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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 β for an annual income less than $25 000 vs $100 000 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: β = 2.63 years; 95% CI, 1.67-3.58 years; lower vs higher annual income: <$25 000 vs ≥$100 000: β = 1.70 years; 95% CI, 0.68-2.72 years; severe obesity vs no obesity: β = 1.57 years; 95% CI, 0.51-2.63 years; no weekly exercise vs ≥5 bouts/week: β = 1.33 years; 95% CI, 0.67-1.99 years; current vs no smoking: β = 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.

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 β = 0.15; 95% CI, 0.02 to 0.28; GrimAge β = 0.27; 95% CI, 0.09 to 0.45; DunedinPACE β = 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 (β = -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.

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., (Copyright © 2024 The Authors.)

Objectives: Cognitive aging is a lifelong process with implications for Alzheimer's disease and dementia. This study aims to fill major gaps in research on the natural history of and social disparities in aging-related cognitive decline over the life span. Methods: We conducted integrative data analysis of four large U.S. population-based longitudinal studies of individuals aged 12 to 105 followed over two decades and modeled age trajectories of cognitive function in multiple domains. Results: We found evidence for the onset of cognitive decline in the 4 th decade of life, varying gender differences with age, and persistent disadvantage among non-Hispanic Blacks, Hispanics, and those without college education. We further found improvement in cognitive function across 20 th century birth cohorts but widening social inequalities in more recent cohorts. Discussion: These findings advance an understanding of early life origins of dementia risk and invite future research on strategies for promoting cognitive health for all Americans., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Disparities in socio-economic status (SES) predict many immune system-related diseases, and previous research documents relationships between SES and the immune cell transcriptome. Drawing on a bioinformatically-informed network approach, we situate these findings in a broader molecular framework by examining the upstream regulators of SES-associated transcriptional alterations. Data come from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a nationally representative sample of 4543 adults in the United States. Results reveal a network-of differentially expressed genes, transcription factors, and protein neighbors of transcription factors-that shows widespread SES-related dysregulation of the immune system. Mediational models suggest that body mass index (BMI) plays a key role in accounting for many of these associations. Overall, the results reveal the central role of upstream regulators in socioeconomic differences in the molecular basis of immunity, which propagate to increase risk of chronic health conditions in later-life., (© 2024. The Author(s).)

Background: Alzheimer's disease and Alzheimer's disease related dementias (AD/ADRD) have increased in prevalence., Objective: This article describes the Add Health Parent Study (AHPS) Phase 2, a study of social, behavioral, and biological factors influencing healthy aging and risk for AD/ADRD, in a national sample of adults aged 58-90., Methods: Sample members are parents of the National Longitudinal Study of Adolescent to Adult Health (Add Health) cohort, initially interviewed in Add Health in midlife (1994-95). AHPS Phase 1 (2015-17) collected longitudinal data on a random subsample of parents and their spouse/partners, who were mostly Non-Hispanic (NH) White. AHPS Phase 2 will collect the same longitudinal socio-behavioral, and health survey data on all remaining NH Black and Hispanic parents (Black and Hispanic Supplement, BHS). Additionally, Phase 2 will collect cognitive and DNA data from AHPS Phase 1 and BHS sample parents and their current spouse/partners., Results: Funded by the National Institute on Aging, recruitment will occur between June 2025 and May 2026, producing an expected total AHPS sample of 5506 parents and their spouse/partners., Conclusions: The AHPS will be the first longitudinal cohort study powered to address multigenerational racial/ethnic disparities in AD/ADRD risk and protective factors across race/ethnic groups and socioeconomic strata.

