ABSTRACT
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.
Subject(s)
Electronic Nicotine Delivery Systems , Racism , Smoking Cessation , Adult , Humans , Delivery of Health Care , Smoking Cessation/methods , Tobacco Use Cessation Devices , Black or African AmericanABSTRACT
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.
Subject(s)
Cigarette Smoking , Racism , Young Adult , Child , Humans , Adolescent , Adult , Black or African American , Longitudinal Studies , Racial GroupsABSTRACT
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 (nâ =â 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 (pâ <â .01). More experiences of racial discrimination were associated with past month cigarillo use, but not hookah or large cigars (pâ <â .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.
Subject(s)
Advertising , Electronic Nicotine Delivery Systems , Racism , Tobacco Products , Tobacco Use , Tobacco, Smokeless , Adult , Humans , United States , Black or African AmericanABSTRACT
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.
Subject(s)
Income , Loneliness , Adult , Middle Aged , Humans , Aging , Black People , DNAABSTRACT
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.
Subject(s)
Cotinine , Proteomics , Adult , Humans , Self Report , Alcohol Drinking/genetics , Biomarkers , Aging/genetics , Epigenesis, Genetic , CarbohydratesABSTRACT
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.
Subject(s)
Smoking , Tobacco Products , Humans , Smoking/genetics , DNA Methylation , Aging/genetics , Ethanol , Epigenesis, Genetic , Alcohol Drinking/genetics , Alcohol Drinking/adverse effectsABSTRACT
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.
Subject(s)
Epigenomics , Life Style , Aging/genetics , DNA Methylation , Epigenesis, Genetic , Female , Humans , Middle Aged , Socioeconomic FactorsABSTRACT
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).
Subject(s)
Adverse Childhood Experiences , DNA Methylation , Animals , Humans , Young Adult , Child , Adolescent , Adult , Hylobates/genetics , Aging/genetics , DNA , Epigenesis, GeneticABSTRACT
Methylation of FKBP5 is involved in the regulation of the stress response and is influenced by early stress exposure. Two CpG sites, cg20813374 and cg00130530, have been identified as potential reporters of early stress. We examined whether FKBP5 methylation was associated with accelerated DNA methylation ageing and indirectly predicted poorer cardiovascular health among both young adult and middle-aged Black Americans. Four hundred and forty-nine young adults, with a mean age of 28.67 and N = 469 middle-age parents and their current partners with a mean age of 57.21, provided self-reports, biometric assessments, and blood draws. Methylation values were obtained using the Illumina Epic Array. Cardiometabolic risk was calculated by summing the standardized log-transformed scores for the body mass index, mean arterial blood pressure, and HbA1c. We also used a more standard index of risk, the Framingham 10-year cardiometabolic risk index, as an alternative measure of cardiometabolic risk. To measure accelerated ageing, four widely used indices of accelerated, DNA methylation-based ageing were used controlling sex, age, other variation in FKBP5, and cell-type. Exposure to community danger was associated with demethylation of FKBP5. FKBP5 methylation was significantly associated with accelerated ageing for both young-adult and middle-aged samples, with significant indirect effects from FKBP5 methylation to cardiometabolic risk through accelerated ageing for both. Early exposure to danger may influence FKBP5 methylation. In turn, FKBP5 methylation may help explain intrinsic accelerated ageing and elevated cardiometabolic risk in adulthood for Black Americans.
Subject(s)
Cardiovascular Diseases , DNA Methylation , Adult , Aging/genetics , Body Mass Index , Cardiovascular Diseases/genetics , Glycated Hemoglobin/genetics , Humans , Middle Aged , Tacrolimus Binding Proteins/genetics , Tacrolimus Binding Proteins/metabolism , Young AdultABSTRACT
Given the potential for unintended pregnancy and exposure to sexually transmitted infections, both of which can have long-term deleterious health consequences, the identification of predictors of adolescent risky sexual behavior remains an important line of inquiry. Although prior research has identified a variety of family and individual factors that are associated with risky sexual behavior, few studies have examined the role of family economic stress. The current study utilized three waves of data from a community sample of African American families with adolescents (N = 778, 54% girls, average age = 10.4 years old at Wave 1, 12.3 years old at Wave 2, 15.6 years old at Wave 3) to test the family stress model as an explanation of adolescent risky sexual behavior. Multi-group analyses examined gender differences in the family processes expected to link economic stress and risky sexual behavior. Unlike most studies utilizing this theoretical perspective, family structure was also taken into account. The results supported the propositions of the family stress model for boys and girls for both two-caregiver and single-mother households. Further, in single-mother households, maternal psychological distress continued to have a positive effect on adolescent risky sex even after taking into account the impact of parenting behaviors. Overall, the results suggest that economic stress ripples through the family system, increasing adolescent risky sexual behavior through its negative impact on family processes, highlighting the need for systemic policy changes rather than individual-level intervention/prevention efforts.
