Articles

Background:</b> Early life socioeconomic conditions and race/ethnicity are critical determinants of long-term health and behavioral outcomes. Epigenetic changes, particularly those measured by the GrimAge biomarker, may mediate the impact of these early adversities on later life outcomes. This study investigates the relationships between race/ethnicity, poverty at birth, epigenetic aging at age 15, and subsequent self-rated health, school discipline, depression, and school dropout at age 22. We explored sex differences in these paths. <b>Methods:</b> Data were drawn from the Fragile Families and Child Wellbeing Study (FFCWS), which included 733 youth with comprehensive follow-up data up to age 22. Structural Equation Modeling (SEM) was employed to assess the pathways from race/ethnicity and poverty at birth to epigenetic aging (GrimAge) at age 15, and subsequently to self-rated health and school discipline at age 22. The model controlled for potential confounders including sex, family structure, and parental education. <b>Results:</b> Race/ethnicity and poverty at birth were significantly associated with higher GrimAge scores at age 15 (p < 0.05). Higher GrimAge scores were predictive of poorer self-rated health (β = -0.08, p < 0.05) and increased instances of school discipline (β = 0.13, p < 0.01) at age 22. The indirect effects of race/ethnicity and poverty at birth on self-rated health and school discipline through GrimAge were also significant (p < 0.05), suggesting that epigenetic aging partially mediates these relationships. Sex differences were also observed. Poverty at birth predicted faster epigenetic aging at age 15 for males not females. We also observed that faster epigenetic aging at age 15 was predictive of school discipline of male not female participants at age 22. In contrast, faster epigenetic aging at age 15 was predictive of self-rated health (SRH) of female not male participants at age 22. <b>Conclusions:</b> This study provides evidence that with some sex differences, race/ethnicity and poverty at birth contribute to accelerated epigenetic aging (GrimAge) by age 15, which in turn predicts poorer self-rated health and increased school discipline issues by age 22. These findings emphasize the importance of early interventions targeting social determinants to mitigate long-term health and behavioral disparities. Addressing these early life conditions is crucial for improving health equity and outcomes in young adulthood.

<b>Objective: </b>This study aims to investigate the relationship between the presence of chronic medical conditions and cessation among U.S. adults who use combustible tobacco. We hypothesized that having chronic medical conditions would be associated with a higher likelihood of successfully quitting combustible tobacco.<b> </b><b>Methods: </b>We utilized longitudinal data from the Population Assessment of Tobacco and Health (PATH) Study, using data from Waves 1 to 6. Only current daily smokers were included in our analysis. The independent variable was the number of chronic medical conditions, defined as zero, one, or two or more. The outcome was becoming a former smoker (quitting smoking). Using multivariate regression analyses, we assessed the association between the number of chronic conditions and tobacco cessation over the six waves. We controlled for potential confounding variables, including demographic factors and socioeconomic status.<b> </b><b>Results: </b>Our analysis revealed a significant association between the number of chronic medical conditions and the likelihood of quitting smoking. Specifically, individuals with two or more chronic conditions exhibited a greater probability of quitting smoking compared to those with no chronic conditions. The results remained significant after adjusting for potential confounders.<b> </b><b>Conclusions: </b>Multiple chronic medical conditions may act as a catalyst for smoking cessation among U.S. adults. This suggests that the presence of multimorbidity, defined as multiple chronic disease diagnoses, may serve as “teachable moments,” prompting significant health behavior changes. These findings highlight the potential for leveraging chronic disease management and healthcare interventions to promote tobacco cessation, particularly among individuals with multiple chronic conditions.

<b>Background:</b> Telomere length is a critical biomarker of cellular aging and overall health. While childhood socioeconomic status (SES) indicators such as education and poverty can have long-lasting effects on biological aging, research has shown contradictory results regarding the impact of adulthood SES on future telomere length, particularly in racially and ethnically diverse individuals. This study investigates the effects of baseline adulthood SES indicators such as education and poverty on telomere length nine years later in women, using data from the Future of Families and Child Wellbeing Study (FFCWS). <b>Methods:</b> We analyzed data from the FFCWS, a longitudinal cohort study. The sample included baseline adulthood SES and follow-up telomere length measure of women (n = 2,421) with varying socioeconomic conditions. Telomere length was measured from saliva samples nine years after the baseline measure of adulthood SES. Education, poverty, and marital status at baseline were assessed. Multivariate linear regression models were used to examine the association between adulthood SES indicators at baseline and future telomere length, controlling for potential confounders. <b>Results:</b> From the total 2,421 women, 675 were Latino White, 1,158 were non-Latino Black, and 588 were non-Latino White. Our findings indicate that for women in our study, no adulthood SES indicators such as poverty status, education, or marital status at baseline were predictive of telomere lengths nine years later. <b>Conclusion: </b>Our observations challenge that expected longitudinal association between adulthood SES indicators and subsequent telomere length almost a decade later in racially and ethnically diverse group of women. These findings underscore the need for additional research on the validity of TL as a mediator of the effects of adulthood SES on future rate of biological aging.