Articles

<b>Background:</b> The Minorities' Diminished Returns (MDRs) theory posits that social determinants of health, such as parental education, exert weaker protective effects on health and educational outcomes in racialized and minoritized populations compared to White populations. <b>Aim: </b>This study examines whether higher maternal education is associated with better high school GPA in Black youth and whether this association aligns with the MDRs framework. <b>Methods:</b> Data were drawn from the Future of Families and Child Wellbeing Study also known as Fragile Families and Child Wellbeing Study (FFCWS) baseline and 22nd year follow-up (1990-2022). This study included 1873 Black or White participants who were followed from birth to age 22. Linear regression models were used to assess the association between maternal education and high school GPA, adjusting for sociodemographic covariates. Analyses focused on the differential effects of maternal education across racial groups, particularly among Black youth. <b>Results:</b> While maternal education was positively associated with high school GPA, this effect was weaker for Black students compared to their White counterparts. Specifically, each additional year of maternal education corresponded to a lower GPA increase in Black students, consistent with the MDRs hypothesis. <b>Conclusion:</b> Findings support the MDRs theory, indicating that maternal education has a reduced protective effect on high school GPA among Black youth. These results underscore the need for policies that address structural factors beyond education to promote equitable academic achievement.

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>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.

We used 15 years of follow up of<b> </b>854 racially and ethnically diverse birth cohort who were followed from birth to age 15. Structural equation modeling (SEM) was used to examine the effects of race/ethnicity, maternal education, and family structure on poverty at birth, as well as the effects of poverty at birth on epigenetic changes at age 15. We also explored variations by sex. <b>Results: </b>Our findings indicate that Black and Latino families had lower maternal education and married family structure which in turn predicted poverty at birth. Poverty at birth then was predictive of epigenetic changes 15 years later when the index child was 15. This suggested that poverty at birth partially mediates the effects of race/ethnicity, maternal education, and family structure on epigenetic changes of youth at age 15. There was an effect of poverty status at birth on DNA methylation of male but not female youth at age 15. Thus, poverty at birth may have a more salient effect on long term epigenetic changes of male than female youth. <b>Conclusions: </b>Further studies are needed to understand the mechanisms underlying the observed sex differences in the effects of poverty as a mechanism that connects race/ethnicity, maternal education, and family structure to epigenetic changes later in life.

</b><b> </b>Epigenetic studies, which can reflect biological aging, have shown that measuring DNA methylation (DNAm) levels provides new insights into the biological effects of social environment and socioeconomic position (SEP). This study explores how race, family structure, and SEP (income to poverty ratio) at birth influence youth epigenetic aging at age 15. Data were obtained from the Future of Families and Child Wellbeing Study (FFCWS) cohort, with GrimAge used as a measure of DNAm levels and epigenetic aging. Our analysis included 854 racially and ethnically diverse participants followed from birth to age 15. Structural equation modeling (SEM) examined the relationships among race, SEP at birth, and epigenetic aging at age 15, controlling for sex, ethnicity, and family structure at birth. Findings indicate that race was associated with lower SEP at birth and faster epigenetic aging. Specifically, income to poverty ratio at birth partially mediated the effects of race on accelerated aging by age 15. The effect of income to poverty ratio at birth on DNAm was observed in male but not female youth at age 15. Thus, SEP partially mediated the effect of race on epigenetic aging in male but not female youth. These results suggest that income to poverty ratio at birth partially mediates the effects of race on biological aging into adolescence. These findings highlight the long-term biological impact of early-life poverty in explaining racial disparities in epigenetic aging and underscore the importance of addressing economic inequalities to mitigate these disparities. Policymakers should focus on poverty prevention in Black communities to prevent accelerated biological aging and associated health risks later in life. Interventions aimed at eliminating poverty and addressing racial inequities could have significant long-term benefits for public health. Future research should explore additional factors contributing to epigenetic aging and investigate potential interventions to slow down the aging process. Further studies are needed to understand the mechanisms underlying these associations and to identify effective strategies for mitigating the impact of SEP and racial disparities on biological aging.