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Many common chronic diseases of aging are negatively associated with socioeconomic status (SES). This study examines whether inequalities can already be observed in the molecular underpinnings of such diseases in the 30s, before many of them become prevalent. Data come from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a large, nationally representative sample of US subjects who were followed for over two decades beginning in adolescence. We now have transcriptomic data (mRNA-seq) from a random subset of 4,543 of these young adults. SES in the household-of-origin and in young adulthood were examined as covariates of a priori-defined mRNA-based disease signatures and of specific gene transcripts identified de novo. An SES composite from young adulthood predicted many disease signatures, as did income and subjective status. Analyses highlighted SES-based inequalities in immune, inflammatory, ribosomal, and metabolic pathways, several of which play central roles in senescence. Many genes are also involved in transcription, translation, and diverse signaling mechanisms. Average causal-mediated effect models suggest that body mass index plays a key role in accounting for these relationships. Overall, the results reveal inequalities in molecular risk factors for chronic diseases often decades before diagnoses and suggest future directions for social signal transduction models that trace how social circumstances regulate the human genome.
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Classe Social , Adolescente , Adulto , Índice de Massa Corporal , Doença Crônica , Humanos , Estudos Longitudinais , RNA Mensageiro , Fatores Socioeconômicos , Adulto JovemRESUMO
Telomere length (TL) serves as a biomarker of exposure to stressors, including material hardship. Data from the Future of Families and Child Wellbeing Study (1998-2015) were utilized to determine whether prior material hardship was associated with shorter salivary TL at years 9 and 15. 49% of the year 9 study population were female, 49% were Black, and 25% were Hispanic. At year 9 (N = 1990), regression analyses found a significant association between prior material hardship and shorter TL (ß = -.005, p < .01). Additionally, at year 15 (N = 1874), material hardship experienced during infancy and toddlerhood was associated with shorter TL (ß = -.009, p < .01), pointing toward infancy and toddlerhood as a sensitive period.
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Greater educational attainment is generally associated with healthier and longer lives. However, important heterogeneity in who benefits from educational attainment, how much, and why remains underexplored. In particular, in the United States, the physical health returns to educational attainment are not as large for minoritized racial and ethnic groups compared with individuals racialized as White. Yet, our current understanding of ethnoracial differences in educational health disparities is limited by an almost exclusive focus on the quantity of education attained without sufficient attention to heterogeneity within educational attainment categories, such as different institution types among college graduates. Using biomarker data from the National Longitudinal Study of Adolescent to Adult Health (Add Health), we test whether the physical health of college graduates in early adulthood (aged 24-32) varies by institution type and for White, Black, and Hispanic adults. In considering the role of the college context, we conceptualize postsecondary institutions as horizontally stratified and racialized institutional spaces with different implications for the health of their graduates. Finally, we quantify the role of differential attendance at and returns to postsecondary institution type in shaping ethnoracialized health disparities among college graduates in early adulthood.
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Negro ou Afro-Americano , Disparidades nos Níveis de Saúde , Nível de Saúde , Hispânico ou Latino , População Branca , Humanos , Masculino , Adulto , Hispânico ou Latino/estatística & dados numéricos , Feminino , Estados Unidos , Adulto Jovem , Estudos Longitudinais , População Branca/estatística & dados numéricos , Negro ou Afro-Americano/estatística & dados numéricos , Escolaridade , Universidades , Fatores Socioeconômicos , BrancosRESUMO
Can positive transitions into young adulthood at age 25 prevent problematic substance use at age 31, even in the context of childhood adverse family environments, conduct problems, and adolescent substance use? We lean on John Schulenberg's developmental framework to examine this question, focusing on the potential young adult milestones of high school and college graduation, employment, residential independence, romantic partnership, and parenthood. Data came from a prospective-longitudinal multi-method study with N = 1199 participants who were first assessed at age 5 years old and followed to age 31. An accumulation of positive transitions in young adulthood (age 25) was associated with lower likelihood of age 31 problematic cannabis use. The protective effect for problematic cannabis use remained even when adjusting for childhood adverse family environments and was primarily driven by successful college graduation and/or home ownership. The accumulation of positive transitions protected individuals at modest to somewhat elevated risk due to childhood adverse family environments from experiencing age 31 cannabis use problems. However, for other individuals with very high numbers of conduct problems, or with high levels of adolescent substance use, the protective effects of accumulated positive transitions to young adulthood were less strong or nonexistent. Moreover, individuals who completed college or obtained full-time employment by 25 were more likely to report problematic age 31 alcohol use. These findings highlight the central tenets of John Schulenberg's developmental framework, including the examination of ontogenetic continuity and discontinuity, the interplay of developmentally distal and proximal effects, and the identification of developmental protective factors that may sway people toward or away from substance use.