Background: Air pollution exposure is associated with cardiovascular morbidity and mortality. Although exposure to air pollution early in life may represent a critical window for development of cardiovascular disease risk factors, few studies have examined associations of long-term air pollution exposure with markers of cardiovascular and metabolic health in young adults., Objectives: By combining health data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) with air pollution data from the Fused Air Quality Surface using Downscaling (FAQSD) archive, we: (1) calculated multi-year estimates of exposure to ozone (O 3 ) and particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM 2.5 ) for Add Health participants; and (2) estimated associations between air pollution exposures and multiple markers of cardiometabolic health., Methods: Add Health is a nationally representative longitudinal cohort study of over 20,000 adolescents aged 12-19 in the United States (US) in 1994-95 (Wave I). Participants have been followed through adolescence and into adulthood with five in-home interviews. Estimated daily concentrations of O 3 and PM 2.5 at census tracts were obtained from the FAQSD archive and used to generate tract-level annual averages of O 3 and PM 2.5 concentrations. We estimated associations between average O 3 and PM 2.5 exposures from 2002 to 2007 and markers of cardiometabolic health measured at Wave IV (2008-09), including hypertension, hyperlipidemia, body mass index (BMI), diabetes, C-reactive protein, and metabolic syndrome., Results: The final sample size was 11,259 individual participants. The average age of participants at Wave IV was 28.4 years (range: 24-34 years). In models adjusting for age, race/ethnicity, and sex, long-term O 3 exposure (2002-07) was associated with elevated odds of hypertension, with an odds ratio (OR) of 1.015 (95% confidence interval [CI]: 1.011, 1.029); obesity (1.022 [1.004, 1.040]); diabetes (1.032 [1.009,1.054]); and metabolic syndrome (1.028 [1.014, 1.041]); PM 2.5 exposure (2002-07) was associated with elevated odds of hypertension (1.022 [1.001, 1.045])., Conclusion: Findings suggest that long-term ambient air pollution exposure, particularly O 3 exposure, is associated with cardiometabolic health in early adulthood., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Violence victimization has been associated with low-grade inflammation. Lesbian, Gay, and Bisexual (LGB) individuals are at greater risk for victimization in childhood and young adulthood compared to heterosexuals. Moreover, the intersection of LGB identity with gender, race/ethnicity, and educational attainment may be differentially associated with victimization rates. However, no previous study has examined the role of cumulative life-course victimization during childhood and young adulthood in the association between 1) LGB identity and low-grade inflammation during the transition to midlife, and 2) intersection of LGB identity with gender, race/ethnicity, and educational attainment and low-grade inflammation during the transition to midlife. We utilized multi-wave data from a national sample of adults entering midlife in the United States- the National Longitudinal Study of Adolescent to Adult Health (Add Health; n = 4573) - and tested four bootstrapped mediation models. Results indicate LGB identity, LGB and White, and LGB and Black identities were indirectly associated with low-grade inflammation during the transition to midlife via higher levels of cumulative life-course victimization. Moreover, among LGB adults, the association between 1) less than college education and 2) some college education, and low-grade inflammation was mediated by cumulative life-course victimization. For LGB females, there was a direct association between identity and low-grade inflammation and this association was mediated by cumulative life-course victimization . Reducing accumulation of victimization could be critical for preventing biological dysregulation and disease onset among LGB individuals, particularly for those with multiple marginalized identities., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Inc.)

