher odds of using cigarillos, large cigars, and hookah (p < .01). More experiences of racial discrimination were associated with past month cigarillo use, but not hookah or large cigars (p < .01). CONCLUSIONS: Non-cigarette tobacco advertisement exposure was associated with the use of non-cigarette tobacco products. Experiences of racial discrimination were associated with the most used non-cigarette tobacco product among Black adults, cigarillos. IMPLICATIONS: This is the first time that a specific type of cigar (ie cigarillos) has been associated with experiences of racial discrimination among Black adults. Efforts to reduce non-cigarette tobacco marketing and eradicate exposure to racial discrimination among Black adults may aid in eliminating tobacco-related health disparities.

Do Loneliness and Per Capita Income Combine to Increase the Pace of Biological Aging for Black Adults across Late Middle Age?

In a sample of 685 late middle-aged Black adults (M age at 2019 = 57.17 years), we examined the effects of loneliness and per capita income on accelerated aging using a newly developed DNA-methylation based index: the DunedinPACE. First, using linear, mixed effects regression in a growth curve framework, we found that change in DunedinPACE was dependent on age, with a linear model best fitting the data (b = 0.004, p < 0.001), indicating that average pace of change increased among older participants. A quadratic effect was also tested, but was non-significant. Beyond the effect of age, both change in loneliness (b = 0.009, p < 0.05) and change in per capita income (b = -0.016, p < 0.001) were significantly associated with change in DunedinPACE across an 11-year period, accounting for significant between person variability observed in the unconditional model. Including non-self-report indices of smoking and alcohol use did not reduce the association of loneliness or per capita income with DunedinPACE. However, change in smoking was strongly associated with change in DunedinPACE such that those reducing their smoking aged less rapidly than those continuing to smoke. In addition, both loneliness and per capita income were associated with DunedinPACE after controlling for variation in cell-types.

Epigenetic and Proteomic Biomarkers of Elevated Alcohol Use Predict Epigenetic Aging and Cell-Type variation Better Than Self-Report.

Excessive alcohol consumption (EAC) has a generally accepted effect on morbidity and mortality, outcomes thought to be reflected in measures of epigenetic aging (EA). As the association of self-reported EAC with EA has not been consistent with these expectations, underscoring the need for readily employable non-self-report tools for accurately assessing and monitoring the contribution of EAC to accelerated EA, newly developed alcohol consumption DNA methylation indices, such as the Alcohol T Score (ATS) and Methyl DetectR (MDR), may be helpful. To test that hypothesis, we used these new indices along with the carbohydrate deficient transferrin (CDT), concurrent as well as past self-reports of EAC, and well-established measures of cigarette smoking to examine the relationship of EAC to both accelerated EA and immune cell counts in a cohort of 437 young Black American adults. We found that MDR, CDT, and ATS were intercorrelated, even after controlling for gender and cotinine effects. Correlations between EA and self-reported EAC were low or non-significant, replicating prior research, whereas correlations with non-self-report indices were significant and more substantial. Comparing non-self-report indices showed that the ATS predicted more than four times as much variance in EA, CDT4 cells and B-cells as for both the MDR and CDT, and better predicted indices of accelerated EA. We conclude that each of the non-self-report indices have differing predictive capacities with respect to key alcohol-related health outcomes, and that the ATS may be particularly useful for clinicians seeking to understand and prevent accelerated EA. The results also underscore the likelihood of substantial underestimates of problematic use when self-report is used and a reduction in correlations with EA and variance in cell-types.

Digital methylation assessments of alcohol and cigarette consumption account for common variance in accelerated epigenetic ageing.

Smoking and Heavy Alcohol Consumption (HAC) are established risk factors for myriad complex disorders of ageing. Yet many prior studies of Epigenetic Ageing (EA) have shown only modest effects of smoking and drinking on accelerated ageing. One potential reason for this conundrum might be the reliance of some prior EA studies on self-reported substance use, which may be unreliable in many samples. To test whether novel, non-self-reported indices would show a stronger association of smoking and HAC to EA, we used methylation sensitive digital PCR (MSdPCR) and data from 437 African American subjects from Wave 7 of the Family and Community Health Study Offspring Cohort to examine the effects of subjective and objective measures of smoking and HAC on 7 indices of EA. Because of limited overall correlations between the various EA indices, we examined patterns of association separately for each index. Consistent with expectations, MSdPCR assessments of smoking and HAC, but not self-reported alcohol consumption, were strongly correlated with accelerated EA. MSdPCR assessments of smoking and HAC accounted for 57% of GrimAge acceleration and the shared variance in GrimAge and DunedinPOAM accelerated EA. We conclude that MSdPCR assessments of smoking and HAC are valuable tools for understanding EA, represent directly targetable conditions for the prevention of premature ageing, and substantially improve upon self-reported assessment of smoking and HAC.