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Diverse manifestations of biological aging often reflect disparities in socioeconomic status (SES). In this paper, we examine associations between indicators of SES and an mRNA-based aging signature during young adulthood, before clinical indications of aging are common. We use data from wave V (2016-2018) of the National Longitudinal Study of Adolescent to Adult Health, a nationally representative study of adults aged 33-43 years, with transcriptomic data from a subset of 2,491 participants. Biological aging is measured using 1) a composite transcriptomic aging signature previously identified by Peters et al.'s out-of-sample meta-analysis (Nat Commun. 2015;6:8570) and 2) 9 subsets that represent functional pathways of coexpressed genes. SES refers to income, education, occupation, subjective social status, and a composite measure combining these 4 dimensions. We examine hypothesized mechanisms through which SES could affect aging: body mass index, smoking, health insurance status, difficulty paying bills, and psychosocial stress. We find that SES-especially the composite measure and income-is associated with transcriptomic aging and immune, mitochondrial, ribosomal, lysosomal, and proteomal pathways. Counterfactual mediational models suggest that the mediators partially account for these associations. The results thus reveal that numerous biological pathways associated with aging are already linked to SES in young adulthood.
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Envelhecimento , Classe Social , Adulto , Adolescente , Humanos , Adulto Jovem , Estudos Longitudinais , Envelhecimento/genética , Fumar , Renda , Fatores SocioeconômicosRESUMO
Health in later life varies significantly by individual demographic characteristics such as age, sex, and race/ethnicity, as well as by social factors including socioeconomic status and geographic region. This study examined whether sociodemographic variations in the immune and inflammatory molecular underpinnings of chronic disease might emerge decades earlier in young adulthood. Using data from 1,069 young adults from the National Longitudinal Study of Adolescent to Adult Health (Add Health)-the largest nationally representative and ethnically diverse sample with peripheral blood transcriptome profiles-we analyzed variation in the expression of genes involved in inflammation and type I interferon (IFN) response as a function of individual demographic factors, sociodemographic conditions, and biobehavioral factors (smoking, drinking, and body mass index). Differential gene expression was most pronounced by sex, race/ethnicity, and body mass index (BMI), but transcriptome correlates were identified for every demographic dimension analyzed. Inflammation-related gene expression showed the most pronounced variation as a function of biobehavioral factors (BMI and smoking) whereas type I IFN-related transcripts varied most strongly as a function of individual demographic characteristics (sex and race/ethnicity). Bioinformatic analyses of transcription factor and immune-cell activation based on transcriptome-wide empirical differences identified additional effects of family poverty and geographic region. These results identify pervasive sociodemographic differences in immune-cell gene regulation that emerge by young adulthood and may help explain social disparities in the development of chronic illness and premature mortality at older ages.