Objectives: To better understand the temporal dynamics of progression from cognitive decline to onset of dementia in the dementia-free older population in the United States., Methods: We used longitudinal data from a diverse national population-based sample of older adults (N = 531) in the Aging, Demographics, and Memory Study from the Health and Retirement Study with repeated measures of cognitive function and dementia diagnosis during 12 years of follow-up from 1996 to 2009. We employed joint latent class mixed models to estimate the association between cognitive change and competing risks of dementia and nondementia death and identify heterogeneity in the age profiles of such association adjusting for baseline characteristics., Results: Our analyses found 3 latent classes with distinct age profiles of cognitive decline and associated risk of dementia and mortality: "Rapid Cognitive Decline" (19.6%), "Moderate Progression" (44.6%), and "Optimal Cognitive Aging" (35.8%). When simultaneously accounting for cognitive trajectories and time-to-dementia/death, we also found associations of baseline covariates with slope of cognitive decline (e.g., steeper decline among non-Hispanic Blacks and more educated) and risk of dementia (e.g., greater risk for females and apolipoprotein E-4 carriers, but no difference by education level) that differ substantially from those in separate longitudinal mixed models or survival models., Discussion: The differential age patterns of cognitive decline predicting dementia incidences identified in this study suggest variation in the course of cognitive aging in older adults that may inform future etiological and intervention studies., (© The Author(s) 2022. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Messenger RNA (mRNA) BNT162b2 (Pfizer-BioNTech) and mRNA-1273 (Moderna) COVID-19 vaccines have been shown to be effective in preventing symptomatic COVID-19 in randomized placebo-controlled Phase III trials (1,2); however, the benefits of these vaccines for preventing asymptomatic and symptomatic SARS-CoV-2 (the virus that causes COVID-19) infection, particularly when administered in real-world conditions, is less well understood. Using prospective cohorts of health care personnel, first responders, and other essential and frontline workers* in eight U.S. locations during December 14, 2020-March 13, 2021, CDC routinely tested for SARS-CoV-2 infections every week regardless of symptom status and at the onset of symptoms consistent with COVID-19-associated illness. Among 3,950 participants with no previous laboratory documentation of SARS-CoV-2 infection, 2,479 (62.8%) received both recommended mRNA doses and 477 (12.1%) received only one dose of mRNA vaccine. † Among unvaccinated participants, 1.38 SARS-CoV-2 infections were confirmed by reverse transcription-polymerase chain reaction (RT-PCR) per 1,000 person-days. § In contrast, among fully immunized (≥14 days after second dose) persons, 0.04 infections per 1,000 person-days were reported, and among partially immunized (≥14 days after first dose and before second dose) persons, 0.19 infections per 1,000 person-days were reported. Estimated mRNA vaccine effectiveness for prevention of infection, adjusted for study site, was 90% for full immunization and 80% for partial immunization. These findings indicate that authorized mRNA COVID-19 vaccines are effective for preventing SARS-CoV-2 infection, regardless of symptom status, among working-age adults in real-world conditions. COVID-19 vaccination is recommended for all eligible persons., Competing Interests: All authors have completed and submitted the International Committee of Medical Journal Editors form for disclosure of potential conflicts of interest. Allison L. Naleway reported funding from Pfizer for a meningococcal B vaccine study unrelated to the submitted work. Kurt T. Hegmann serves at the Editor of the American College of Occupational and Environmental Medicine’s evidence-based practice guidelines. Matthew S. Thiese reported grants and personal fees from Reed Group and the American College of Occupational and Environmental Medicine, outside the submitted work. No other potential conflicts of interest were disclosed.

While disparities in depressive symptoms by race/ethnicity and gender have been documented, left unclear is how such status characteristics intersect to influence mental health, particularly across early life and among a diverse set of population subgroups. This study investigates how intra- and inter-individual trends in depressive symptoms unfold across a 30-year span (ages 12-42) and are structured by the intersection of race/ethnicity and gender among White, Black, Hispanic, and Asian American young adults (N = 18,566). Analyses use data from the National Longitudinal Study of Adolescent to Adult Health, a nationally representative study of adolescents who have been followed through their fourth decade of life. We draw on Waves I-IV and a representative subsample of the brand new Wave V data. Growth curve models indicated depressive symptoms decreased across adolescence and young adulthood before increasing in the early 30s. Racial/ethnic minorities reported more depressive symptoms than Whites. Women reported more depressive symptoms than men and experienced especially steep increases in their late 30s. Racial/ethnic-gender disparities remained stable with age, except for Hispanic-White disparities among women and Asian American-White disparities among men, which narrowed with age. Overall, findings demonstrate dynamic inequalities across a longer period of the life span than was previously known, as well as heterogeneity in trajectories of poor mental health within and between racial/ethnic-gender groups. Results also suggest that Black and Asian American women experience the highest mental health risks and that interventions for reducing disparities in depressive symptoms should focus on adults in their late 20s/early 30s, particularly women of color.