Subject(s)
Adolescent Behavior , Sexually Transmitted Diseases , Adolescent , Adolescent Behavior/psychology , Black or African American/psychology , Child , Female , Humans , Male , Pregnancy , Risk-Taking , Sexual Behavior/psychologyABSTRACT
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.
ABSTRACT
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).
Subject(s)
Black or African American/psychology , Health Behavior , Racism/psychology , Social Perception/psychology , Adolescent , Adult , Aged , Aged, 80 and over , Anxiety/ethnology , Caregivers/psychology , Child , Depression/ethnology , Female , Health Status , Humans , Male , Middle Aged , Prospective Studies , Substance-Related Disorders , Young AdultABSTRACT
The NIMH Research Domain Criteria (RDoC) initiative aims to understand the mechanisms influencing psychopathology through a dimensional approach. Limited research thus far has considered potential racial/ethnic differences in RDoC constructs that are influenced by developmental and contextual processes. A growing body of research has demonstrated that racial trauma is a pervasive chronic stressor that impacts the health of Black Americans across the life course. In this review article, we examine the ways that an RDOC framework could allow us to better understand the biological embedding of racial trauma among Black Americans. We also specifically examine the Negative Valence System domain of RDoC to explore how racial trauma is informed by and can help expand our understanding of this domain. We end the review by providing some additional research considerations and future research directives in the area of racial trauma that build on the RDoC initiative.
Subject(s)
Mental Disorders , Black or African American , Humans , National Institute of Mental Health (U.S.) , Psychopathology , United StatesABSTRACT
It is widely accepted that socioeconomic status (SES) is a fundamental cause of health inequality. There is evidence, however, that race is also a fundamental cause of disparities in health. Based on this idea, the weathering hypothesis developed by Geronimus and her colleagues views the elevated rates of illness and disability seen among Black Americans as a physiological response to the structural barriers, daily slights, and other threats to identity that comprise the Black experience. The current study tests the weathering hypothesis using chronic inflammation as an indicator of biological weathering. Specifically, we examine the extent to which persistent exposure to racial discrimination predicts elevated inflammation and, in turn, diagnosed chronic illness, after taking into account SES and several control variables. This mediation model was tested using zero-inflated Poisson path modeling with five waves of data collected from 391 African American women participating in the Family and Community Health Study (FACHS). A 13-item index was used to assess exposure to racial discrimination across 8 years. ELISA blood assays of seven cytokines central to the inflammatory response were used to construct an inflammatory index. Respondents reported their diagnosed chronic diseases. Consonant with the weathering hypothesis, persistent exposure to discrimination predicted inflammation which, in turn, predicted number of chronic diseases. This indirect effect was statistically significant. SES predicted having a chronic disease and the various controls showed no effect. The findings support the idea that race, like SES, is a fundamental cause of health inequalities.
Subject(s)
Black or African American/statistics & numerical data , Chronic Disease/ethnology , Health Status Disparities , Inflammation/ethnology , Racism/statistics & numerical data , Female , Humans , Middle Aged , Social ClassABSTRACT
BACKGROUND: The weathering hypothesis views the elevated rates of illness, disability, and mortality seen among Black Americans as a physiological response to the structural barriers, material hardships, and identity threats that comprise the Black experience. While granting that lifestyle may have some significance, the fundamental explanation for heath inequalities is seen as race-related stressors that accelerate biological aging. OBJECTIVE: The present study tests the weathering hypothesis by examining the impact on accelerated aging of four types of adversity frequently experienced by Black Americans. Further, we investigate whether health risk behaviors mediate the effect of these conditions. METHOD: Our analyses utilize data from 494 middle-age, African American men and women participating in the Family and Community Healthy Study. The newly developed GrimAge index of accelerated aging is used as an indicator of weathering. Education, income, neighborhood disadvantage, and discrimination serve as the independent variables. Three health risk behaviors - diet, exercise, and alcohol consumption - are included as potential mediators of the four types of adversity. Marital status and gender are entered as controls. RESULTS: Multivariate analyses indicated that the four types of adversity predicted acceleration whereas marriage predicted deceleration in speed of aging. Males showed greater accelerated aging than females, but there was no evidence that gender conditioned the effect of adversity. The health risk behaviors were unrelated to accelerated aging and did not mediate the effect of the stressors. CONCLUSION: Modern medicine's emphasis on life style as the primary explanation for race-based health disparities ignores the way race-related adversity rooted in structural and cultural conditions serves to accelerate biological decline, thereby increasing risk of early onset of illness and death. Importantly, these social conditions can only be addressed through social policies and programs that target institutional racism and promote economic equity.