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Status Econômico , Disparidades nos Níveis de Saúde , Classe Social , Transcriptoma , Adolescente , Adulto , Fatores Etários , Feminino , Comportamentos Relacionados com a Saúde , Humanos , Imunidade/genética , Inflamação/genética , Interferons/genética , Longevidade , MasculinoRESUMO
Educational disparities in health are well documented, yet the education-health relationship is inconsistent across racial/ethnic and nativity groups. These inconsistencies may arise from characteristics of the early life environments in which individuals attain their education. We evaluate this possibility by investigating (1) whether educational disparities in cardiometabolic risk vary by race/ethnicity and nativity among Black, Hispanic, and White young adults; (2) the extent to which racial/ethnic-nativity differences in the education-health relationship are contingent on economic, policy, and social characteristics of counties of early life residence; and (3) the county characteristics associated with the best health at higher levels of education for each racial/ethnic-nativity group. Using data from the National Longitudinal Study of Adolescent to Adult Health, we find that Black young adults who achieve high levels of education exhibit worse health across a majority of contexts relative to their White and Hispanic counterparts. Additionally, we observe more favorable health at higher levels of education across almost all contexts for White individuals. For all other racial/ethnic-nativity groups, the relationship between education and health depends on the characteristics of the early life counties of residence. Findings highlight place-based factors that may contribute to the development of racial/ethnic and nativity differences in the education-health relationship among U.S. young adults.
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Etnicidade , Grupos Raciais , Adolescente , Escolaridade , Hispânico ou Latino , Humanos , Estudos Longitudinais , Estados Unidos , Adulto JovemRESUMO
We examined the way body-weight patterns through the first 4 decades of life relate to gene expression signatures of common forms of morbidity, including cardiovascular disease (CVD), type 2 diabetes (T2D), and inflammation. As part of wave V of the nationally representative National Longitudinal Study of Adolescent to Adult Health (1997-2018) in the United States, mRNA abundance data were collected from peripheral blood (n = 1,132). We used a Bayesian modeling strategy to examine the relative associations between body size at 5 life stages-birth, adolescence, early adulthood, young adulthood, and adulthood-and gene expression-based disease signatures. We compared life-course models that consider critical or sensitive periods, as well as accumulation over the entire period. Our results are consistent with a sensitive-period model when examining CVD and T2D gene expression signatures: Birth weight has a prominent role for the CVD and T2D signatures (explaining 33.1% and 22.1%, respectively, of the total association accounted for by body size), while the most recent adult obesity status (ages 33-39) is important for both of these gene expression signatures (24.3% and 35.1%, respectively). Body size in all life stages was associated with inflammation, consistent with the accumulation model.
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Doenças Cardiovasculares/epidemiologia , Diabetes Mellitus Tipo 2/epidemiologia , Inflamação/epidemiologia , Obesidade/epidemiologia , Transcriptoma , Adolescente , Adulto , Teorema de Bayes , Peso ao Nascer , Índice de Massa Corporal , Doenças Cardiovasculares/genética , Criança , Diabetes Mellitus Tipo 2/genética , Feminino , Humanos , Recém-Nascido , Inflamação/genética , Estudos Longitudinais , Masculino , Obesidade/genética , RNA Mensageiro , Fatores de Risco , Adulto JovemRESUMO
Individuals with higher educational attainment live healthier and longer lives. However, not everyone benefits equally from higher education. In particular, the black-white gap in life expectancy is greater at higher levels of educational attainment. Furthermore, recent research suggests that disadvantaged African Americans in the rural Southeast who attend college have worse physical health than their similarly disadvantaged peers who do not attend college. The extent to which this pattern generalizes to a nationally representative, mixed-race sample is unknown. Using data from the National Longitudinal Study of Adolescent to Adult Health, we test whether the health benefits associated with college completion vary by level of childhood disadvantage for depression and metabolic syndrome in young adulthood, across race/ethnicity. We find uniform lower depression associated with college completion regardless of childhood disadvantage, and across non-Hispanic white, non-Hispanic black, and Hispanic young adults. College completion is associated with lower metabolic syndrome for whites across all levels of childhood disadvantage. In contrast, college completion is associated with higher metabolic syndrome among black and Hispanic young adults from disadvantaged childhood environments. Our findings suggest that, for minorities from disadvantaged backgrounds, finishing college pays substantial dividends for mental health but simultaneously exacts costs with regard to physical health. This pattern contrasts starkly with whites and minorities from more privileged backgrounds, for whom college completion is associated with benefits to both mental and physical health. These results suggest that racial disparities in health may persist in part because the health of upwardly mobile minorities is compromised in young adulthood.