Objectives: We assess the temporal properties and biosocial mechanisms underlying the associations between early-life socioeconomic status (SES) and later health. Using a life-course design spanning adolescence to older adulthood, we assess how early life and various dimensions of adult SES are associated with immune and metabolic function in different life stages and examine possible bio-behavioral and psychosocial mechanisms underlying these associations., Method: Data for this study come from 3 national studies that collectively cover multiple stages of the life course (Add Health, MIDUS, and HRS). We estimated generalized linear models to examine the prospective associations between early-life SES, adult SES, and biomarkers of chronic inflammation and metabolic disorder assessed at follow-up. We further conducted formal tests of mediation to assess the role of adult SES in linking early SES to biological functions., Results: We found that early-life SES exerted consistent protective effects for metabolic disorder across the life span, but waned with time for CRP. The protective effect of respondent education remained persistent for CRP but declined with age for metabolic disorder. Adult income and assets primarily protected respondents against physiological dysregulation in middle and old ages, but not in early adulthood., Discussion: These findings are the first to elucidate the life-course patterns of SES that matter for underlying physiological functioning during the aging process to produce social gradients in health., (© The Author(s) 2018. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: We constructed measures of an individual's gendered behaviour and their gendered environment to investigate the salience of gender norms during adolescence for social mobility during the next decade of life., Methods: In this nationally representative observational study, we collected individual-level data from the National Longitudinal Study of Adolescent to Adult Health (Add Health), which enrolled a cohort of nationally representative school students aged 11-19 years from across the USA and followed them up for 14 years (ie, to age 25-33 years). We characterised gendered behaviour for adolescents in a performative sense via self-reports of behaviours and beliefs. We aggregated this individual-level measure to create a proxy measure of an individual's social context by taking averages for an individual's peers of the same sex and school year., Findings: Between Jan 5, 1994, and Dec 26, 1995, Add Health collected data on a cohort of 20 745 students. 14 540 respondents were followed-up 14 years later between April 3, 2007, and Feb 1, 2009, of whom 7722 (53·1%) were female. More masculine male respondents were downwardly mobile; they were enrolled in school for fewer years and were more likely to have lower status jobs than their less masculine same-sex school peers. More masculine male respondents were also more likely to have jobs in occupational categories with larger proportions of males than their same-sex school peers. Gendered behaviour was not predictive of future educational and occupational attainment for female respondents. Male adolescents in school years with more masculine same-sex peers than male adolescents in other school years also tended to have lower educational and occupational attainment than their male peers. Educational and occupational attainment in early midlife for female respondents was not affected by their gendered environment., Interpretation: Gender, when measured as a set of gender-distinct behaviours in adolescence, was associated with differential patterns of social mobility from adolescence to young adulthood. Moreover, variation in an individual's local gender norms has implications for subsequent socioeconomic attainment, especially for male adolescents. These findings have potential implications for observed health disparities., Funding: Bill & Melinda Gates Foundation., (Copyright © 2019 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Recent scholarship suggests that the genomes of those around us affect our own phenotypes. Much of the empirical evidence for such "metagenomic" effects comes from animal studies, where the socio-genetic environment can be easily manipulated. Among humans, it is more difficult to identify such effects given the nonrandom distribution of genes and environments. Here we leverage the as-if-random distribution of grade-mates' genomes conditional on school-level variation in a nationally representative sample. Specifically, we evaluate whether one's peers' genetic propensity to smoke affects one's own smoking behavior net of one's own genotype. Results show that peer genetic propensity to smoke has a substantial effect on an individual's smoking outcome. This is true not only when the peer group includes direct friends, and therefore where the individual plays an active role in shaping the metagenomic context but also when the peer group includes all grade-mates and thus in cases where the individual does not select the metagenomic environment. We explore these effects further and show that a small minority with high genetic risk to smoke ('bad apples') can greatly affect the smoking behavior of an entire grade. The methodology used in this paper offers a potential solution to many of the challenges inherent in estimating peer effects in nonexperimental settings and can be utilized to study a wide range of outcomes with a genetic basis. On a policy level, our results suggest that efforts to reduce adolescent smoking should take into account metagenomic effects, especially bad apples, within social networks., Competing Interests: The authors declare no conflict of interest., (Copyright © 2019 the Author(s). Published by PNAS.)