Shifts in lifestyle and socioeconomic circumstances predict change-for better or worse-in speed of epigenetic aging: A study of middle-aged black women.

BACKGROUND: While numerous studies have documented the power of new generation epigenetic clocks to predict morbidity and mortality, research regarding the causes of variation in speed of epigenetic aging is in the early stages. To the extent that these epigenetic clocks are robust measures of biological aging, they should be sensitive to various nutritional, behavioral, ecological, and social factors that have been shown to affect health. OBJECTIVE: Investigate over an 11-year period the extent to which changes in socioeconomic stress and lifestyle predict changes in speed of epigenetic aging among a sample of middle-aged African American women. METHODS: Using data from the Family and Community Health Study, we investigated whether changes in socioeconomic stress, diet, smoking, exercise, alcohol consumption, and relationship status predict changes in speed of biological aging assessed with 3 s-generation epigenetic clocks: AccelGrimAge, DunedinPoAm, and AccelPhenoAge. The study was able to avoid the challenges associated with self-reports of diet and smoking by employing recently developed epigenetic measures. RESULTS: Changes in socioeconomic stress and diet were associated with changes in speed of biological aging as assessed by all three epigenetic clocks, and changes in smoking was related to changes in AccelGrimAge and DunedinPoAm. Analyses controlling for cell-type indicated that in large measure diet exerts its effect on aging through its impact on the immune system. CONCLUSIONS: These findings suggest that adoption of a healthy diet and reduction in the use of tobacco are related to a decrease in epigenetic aging, whereas increased pressure relating to income, housing and economic independence are associated with an increase in the speed of aging. These effects were especially strong for the two epigenetic clocks AccelGrimAge and DunedinPoAm. Overall, the results indicate that stress and lifestyle changes may, for better or worse, influence the "biological weathering" often experienced by middle-aged African American women.

An Examination of Risk Factors for Tobacco and Cannabis Smoke Exposure in Adolescents Using an Epigenetic Biomarker.

Objective: Evolving patterns of nicotine and cannabis use by adolescents require new tools to understand the changing epidemiology of these substances. Here we describe the use of a novel epigenetic biomarker sensitive to both tobacco and cannabis smoke in a longitudinal sample of high-risk adolescents. We examine risk factors for positivity for this epigenetic biomarker in comparison to positivity for conventional serum biomarkers of nicotine and cannabis use. Method: Eastern Iowa 10th graders who had a friend or family member who smoked were eligible to participate in a longitudinal study over 10-12th grades. Subjects provided self-report data on nicotine, tobacco, and cannabis use patterns as well as blood samples that were used for serum cotinine and THC assays. DNA was prepared for analysis of methylation at the CpG cg05575921, a sensitive indicator of smoke exposure. Relationships between positivity for each these biomarkers and a variety of risk factors, including demographics, family and peer relationships, psychopathology, willingness to smoke, and perceptions of typical cigarette and cannabis users, were examined at the 10th (n = 442), 11th (n = 376), and 12th (n = 366) grade timepoints. Results: A increasing proportion of subjects were positive for cotinine (5-16%), THC (3-10%), and cg05575921 methylation (5-7%) across timepoints, with some overlap. Self-reported combusted tobacco and cannabis use was strongly correlated with all biomarkers, whereas cg05575921 methylation was not correlated with reported e-cigarette use. Dual users, defined as those positive for nicotine and THC in the 12th grade showed the greatest cumulative smoke exposure, indicated by cg05575921 methylation. Subjects reported more positive attitudes toward cannabis users than cigarette smokers, and willingness to smoke and positive perceptions of tobacco and cannabis smokers were significant risk factors for biomarker positivity across timepoints. Conclusion: We conclude that measurement of cg05575921 methylation in adolescents is a useful tool in detecting tobacco smoking in adolescents, and may be a novel tool for the detection of cannabis smoking and cannabis and tobacco co-use, though non-combusted forms of nicotine use do not appear to be detectable by this method.

Perceived racial discrimination and healthy behavior among African Americans.