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Depressão/epidemiologia , Educação Profissionalizante , Síndrome Metabólica/epidemiologia , Grupos Minoritários , Adolescente , Adulto , Feminino , Humanos , Masculino , Adulto JovemRESUMO
Two seemingly associated demographic trends have generated considerable interest: income stagnation and rising premature mortality from suicides, drug poisoning, and alcoholic liver disease among US non-Hispanic Whites with low education. Economists interpret these population-level trends to indicate that despair induced by financial stressors is a shared pathway to these causes of death. Although we now have the catchy term "deaths of despair," we have yet to study its central empirical claim: that conceptually defined and empirically assessed "despair" is indeed a common pathway to several causes of death. At the level of the person, despair consists of cognitive, emotional, behavioral, and biological domains. Despair can also permeate social relationships, networks, institutions, and communities. Extant longitudinal data sets feature repeated measures of despair-before, during, and after the Great Recession-offering resources to test the role that despair induced by economic decline plays in premature morbidity and mortality. Such tests must also focus on protective factors that could shield individuals. Deaths of despair is more than a phrase; it constitutes a hypothesis that deserves conceptual mapping and empirical study with longitudinal, multilevel data.
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Mortalidade , Angústia Psicológica , Causas de Morte , Humanos , Renda , Hepatopatias Alcoólicas/mortalidade , Intoxicação/mortalidade , Suicídio/estatística & dados numéricos , Estados Unidos/epidemiologiaRESUMO
OBJECTIVES: To test whether indicators of despair are rising among US adults as they age toward midlife and whether this rise is concentrated among low-educated Whites and in rural areas. METHODS: We used data from the National Longitudinal Study of Adolescent to Adult Health, a nationally representative study of US adolescents in 1994. Our sample was restricted to individuals who participated in 1 or more of 5 waves (1994-2017) and self-identified as non-Hispanic White, non-Hispanic Black, or Hispanic (n = 18 446). We examined change in indicators of despair from adolescence to adulthood using multilevel regression analysis, testing for differences by race/ethnicity, education, and rurality. RESULTS: We found evidence of rising despair among this cohort over the past decade. This increase was not restricted to low-educated Whites or to rural areas. CONCLUSIONS: Results suggest that generally rising despair among the young adult cohort now reaching midlife that cuts across racial/ethnic, educational, and geographic groups may presage rising midlife mortality for these subgroups in the next decade.
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Atitude Frente a Saúde/etnologia , Depressão/etnologia , Etnicidade/estatística & dados numéricos , Adaptação Psicológica , Adulto , Estudos de Coortes , Feminino , Nível de Saúde , Humanos , Estudos Longitudinais , Masculino , Fatores Socioeconômicos , Estados Unidos , Adulto JovemRESUMO
Girls who experience father absence in childhood also experience accelerated reproductive development in comparison with peers with present fathers. One hypothesis advanced to explain this empirical pattern is genetic confounding, wherein gene-environment correlation (rGE) causes a spurious relationship between father absence and reproductive timing. We test this hypothesis by constructing polygenic scores for age at menarche and first birth using recently available genome-wide association study results and molecular genetic data on a sample of non-Hispanic white females from the National Longitudinal Study of Adolescent to Adult Health. We find that young women's accelerated menarche polygenic scores are unrelated to their exposure to father absence. In contrast, polygenic scores for earlier age at first birth tend to be higher in young women raised in homes with absent fathers. Nevertheless, father absence and the polygenic scores independently and additively predict reproductive timing. We find no evidence in support of the rGE hypothesis for accelerated menarche and only limited evidence in support of the rGE hypothesis for earlier age at first birth.