Young people's life chances can be predicted by characteristics of their neighbourhood 1 . Children growing up in disadvantaged neighbourhoods exhibit worse physical and mental health and suffer poorer educational and economic outcomes than children growing up in advantaged neighbourhoods. Increasing recognition that aspects of social inequalities tend, in fact, to be geographical inequalities 2-5 is stimulating research and focusing policy interest on the role of place in shaping health, behaviour and social outcomes. Where neighbourhood effects are causal, neighbourhood-level interventions can be effective. Where neighbourhood effects reflect selection of families with different characteristics into different neighbourhoods, interventions should instead target families or individuals directly. To test how selection may affect different neighbourhood-linked problems, we linked neighbourhood data with genetic, health and social outcome data for >7,000 European-descent UK and US young people in the E-Risk and Add Health studies. We tested selection/concentration of genetic risks for obesity, schizophrenia, teen pregnancy and poor educational outcomes in high-risk neighbourhoods, including genetic analysis of neighbourhood mobility. Findings argue against genetic selection/concentration as an explanation for neighbourhood gradients in obesity and mental health problems. By contrast, modest genetic selection/concentration was evident for teen pregnancy and poor educational outcomes, suggesting that neighbourhood effects for these outcomes should be interpreted with care.

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.

This study investigates the association between neighborhood disadvantage from adolescence to young adulthood and metabolic syndrome using a life course epidemiology framework. Data from the United States-based National Longitudinal Study of Adolescent to Adult Health (n = 9500) and a structural equation modeling approach were used to test neighborhood disadvantage across adolescence, emerging adulthood, and young adulthood in relation to metabolic syndrome. Adolescent neighborhood disadvantage was directly associated with metabolic syndrome in young adulthood. Evidence supporting an indirect association between adolescent neighborhood disadvantage and adult metabolic syndrome was not supported. Efforts to improve cardiometabolic health may benefit from strategies earlier in life., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

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.

In this research note, we use data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) to determine whether darker skin tone predicts hypertension among siblings using a family fixed-effects analytic strategy. We find that even after we account for common family background and home environment, body mass index, age, sex, and outdoor activity, darker skin color significantly predicts hypertension incidence among siblings. In a supplementary analysis using newly released genetic data from Add Health, we find no evidence that our results are biased by genetic pleiotropy, whereby differences in alleles among siblings relate to coloration and directly to cardiovascular health simultaneously. These results add to the extant evidence on color biases that are distinct from those based on race alone and that will likely only heighten in importance in an increasingly multiracial environment as categorization becomes more complex.

The DeBakey classification divides type A acute aortic dissection (AAD) into type I and type II; the latter limited to the ascending aorta. We endeavored to examine differences in DeBakey groups in a contemporary registry. We divided 1,872 patients with noniatrogenic AAD from the International Registry of Acute Aortic Dissection into type I (n = 1691, 90.3%) and type II (n = 181, 9.7%). Patients with type II AAD were older. On presentation, patients with type I AAD reported more back and abdominal pain and were more likely to have pulse deficit. Intramural hematoma was more frequent in type II AAD. Most patients with both types were treated surgically. Lower rates of renal failure, coma, mesenteric and limb ischemia were noted in those with type II AAD. In-hospital death was less frequent (16.6% vs 22.5%) after type II AAD, a trend that did not reach significance. There was no difference in the incidence of new dissection, rapid aortic growth, late aortic intervention or survival at 5 years. In conclusion, AAD limited to the ascending aorta (DeBakey type II) appears to be associated with improved clinical outcomes compared with dissection that extend to the aortic arch or beyond. Although fewer dissection-related complications were noted in patients presenting with type II AAD, as was a trend toward reduced in-hospital mortality, 5-year survival and descending aortic sequelae are not reduced in this contemporary report from International Registry of Acute Aortic Dissection., (Copyright © 2018 Elsevier Inc. All rights reserved.)

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.

We investigated whether darker interviewer-ascribed skin color is associated with worse cardiometabolic health among young adult Blacks and Hispanics in the United States. Our sample was comprised of 2,128 non-Hispanic Blacks and 1603 Hispanics aged 24-32, who were in high school in the United States in 1994. We used logistic and OLS regression to predict obesity, hypertension, diabetes, and cardiometabolic risk. We tested the interaction between Hispanic immigrant generation and ascribed skin color. Darker ascribed skin color predicted worse cardiometabolic health among both young adult Blacks and Hispanics. Among Hispanics, the associations were strongest among third and higher generation respondents. Our findings suggest that among US Blacks and Hispanics how individuals are perceived by others via their skin color is significantly associated with their health and well-being. Gradients in cardiometabolic health in young adulthood will likely contribute to gradients in cardiovascular disease and all-cause mortality later in life.