OBJECTIVE: Numerous studies have found evidence of a link between perceived discrimination and unhealthy behavior, especially substance use. Within this body of literature, however, several studies have found unexpected evidence of a positive relation between perceived racial discrimination among African Americans-mostly women-and certain types of healthy behavior, primarily exercise and healthy eating. The current study further examined this positive relation, including an anticipated moderator: optimism. It also examined the relation between perceived racial discrimination and a correlate of unhealthy behavior: BMI. METHOD: Six waves of data were collected over 14 years in three related samples of African Americans from families participating in the Family and Community Health Study. Each family included an adolescent (Mage = 10.5 at Wave 1), the adolescent's primary caregiver (Mage = 37), and, in some cases, an older sibling of that adolescent (Mage = 13). Wave 1 Ns were 889, 889, and 295, respectively. Healthy behavior was defined as diet and exercise. RESULTS: There was very little evidence of a long-term relation between perceived racial discrimination and BMI in any sample, and no evidence of a relation between discrimination and healthy behavior among the males. However, correlational analyses revealed a positive prospective relation between discrimination and healthy behavior among all three groups of females; structural equation modeling indicated that this relation was stronger among women who were high in optimism. CONCLUSIONS: Perceived racial discrimination does not appear to be related to BMI among African Americans, but it is related to healthy behavior among Black females who are high in dispositional optimism. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

A simple, rapid, interpretable, actionable and implementable digital PCR based mortality index.

Mortality assessments are conducted for both civil and commercial purposes. Recent advances in epigenetics have resulted in DNA methylation tools to assess risk and aid in this task. However, widely available array-based algorithms are not readily translatable into clinical tools and do not provide a good foundation for clinical recommendations. Further, recent work shows evidence of heritability and possible racial bias in these indices. Using a publicly available array data set, the Framingham Heart Study (FHS), we develop and test a five-locus mortality-risk algorithm using only previously validated methylation biomarkers that have been shown to be free of racial bias, and that provide specific assessments of smoking, alcohol consumption, diabetes and heart disease. We show that a model using age, sex and methylation measurements at these five loci outperforms the 513 probe Levine index and approximates the predictive power of the 1030 probe GrimAge index. We then show each of the five loci in our algorithm can be assessed using a more powerful, reference-free digital PCR approach, further demonstrating that it is readily clinically translatable. Finally, we show the loci do not reflect ethnically specific variation. We conclude that this algorithm is a simple, yet powerful tool for assessing mortality risk. We further suggest that the output from this or similarly derived algorithms using either array or digital PCR can be used to provide powerful feedback to patients, guide recommendations for additional medical assessments, and help monitor the effect of public health prevention interventions.

Refinement of cg05575921 demethylation response in nascent smoking.

The initiation of adolescent smoking is difficult to detect using carbon monoxide or cotinine assays. Previously, we and others have shown that the methylation of cg05575921 is an accurate predictor of adult smoking status. But the dose and time dependency of the demethylation response to smoking initiation in adolescents is not yet well understood. To this end, we conducted three consecutive annual in-person interviews and biological samplings of 448 high school students (wave 1 (W1)-wave 3 (W3)). At W1 (n = 448), 62 subjects reported using tobacco and 72 subjects reported using cannabis at least once in their life-time with 38 and 20 subjects having a positive cotinine and cannabinoid levels, respectively, at W1 intake. At W3 (n = 383), 67 subjects reported using tobacco and 60 subjects reported using cannabis at least once with 75 and 60 subjects having positive cotinine and cannabinoid levels, respectively, at W3. Subjects with undetectable cotinine levels at all three-time waves had stable levels of cg05575921 methylation throughout the study (88.7% at W1 and 88.8% at W3, n = 149), while subjects with positive cotinine levels at all 3 time points manifested a steady decrease in cg05575921 methylation (81.8% at W1 and 71.3% at the W3, n = 12). In those subjects with an affirmative smoking self-report at W3 (n = 17), the amount of demethylation at cg05575921 was correlated with time and intensity of smoking. We conclude that cg05575921 methylation is a sensitive, dose-dependent indicator of early stages of smoking, and may help to identify smokers in the early stages of smoking.

The Effect of Tobacco Smoking Differs across Indices of DNA Methylation-Based Aging in an African American Sample: DNA Methylation-Based Indices of Smoking Capture These Effects.