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Interação Gene-Ambiente , Menarca/genética , Menarca/fisiologia , Ciclo Menstrual/fisiologia , Pais Solteiros/estatística & dados numéricos , Adolescente , Adulto , Fatores Etários , Criança , Desenvolvimento Infantil/fisiologia , Coito , Pai , Feminino , Estudo de Associação Genômica Ampla , Genótipo , Humanos , Entrevistas como Assunto , Estimativa de Kaplan-Meier , Estudos Longitudinais , Ciclo Menstrual/genética , Herança Multifatorial , Gravidez , Puberdade/genética , Puberdade/fisiologia , Reprodução/fisiologia , Estados Unidos , População Branca , Adulto JovemRESUMO
Although parents might not live with their children for a variety of reasons, existing accounts of parental absence often examine one cause in isolation. Using detailed longitudinal demographic surveillance data from Rufiji, Tanzania, this article examines parental absence due to death, migration, child relocation, union dissolution, and union formation from 2001-2011. Employing survival analysis, the article quantifies children's risk of absence by cause and investigates sociodemographic variation in this risk. Of children born into two-parent households, 25% experience maternal absence by age 10, and 40% experience paternal absence by the same age. Roughly one-quarter of children are born into single-mother families with an absent father at birth, and nearly 70% of these children experience maternal absence as well by age 10. Despite the emphasis on orphanhood in the research and policy communities, parental death is the least common cause of absence. Furthermore, although demographic and socioeconomic characteristics are strong predictors of absence, variation in these relationships across causes underscores the distinctiveness and similarity of different reasons for absence.
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Características da Família , Adulto , Criança , Crianças Órfãs/estatística & dados numéricos , Feminino , Cuidados no Lar de Adoção/estatística & dados numéricos , Humanos , Estimativa de Kaplan-Meier , Estudos Longitudinais , Masculino , Morte Parental/estatística & dados numéricos , Fatores de Risco , Família Monoparental/estatística & dados numéricos , Fatores Socioeconômicos , TanzâniaRESUMO
BACKGROUND: Health professionals and public health experts in maternal and newborn health encourage women to deliver at health facilities in an effort to reduce maternal and newborn mortality. In the existing literature, there is scant information on how migration, family members and community influence facility delivery. This study addresses this knowledge gap using 10 years of longitudinal surveillance data from a rural district of Tanzania. METHODS: Multilevel logistic regression was used to quantify the influence of hypothesized migration, family and community-level factors on facility delivery while adjusting for known confounders identified in the literature. We report adjusted odds ratios (AOR). RESULTS: Overall, there has been an increase of 14% in facility delivery over the ten years, from 63% in 2001 to 77% in 2010 (p < .001). Women residing in households with female migrants from outside their community were more likely to give birth in a facility AOR = 1.2 (95% CI 1.11-1.29). Furthermore, the previous facility delivery of sisters and sisters-in-law has a significant influence on women's facility delivery; AOR = 1.29, 95% CI 1.15-1.45 and AOR = 1.7, 95% CI 1.35-2.13 respectively. Community level characteristics play a role as well; women in communities with higher socioeconomic status and older women of reproductive age had increased odds of facility delivery; AOR = 2.37, 95% CI 1.88-2.98 and AOR = 1.17, 95% CI 1.03-1.32 respectively. CONCLUSION: Although there has been an increase in facility delivery over the last decade in Rufiji, this study underscores the importance of female migrants, family members and community in influencing women's place of delivery. The findings of this study suggest that future interventions designed to increase facility delivery must integrate person-to-person facility delivery promotion, especially through women of the community and within families. Furthermore, the results suggest that investment in formal education of the community and increased community socio-economic status may increase facility delivery.