Purpose: We investigated the influence of depression on subsequent risk of unintended pregnancy and social disparities within this relationship, during adolescence and young adulthood., Methods: Drawing upon 15-year, nationally representative data from 8,810 young U.S. women in the National Longitudinal Study of Adolescent to Adult Health, we estimated associations between depression and time to first pregnancies reported as unintended, overall and stratified by race/ethnicity, socioeconomic status, and age with Cox proportional hazard models., Results: Moderate/severe depression symptoms were associated with an increased risk of unintended first pregnancy (hazard ratio [HR], 1.21; confidence interval [CI], 1.02-1.44). In stratified models, depression increased the pregnancy risk for all minority groups (HRs, 1.36-3.25) but not white women. Depression increased the pregnancy risk for women with $0-$19,999 (HR, 1.48; CI, 1.11-1.98) and $20,000-$49,999 (HR, 1.33; CI, 1.05-1.68) income levels but not those at higher levels. Depression increased the pregnancy risk for adolescents <20 years (HR, 1.35; CI, 1.07-1.71) but decreased the risk for women >24 years (HR, .47; CI, .25-.86)., Conclusions: Findings may inform more equitable, holistic public health strategies that target depression as a modifiable risk factor for adverse reproductive outcomes during adolescence and young adulthood., (Copyright © 2016 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.)

Based on prior research finding the 5HTTLPR L allele associated with increased cardiovascular reactivity to laboratory stressors and increased risk of myocardial infarction, we hypothesized that the 5HTTLPR L allele will be associated with increased blood pressure (BP) and increased hypertension prevalence in 2 large nationally representative samples in the United States and Singapore., Methods: Logistic regression and linear models tested associations between triallelic (L'S', based on rs25531) 5HTTLPR genotypes and hypertension severity and mean systolic and diastolic blood pressure (SBP and DBP) collected during the Wave IV survey of the National Longitudinal Study of Adolescent to Adult Health (Add Health, N=11,815) in 2008-09 and during 2004-07 in 4196 Singaporeans., Results: In US Whites, L' allele carriers had higher SBP (0.9 mm Hg, 95% CI=0.26-1.56) and greater odds (OR=1.23, 95% CI=1.10-1.38) of more severe hypertension than those with S'S' genotypes. In African Americans, L' carriers had lower mean SBP (-1.27mm Hg, 95% CI=-2.53 to -0.01) and lower odds (OR = 0.78, 95% CI=0.65-0.94) of more severe hypertension than those with the S'S' genotype. In African Americans, those with L'L' genotypes had lower DBP (-1.13mm Hg, 95% CI=-2.09 to -0.16) than S' carriers. In Native Americans, L' carriers had lower SBP (-6.05mm Hg, 95% CI=-9.59 to -2.51) and lower odds of hypertension (OR = 0.34, 95% CI=0.13-0.89) than those with the S'S' genotype. In Asian/Pacific Islanders those carrying the L' allele had lower DBP (-1.77mm Hg, 95% CI=-3.16 to -0.38) and lower odds of hypertension (OR = 0.68, 95% CI=0.48-0.96) than those with S'S'. In the Singapore sample S' carriers had higher SBP (3.02mm Hg, 95% CI=0.54-5.51) and DBP (1.90mm Hg, 95% CI=0.49-3.31) than those with the L'L' genotype., Conclusions: These findings suggest that Whites carrying the L' allele, African Americans and Native Americans with the S'S' genotype, and Asians carrying the S' allele will be found to be at higher risk of developing cardiovascular disease and may benefit from preventive measures., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Little is known about how obesity susceptibility single nucleotide polymorphisms (SNPs) interact with moderate to vigorous physical activity (MVPA) in relation to BMI during adolescence, once obesogenic neighborhood factors are accounted for. In race stratified models, including European (EA; N=4977), African (AA; N=1726), and Hispanic Americans (HA; N=1270) from the National Longitudinal Study of Adolescent to Adult Health (1996; ages 12-21), we assessed the evidence for a SNPxMVPA interaction with BMI-for-age Z score, once accounting for obesogenic neighborhood factors including physical activity amenities, transportation and recreation infrastructure, poverty and crime. Eight SNPxMVPA interactions with suggestive significance (p<0.10; three in each EA, and AA, two in HA) were observed showing attenuation on BMI-for-age Z score in adolescents with ≥5 versus <5 bouts/week MVPA, except for rs10146997 (near NRXN3). Findings were robust to the inclusion of neighborhood-level variables as covariates. These findings suggest that any attenuation from MVPA on a genetic susceptibility to obesity during adolescence is likely not operating through obesogenic neighborhood factors., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Glycated hemoglobin (HbA1c) is used to classify glycaemia and type 2 diabetes (T2D). Body mass index (BMI) is a predictor of HbA1c levels and T2D. We tested 43 established BMI and obesity loci for association with HbA1c in a nationally representative multiethnic sample of young adults from the National Longitudinal Study of Adolescent to Adult Health [Add Health: age 24-34 years; n = 5641 European Americans (EA); 1740 African Americans (AA); 1444 Hispanic Americans (HA)] without T2D, using two levels of covariate adjustment (Model 1: age, sex, smoking, and geographic region; Model 2: Model 1 covariates plus BMI). Bonferroni adjustment was made for 43 SNPs and we considered P < 0.0011 statistically significant. Means (SD) for HbA1c were 5.4% (0.3) in EA, 5.7% (0.4) in AA, and 5.5% (0.3) in HA. We observed significant evidence for association with HbA1c for two variants near SH2B1 in EA (rs4788102, P = 2.2 × 10(-4) ; rs7359397, P = 9.8 × 10(-4) ) for Model 1. Both results were attenuated after adjustment for BMI (rs4788102, P = 1.7 × 10(-3) ; rs7359397, P = 4.6 × 10(-3) ). No variant reached Bonferroni-corrected significance in AA or HA. These results suggest that SH2B1 polymorphisms are associated with HbA1c, largely independent of BMI, in EA young adults., (© 2016 John Wiley & Sons Ltd/University College London.)

