Bedtime Schedules and Sleep Regulation among Children of Incarcerated Parents.

OBJECTIVES: To investigate variation by parental incarceration history in the bedtime schedules set for elementary-age children and whether sleep was effectively regulated. STUDY DESIGN: We ran multivariate regression models estimating the relationship between parental incarceration and 6 measures of bedtime schedules and sleep regulation. Our sample included 9-year-olds in the Fragile Families and Child Wellbeing Study (n = 3246), a survey of children born in large US cities between 1998 and 2000 that has an oversample of unmarried mothers. RESULTS: Children's bedtime schedules did not differ at a statistically significant level by parental incarceration history, but children of ever- vs never-incarcerated fathers had lower odds of consistently adhering to a set bedtime. Children of ever-incarcerated fathers also slept for less time on average than did children of never-incarcerated fathers, and they had lower odds of obtaining sufficient sleep. Bedtime consistency partly mediated the association between paternal incarceration and total sleep duration. CONCLUSIONS: Although caregivers set appropriate bedtime schedules for children of ever-incarcerated fathers, consistent adherence to those schedules may be particularly challenging given the structural hardships of paternal incarceration. Policymakers, researchers, and practitioners working to improve sleep among children of incarcerated fathers should focus on helping families to develop strategies for implementing bedtime schedules as consistently and effectively as possible.

Social and physical environments early in development predict DNA methylation of inflammatory genes in young adulthood.

Chronic inflammation contributes to a wide range of human diseases, and environments in infancy and childhood are important determinants of inflammatory phenotypes. The underlying biological mechanisms connecting early environments with the regulation of inflammation in adulthood are not known, but epigenetic processes are plausible candidates. We tested the hypothesis that patterns of DNA methylation (DNAm) in inflammatory genes in young adulthood would be predicted by early life nutritional, microbial, and psychosocial exposures previously associated with levels of inflammation. Data come from a population-based longitudinal birth cohort study in metropolitan Cebu, the Philippines, and DNAm was characterized in whole blood samples from 494 participants (age 20-22 y). Analyses focused on probes in 114 target genes involved in the regulation of inflammation, and we identified 10 sites across nine genes where the level of DNAm was significantly predicted by the following variables: household socioeconomic status in childhood, extended absence of a parent in childhood, exposure to animal feces in infancy, birth in the dry season, or duration of exclusive breastfeeding. To evaluate the biological significance of these sites, we tested for associations with a panel of inflammatory biomarkers measured in plasma obtained at the same age as DNAm assessment. Three sites predicted elevated inflammation, and one site predicted lower inflammation, consistent with the interpretation that levels of DNAm at these sites are functionally relevant. This pattern of results points toward DNAm as a potentially important biological mechanism through which developmental environments shape inflammatory phenotypes across the life course.

The Sociodemographic and Lifestyle Correlates of Epigenetic Aging in a Nationally Representative U.S. Study of Younger Adults.

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.

Sleep Duration Differences by Education from Middle to Older Adulthood: Does Employment Stratification Contribute to Gendered Leveling?

Sleep duration changes across the life course and differs by education in the United States. However, little research has examined whether educational differences in sleep duration change over age-or whether sleep duration trajectories over age differ by education. This study uses a life course approach to analyze American Time Use Survey data (N = 60,908), examining how educational differences in weekday sleep duration change from middle to older adulthood (ages 40-79). For men only, differences in total sleep time between individuals with less than a high school degree and those with more education converge in older adulthood. Results suggest that this leveling is explained by decreasing educational stratification in work hours as men enter older adulthood. Findings highlight the importance of employment for shaping gendered socioeconomic differences in sleep and demonstrate differences by education in how sleep duration changes over age, with possible implications for health disparities.

Body mass and the epidemic of chronic inflammation in early mid-adulthood.

OBJECTIVES: Chronic inflammation is a potentially important mechanism through which social inequalities may contribute to health inequalities over the life course. Excess body fat contributes to chronic inflammation, and younger adults in the US have come of age during a pronounced secular increase in body mass index (BMI). We aim to document levels of chronic inflammation in a nationally representative sample of 33-to-44 year-old adults in the US, and to describe associations with BMI, race/ethnicity, and education. METHODS: High sensitivity C-reactive protein (CRP) was measured in Wave V (2016-18) of the National Longitudinal Study of Adolescent to Adult Health, with complete data available for 4349 participants. Sex-stratified weighted regression models were implemented to investigate CRP in association with education, race/ethnicity, and BMI. RESULTS: Geometric mean CRP was 1.9 mg/L, and 35.4% of the sample had CRP >3 mg/L. Females had significantly higher CRP than males. Body mass index was a strong positive predictor of CRP, and education level was negatively associated with CRP. Associations between education and CRP were substantially attenuated after adjusting for BMI. High risk CRP increased linearly with BMI even among the obese: 87.0 percent of females and 74.1 percent of males with class 3 obesity (BMI ≥40) were predicted to have high risk CRP > 3 mg/L. CONCLUSIONS: The obesity epidemic is producing an epidemic of chronic inflammation in early mid-adulthood in the US. Strong associations between BMI and chronic inflammation portend high risk for future disease-and inequitable distribution of disease-as the cohort ages.

Health and Union Dissolution among Parenting Couples: Differences by Gender and Marital Status.

Poor health may destabilize romantic unions by impeding fulfillment of family responsibilities, increasing stress, and causing financial strain. We hypothesized that the associations of health characteristics with union stability for parenting couples vary by the gender of the partner in poor health and the couple's marital status because of gender and marital status differences in family responsibilities and health-related coping behaviors. Using longitudinal data from the Fragile Families and Child Wellbeing Study (n = 2,997), we examined how three health measures predicted union dissolution for urban married and cohabiting couples with young children. Fathers' depression at baseline predicted dissolution for all parenting couples, as did either partner developing depression between baseline and the following interview. For married parents, fathers' health-related work limitations and mothers' poor self-rated health also predicted dissolution. Associations between health conditions and dissolution differ by gender and marital status, possibly reflecting varying social norms about family responsibilities.

Health behaviors and union dissolution among parents of young children: Differences by marital status.

Previous research finds that marriage is associated with better health and lower mortality, and one of the mechanisms underlying this association is health-related selection out of marriage. Using longitudinal survey data from 2,348 couples from the Fragile Families and Child Wellbeing Study, we examine whether certain health behaviors-smoking and binge drinking-are associated with risk of union dissolution among couples with young children. We use discrete time hazard models to test whether associations between health behaviors and union dissolution differ between married and cohabiting parents. We find no statistically significant association between binge drinking and union dissolution for either cohabiting or married couples. Parental smoking, however, is associated with union dissolution. On average, married and cohabiting couples in which both parents smoke have a higher risk of union dissolution than couples in which neither parent smokes. Additionally, father's smoking (in couples in which the mother does not smoke) is associated with union dissolution, but only for married couples. These findings illustrate the importance of considering the health behaviors of both partners and provide further evidence of differences in union dissolution dynamics between married and cohabiting couples.