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Parto Obstétrico/estatística & dados numéricos , Características da Família , Instalações de Saúde/estatística & dados numéricos , Características de Residência , Migrantes , Adolescente , Adulto , Fatores Etários , Escolaridade , Feminino , Humanos , Pessoa de Meia-Idade , Gravidez , Irmãos , Classe Social , Tanzânia , Adulto JovemRESUMO
Structural racism generates racial inequities in U.S. primary education, including segregated schools, inequitable funding and resources, racial disparities in discipline and achievement, and hostile racial climates, which are risk factors for adverse youth health and development. Black youth are disproportionately exposed to adverse school contexts that may become biologically embedded via stress-mediated epigenetic pathways. This study examined whether childhood exposure to adverse school contexts is associated with changes in epigenetic aging during adolescent development. DNA methylation-based epigenetic clocks were calculated from saliva samples at ages 9 and 15 among Black (n = 774) and White (n = 287) youth in the Future of Families and Child Wellbeing Study (2009-2015). We performed latent class analyses to identify race-specific primary school contexts using administrative data on segregation, discipline, achievement, resources, economic disadvantage, and racial harassment. We then estimated change in epigenetic age acceleration from childhood to adolescence across school typologies using GrimAge, PhenoAge, and DunedinPACE epigenetic clocks. Three distinct school contexts were identified for Black youth: segregated and highly-disadvantaged (17.0%), segregated and moderately-disadvantaged (52.1%), and integrated and moderately-disadvantaged (30.8%). Two school contexts emerged for White youth: integrated and unequal (46.5%) and predominantly White & advantaged (53.5%). At age 15, Black youth who attended segregated and highly-disadvantaged primary schools experienced increases in their speed of epigenetic aging with GrimAge and DunedinPACE. Slowed epigenetic aging with GrimAge was observed for Black youth who attended integrated and moderately-disadvantaged schools. School contexts were not associated with changes in epigenetic age acceleration for White youth. Our findings suggest that manifestations of structural racism in primary school contexts are associated with early-life epigenetic age acceleration and may forecast future health inequities.
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Racismo , Racismo Sistêmico , Adolescente , Criança , Humanos , Negro ou Afro-Americano , Epigênese Genética , Instituições Acadêmicas , Brancos , População Branca , Estados UnidosRESUMO
Importance: Epigenetic clocks represent molecular evidence of disease risk and aging processes and have been used to identify how social and lifestyle characteristics are associated with accelerated biological aging. However, most of this research is based on older adult samples who already have measurable chronic disease. Objective: To investigate whether and how sociodemographic and lifestyle characteristics are related to biological aging in a younger adult sample across a wide array of epigenetic clock measures. Design: Nationally representative prospective cohort study. Setting: United States (U.S.). Participants: Data come from the National Longitudinal Study of Adolescent to Adult Health, a national cohort of adolescents in grades 7-12 in U.S. in 1994 followed for 25 years over five interview waves. Our analytic sample includes participants followed-up through Wave V in 2016-18 who provided blood samples for DNA methylation (DNAm) testing (n=4237) at Wave V. Exposure: Sociodemographic (sex, race/ethnicity, immigrant status, socioeconomic status, geographic location) and lifestyle (obesity status, exercise, tobacco, and alcohol use) characteristics. Main Outcome: Biological aging assessed from blood DNAm using 16 epigenetic clocks when the cohort was aged 33-44 in Wave V. Results: While there is considerable variation in the mean and distribution of epigenetic clock estimates and in the correlations among the clocks, we found sociodemographic and lifestyle factors are more often associated with biological aging in clocks trained to predict current or dynamic phenotypes (e.g., PhenoAge, GrimAge and DunedinPACE) as opposed to clocks trained to predict chronological age alone (e.g., Horvath). Consistent and strong associations of faster biological aging were found for those with lower levels of education and income, and those with severe obesity, no weekly exercise, and tobacco use. Conclusions and Relevance: Our study found important social and lifestyle factors associated with biological aging in a nationally representative cohort of younger-aged adults. These findings indicate that molecular processes underlying disease risk can be identified in adults entering midlife before disease is manifest and represent useful targets for interventions to reduce social inequalities in heathy aging and longevity. Key Points: Question: Are epigenetic clocks, measures of biological aging developed mainly on older-adult samples, meaningful for younger adults and associated with sociodemographic and lifestyle characteristics in expected patterns found in prior aging research?Findings: Sociodemographic and lifestyle factors were associated with biological aging in clocks trained to predict morbidity and mortality showing accelerated aging among those with lower levels of education and income, and those with severe obesity, no weekly exercise, and tobacco use.Meaning: Age-related molecular processes can be identified in younger-aged adults before disease manifests and represent potential interventions to reduce social inequalities in heathy aging and longevity.