Smoking is one of the leading preventable causes of morbidity and mortality worldwide, prompting interest in its association with DNA methylation-based measures of biological aging. Considerable progress has been made in developing DNA methylation-based measures that correspond to self-reported smoking status. In addition, assessment of DNA methylation-based aging has been expanded to better capture individual differences in risk for morbidity and mortality. Untested to date, however, is whether smoking is similarly related to older and newer indices of DNA methylation-based aging, and whether DNA methylation-based indices of smoking can be used in lieu of self-reported smoking to examine effects on DNA methylation-based aging measures. In the current investigation we examine mediation of the impact of self-reported cigarette consumption on accelerated, intrinsic DNA methylation-based aging using indices designed to predict chronological aging, phenotypic aging, and mortality risk, as well as a newly developed DNA methylation-based measure of telomere length. Using a sample of 500 African American middle aged smokers and non-smokers, we found that a) self-reported cigarette consumption was associated with accelerated intrinsic DNA methylation-based aging on some but not all DNA methylation-based aging indices, b) for those aging outcomes associated with self-reported cigarette consumption, DNA methylation-based indicators of smoking typically accounted for greater variance than did self-reported cigarette consumption, and c) self-reported cigarette consumption effects on DNA methylation-based aging indices typically were fully mediated by DNA methylation-based indicators of smoking (e.g., PACKYRS from GrimAge; or cg05575921 CpG site). Results suggest that when DNA methylation-based indices of smoking are substituted for self-reported assessments of smoking, they will typically fully reflect the varied impact of cigarette smoking on intrinsic, accelerated DNA methylation-based aging.

Testing Life Course Models Whereby Juvenile and Adult Adversity Combine to Influence Speed of Biological Aging.

The present study extends prior research on the links between social adversity and aging by employing more comprehensive measures of adversity and a new gene expression index of aging. Hierarchical regression and 20 years of data from a sample of 381 black Americans were used to test models regarding the impact of social adversity on speed of aging. Consistent with the early life sensitivity model, early adversity continued to predict accelerated aging after controlling for adult adversity. Contrary to the pathway model, adult adversity was not related to aging following controls for early adversity. The cumulative stress model received partial support as high adversity during adulthood amplified the effect of early adversity on aging. Finally, consonant with the social change model, low adversity during adulthood buffered the effect of early adversity on aging. These findings held after controlling for health behaviors such as smoking, diet, and exercise.

The effect of early discrimination on accelerated aging among African Americans.

OBJECTIVE: This study examined the role of depressive symptoms in mediating the relationship between early life experiences of racial discrimination and accelerated aging in adulthood for African Americans (i.e., prediction over a 19-year period, from ages 10 to 29) after adjusting for gender and health behaviors. METHOD: Longitudinal self-report data over 7 waves of data collection from the Family and Community Health Study were utilized. The sample included 368 African Americans with usable gene expression data to compute accelerated aging, as well as complete data on all self-report variables including racial discrimination (Schedule of Racist Events) and depression (Diagnostic Interview Schedule for Children-Version 4). Blood was collected by antecubital blood draws from participants at age 29. The proposed model was tested by path analysis. RESULTS: Findings revealed that high discrimination at ages 10-15 was associated with depression at ages 20-29 (ß = .19, p = .001), controlling for depression at ages 10-15, which, in turn, was related to accelerated cellular-level aging (ß = .11, p = .048) after controlling for gender, alcohol consumption, and cigarette use. The indirect effect of racial discrimination on aging through depression at ages 20-29 was significant (ß = .021, 95% confidence interval [.001, .057]), accounting for 32.3% of the total variance. CONCLUSION: These findings support research conceptualizations that early life stress due to racial discrimination lead to sustained negative affective states continuing into young adulthood that confer risk for accelerated aging and possibly premature disease and mortality in African Americans. These findings advance knowledge of potential underlying mechanisms that influence racial health disparities. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Saliva DNA Methylation Detects Nascent Smoking in Adolescents.

Objectives: Early identification of smoking, essential for the successful implementation of interventions, arrests the escalation of smoking and smoking-associated risk behaviors in adolescents. However, because nascent smoking is typically episodic and infrequent, enzyme-linked immunoassay reagent-based approaches that detect cotinine, a key nicotine metabolite, are not effective in identifying adolescents in the earliest stages of smoking. Epigenetic methods may offer an alternative approach for detecting early-stage smokers. In prior work, we and others have shown that the methylation status of cg05575921 of whole-blood DNA accurately predicts smoking status in regularly smoking adults and is sensitive to nascent smoking. Yet, the blood draws necessary to obtain DNA for this method may be poorly accepted by adolescents. Saliva could be an alternative source of DNA. However, the ability of saliva DNA methylation status to predict smoking status among adolescents is unknown. Methods: To explore the possibility of using salivary DNA for screening purposes, we examined the DNA methylation status at cg05575921 in saliva DNA samples from 162 high school aged subjects for whom we also had paired serum cotinine values. Results: Overall, the reliability of self-report of nicotine/tobacco use in these adolescents was poor with 67% of all subjects whose serum levels of cotinine was ≥2 ng/mL (n = 75) denying any use of nicotine-containing products in the past 6 months. However, the correspondence of the two biological measures of smoking was high, with serum cotinine positivity being strongly correlated with cg05575921 methylation (p < 0.0001). Receiver operating characteristic (ROC) analyses showed that cg05575921 methylation status could be used to classify those with positive serum cotinine values (≥2 ng/mL) from those denying smoking and have undetectable levels of cotinine. Conclusions: We conclude that saliva DNA methylation assessments hold promise as a means of detecting nascent smoking.