Subject(s)
Black or African American , Racism , Aging , Educational Status , Female , Health Risk Behaviors , Humans , Male , Middle AgedABSTRACT
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.
Subject(s)
Adverse Childhood Experiences , Black or African American , Adolescent , Adult , Black or African American/genetics , Body Mass Index , Humans , Risk Factors , Weight Gain/genetics , Young AdultABSTRACT
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.
Subject(s)
DNA Methylation , Epigenomics , Alcohol Drinking , Epigenesis, Genetic , Humans , Polymerase Chain ReactionABSTRACT
Racial socialization is a culturally relevant parenting strategy known to combat the detrimental consequences of racial discrimination for African American youth. Three limitations hinder our developmental understanding of the racial socialization process. Few studies have accounted for the combination of messages that primary caregivers convey, examined how these messages change over time, or investigated how caregivers and adolescents experiences with racial discrimination predict change in the combination of messages conveyed. Given that African American mothers are often the primary socializers in families, the current study used data from a community sample of 497 African American adolescents (52% Female; Time 1 Mage = 15.69; Time 2 Mage = 18.74) and their mothers (Time 1 Mage = 40.43; Time 2 Mage = 43.39) to identify patterns in mothers' racial socialization messages, identify how mothers' racial socialization patterns change from middle to late adolescence, and investigate whether mother- and adolescent-reported racial discrimination contribute to changes in mothers' racial socialization patterns. Latent profile analysis and latent transition analysis were used to examine these questions. Findings revealed three racial socialization patterns: balanced socializers who mistrust, cultural socialization and preparation for bias emphasizers, and low racial socializers. Most mothers were in the low racial socializers group, and most provided similar messages in middle and late adolescence. Mothers' reports of their own racial discrimination influenced the racial socialization messages mothers delivered; however, adolescent-reported racial discrimination did not. These results have implications for community-based interventions designed to help families manage racial discrimination. (PsycInfo Database Record (c) 2020 APA, all rights reserved).
Subject(s)
Black or African American/psychology , Mothers/psychology , Parenting/psychology , Racism/psychology , Socialization , Adolescent , Adult , Female , Humans , Male , Social IdentificationABSTRACT
Epigenetic aging (EA) indices are frequently used as predictors of mortality and other important health outcomes. However, each of the commonly used array-based indices has significant heritable components which could tag ethnicity and potentially confound comparisons across racial and ethnic groups. To determine if this was possible, we examined the relationship of DNA methylation in cord blood from 203 newborns (112 African American (AA) and 91 White) at the 513 probes from the Levine PhenoAge Epigenetic Aging index to ethnicity. Then, we examined all sites significantly associated with race in the newborn sample to determine if they were also associated with an index of ethnic genetic heritage in a cohort of 505 AA adults. After Bonferroni correction, methylation at 50 CpG sites was significantly associated with ethnicity in the newborn cohort. The five most significant sites predicted ancestry with a receiver operator characteristic area under the curve of 0.97. Examination of the top 50 sites in the AA adult cohort showed that methylation status at 11 of those sites was also associated with percentage European ancestry. We conclude that the Levine PhenoAge Index is influenced by cryptic ethnic-specific genetic influences. This influence may extend to similarly constructed EA indices and bias cross-race comparisons.
Subject(s)
Aging/genetics , DNA Methylation/genetics , Epigenesis, Genetic/genetics , Black or African American/genetics , Aging/blood , Ethnicity/genetics , Female , Fetal Blood/metabolism , Hispanic or Latino/genetics , Humans , Infant, Newborn , Male , White People/geneticsABSTRACT
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.