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For centuries, aging was considered inevitable and immutable. Geroscience provides the conceptual framework to shift this focus toward a new view that regards aging as an active biological process, and the biological age of an individual as a modifiable entity. Significant steps forward have been made toward the identification of biomarkers for and measures of biological age, yet knowledge gaps in geroscience are still numerous. Animal models of aging are the focus of this perspective, which discusses how experimental design can be optimized to inform and refine the development of translationally relevant measures and biomarkers of biological age. We provide recommendations to the field, including: the design of longitudinal studies in which subjects are deeply phenotyped via repeated multilevel behavioral/social/molecular assays; the need to consider sociobehavioral variables relevant for the species studied; and finally, the importance of assessing age of onset, severity of pathologies, and age-at-death. We highlight approaches to integrate biomarkers and measures of functional impairment using machine learning approaches designed to estimate biological age as well as to predict future health declines and mortality. We expect that advances in animal models of aging will be crucial for the future of translational geroscience but also for the next chapter of medicine.
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Envelhecimento , Biomarcadores , Modelos Animais , Animais , Envelhecimento/fisiologia , Gerociência , HumanosRESUMO
Importance: Epigenetic clocks represent molecular evidence of disease risk and aging processes and have been used to identify how social and lifestyle characteristics are associated with accelerated biological aging. However, most research is based on samples of older adults who already have measurable chronic disease. Objective: To investigate whether and how sociodemographic and lifestyle characteristics are associated with biological aging in a younger adult sample across a wide array of epigenetic clock measures. Design, Setting, and Participants: This cohort study was conducted using data from the National Longitudinal Study of Adolescent to Adult Health, a US representative cohort of adolescents in grades 7 to 12 in 1994 followed up for 25 years to 2018 over 5 interview waves. Participants who provided blood samples at wave V (2016-2018) were analyzed, with samples tested for DNA methylation (DNAm) in 2021 to 2024. Data were analyzed from February 2023 to May 2024. Exposure: Sociodemographic (sex, race and ethnicity, immigrant status, socioeconomic status, and geographic location) and lifestyle (obesity status by body mass index [BMI] in categories of reference range or underweight [<25], overweight [25 to <30], obesity [30 to <40], and severe obesity [≥40]; exercise level; tobacco use; and alcohol use) characteristics were assessed. Main Outcome and Measure: Biological aging assessed from banked blood DNAm using 16 epigenetic clocks. Results: Data were analyzed from 4237 participants (mean [SD] age, 38.4 [2.0] years; percentage [SE], 51.3% [0.01] female and 48.7% [0.01] male; percentage [SE], 2.7% [<0.01] Asian or Pacific Islander, 16.7% [0.02] Black, 8.7% [0.01] Hispanic, and 71.0% [0.03] White). Sociodemographic and lifestyle factors were more often associated with biological aging in clocks trained to estimate morbidity and mortality (eg, PhenoAge, GrimAge, and DunedinPACE) than clocks trained to estimate chronological age (eg, Horvath). For example, the ß for an annual income less than $25â¯000 vs $100â¯000 or more was 1.99 years (95% CI, 0.45 to 3.52 years) for PhenoAgeAA, 1.70 years (95% CI, 0.68 to 2.72 years) for GrimAgeAA, 0.33 SD (95% CI, 0.17 to 0.48 SD) for DunedinPACE, and -0.17 years (95% CI, -1.08 to 0.74 years) for Horvath1AA. Lower education, lower income, higher obesity levels, no exercise, and tobacco use were associated with faster biological aging across several clocks; associations with GrimAge were particularly robust (no college vs college or higher: ß = 2.63 years; 95% CI, 1.67-3.58 years; lower vs higher annual income: <$25â¯000 vs ≥$100â¯000: ß = 1.70 years; 95% CI, 0.68-2.72 years; severe obesity vs no obesity: ß = 1.57 years; 95% CI, 0.51-2.63 years; no weekly exercise vs ≥5 bouts/week: ß = 1.33 years; 95% CI, 0.67-1.99 years; current vs no smoking: ß = 7.16 years; 95% CI, 6.25-8.07 years). Conclusions and Relevance: This study found that important social and lifestyle factors were associated with biological aging in a nationally representative cohort of younger adults. These findings suggest that molecular processes underlying disease risk may be identified in adults entering midlife before disease is manifest and inform interventions aimed at reducing social inequalities in heathy aging and longevity.