Inflammation mediates the effect of discrimination, religiosity, and friendship network on expression of the Tp53 cancer suppressor gene.

OBJECTIVE: Chronic inflammation and expression of the TP53 gene are two biomarkers that have been identified as particularly important in the etiology and progression of cancer. While much is known about the determinants of inflammation, there is currently little information regarding the causes of variation in the functioning of TP53, even though it has been recognized for 40 years as the most potent of the cancer suppressor genes. The current paper explores the interrelationship between these two biomarkers and investigates the extent to which they are influenced by the social environment. METHODS: Using structural equation modeling (SEM) and longitudinal observational data from a sample of several hundred African Americans, we tested the hypothesis that adversity - operationalized as racial discrimination- and coping resources - operationalized as religiosity and black friends - influence expression of TP53, for better or worse, through their impact on inflammation. RESULTS: Correlational analysis showed inflammation and TP53 to be inversely related. Further, discrimination was positively related to inflammation and negatively related to TP53 expression, whereas religiosity and black friends were both negatively related to inflammation and positively related to TP53 expression. Finally, SEM indicated that the effect of the social environmental variables on TP53 expression was indirect through level of inflammation. CONCLUSIONS: In addition to its established contribution to cancer through DNA damage and cell proliferation, inflammation likely increases cancer risk indirectly by inhibiting expression of the TP53 cancer suppressor gene. Hence environmental and stress management interventions may do more than reduce inflammation's cell damaging effects; they may also lessen the chances of cancer by increasing expression of TP53.

A Direct Comparison of the Relationship of Epigenetic Aging and Epigenetic Substance Consumption Markers to Mortality in the Framingham Heart Study.

A number of studies have examined the relationship of indices of epigenetic aging (EA) to key health outcomes. Unfortunately, our understanding of the relationship of EA to mortality and substance use-related health variables is unclear. In order to clarify these interpretations, we analyzed the relationship of the Levine EA index (LEA), as well as established epigenetic indices of cigarette (cg05575921) and alcohol consumption (cg04987734), to all-cause mortality in the Framingham Heart Study Offspring Cohort (n = 2256) Cox proportional hazards regression. We found that cg05575921 and cg04987734 had an independent effect relative to LEA and vice versa, with the model including all the predictors having better performance than models with either LEA or cg05575921 and cg04987734 alone. After correction for multiple comparisons, 195 and 327, respectively, of the 513 markers in the LEA index, as well as the overall index itself, were significantly associated with cg05575921 and cg04987734 methylation status. We conclude that the epigenetic indices of substance use have an independent effect over and above LEA, and are slightly stronger predictors of mortality in head-to-head comparisons. We also conclude that the majority of the strength of association conveyed by the LEA is secondary to smoking and drinking behaviors, and that efforts to promote healthy aging should continue to focus on addressing substance use.

Reports of perceived racial discrimination among African American children predict negative affect and smoking behavior in adulthood: A sensitive period hypothesis.

We examined the prospective relations between a cultural risk factor, perceived racial discrimination (PRD), and subsequent negative affect and health behavior (smoking) in a panel of 889 African American children (part of the Family and Community Health Study). Cultural moderators (protective factors) of these relations were also examined. PRD was assessed six times from ages 10.5 (Wave 1) to 24.5 (Wave 6), and negative affect (anger and depressive symptoms) was assessed at Wave 2 (age 12.5) and Wave 6 (age 24.5). Results indicated that Wave 1 PRD predicted Wave 6 smoking, controlling for multiple factors related to smoking and/or PRD, including smoking at age 15.5. Structural equation models indicated that these relations between Wave 1 PRD and smoking were mediated by both early and later negative affect. The models also indicated that Wave 1 PRD had a direct impact on Wave 6 anger (assessed 14 years later), controlling for the effects of PRD on early affect. Cultural socialization was associated with lower rates of adolescent smoking, and it buffered the relation between PRD and Wave 6 anger. The impact of early PRD experiences along with suggestions for culturally informed interventions and preventive interventions that might buffer against early PRD effects are discussed.

Discrimination, segregation, and chronic inflammation: Testing the weathering explanation for the poor health of Black Americans.

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