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Envelhecimento , Epigênese Genética , Estilo de Vida , Humanos , Masculino , Feminino , Adulto Jovem , Estados Unidos/epidemiologia , Estudos Longitudinais , Adulto , Envelhecimento/genética , Epigênese Genética/genética , Adolescente , Epigenômica , Metilação de DNA/genética , Fatores Sociodemográficos , Estudos de CoortesRESUMO
Importance: The link between familial loss of a loved one and long-term health decline is complex and not fully understood. Objective: To test associations of losing a parent, sibling, child, or partner or spouse with accelerated biological aging. Design, Setting, and Participants: Data from the National Longitudinal Study of Adolescent to Adult Health, a US population-based longitudinal cohort study, were analyzed. Participants were enrolled from 1994 to 1995 for wave 1, while in grades 7 to 12, and followed up through wave 5 in 2018. The study analyzed participant reports of loss collected at each wave from 1 to 5 over 24 years and used a banked wave 5 blood sample for subsequent DNA methylation testing and epigenetic clock calculation from 2018 to 2024. Data were analyzed from January 2022 to July 2024. Exposure: Loss of biological parents or parental figures, partners or spouses, siblings, or children at waves 1 to 3 or during childhood, adolescence (aged <18 years), or adulthood at wave 4 to wave 5 (aged 18-43 years). Main Outcomes and Measures: Biological aging assessed from blood DNA methylation using the Horvath, PhenoAge, GrimAge, and DunedinPACE epigenetic clocks at wave 5. Results: Data from 3963 participants were analyzed, with a weighted mean (range) age of 38.36 (36.78-39.78) years at wave 5; 2370 (50.3%) were male, 720 (15.97%) were Black, 400 (8.18%) were Hispanic, and 2642 (72.53%) were White. Nearly 40% of participants experienced loss by wave 5 when they were aged 33 to 43 years, and participants who were Black (379 participants [56.67%]), Hispanic (152 participants [41.38%]), and American Indian (18 participants [56.08%]) experienced a greater proportion of losses compared with White participants (884 participants [34.09%]). Those who experienced 2 or more losses tended to have older biological ages for several of the clocks (PhenoAge ß = 0.15; 95% CI, 0.02 to 0.28; GrimAge ß = 0.27; 95% CI, 0.09 to 0.45; DunedinPACE ß = 0.22; 95% CI, 0.10 to 0.34) compared with those with no losses. In contrast, there were no associations with 2 or more losses for the Horvath clock (ß = -0.08; 95% CI, -0.23 to 0.06). Conclusions and Relevance: This study reveals associations between various measures of loss experienced from childhood to adulthood and biological aging in a diverse sample of the US population. These findings underscore the potentially enduring impact of loss on biological aging even before middle age and may contribute to understanding racial and ethnic disparities in health and mortality.