Background: Adolescent obesity is predictive of future weight gain, obesity and adult onset severe obesity (body mass index [BMI] ≥40 kg m(-2) ). Despite successful efforts to identify Single Nucleotide Polymorphisms (SNPs) influencing BMI, <5% of the 40-80% heritability of the phenotype has been explained. Identification of gene-gene (G-G) interactions between known variants can help explain this hidden heritability as well as identify potential biological mechanisms affecting weight gain during this critical developmental period., Objective: We have recently shown distinct genetic effects on BMI across the life course, and thus it is important to examine the evidence for epistasis in adolescence., Methods: In adolescent participants of European descent from wave II of the National Longitudinal Study of Adolescent Health (Add Health, n = 5072, ages 12-21, 52.5% female), we tested 34 established BMI-related SNPs for G-G interaction effects on BMI z-score. We used mixed-effects regression, assuming multiplicative interaction models adjusting for age, sex and geographic region, with random effects for family and school., Results: For 28 G-G interactions that were nominally significant (P < 0.05), we attempted to replicate our results in an adolescent sample from the Childhood European American Cohort from Philadelphia. In the replication study, one interaction (PRKD1-FTO) was significant after correction for multiple testing., Conclusions: Our results are suggestive of epistatic effects on BMI during adolescence and point to potentially interactive effects between genes in biological pathways important in obesity., (© 2015 World Obesity.)

Here we provide a detailed description of the genome-wide information available on the National Longitudinal Study of Adolescent to Adult Health (Add Health) sibling pair subsample (Harris et al. in Twin Res Hum Genet 16:391-398, 2013). A total of 2,020 samples were genotyped (including duplicates) arising from 1946 Add Health individuals from the sibling pairs subsample. After various steps for quality control (QC) and quality assurance (QA), we have high quality genome-wide data available on 1,888 individuals. In this report, we first highlight the QC and QA steps that were taken to prune the data of poorly performing samples and genetic markers. We further estimate the pairwise biological relationships using genome-wide data and compare those estimates to the assumed relationships in Add Health. Additionally, using genome-wide data from known regional reference populations from Europe, West Africa, North and South America, Japan and China, we estimate the relative genetic ancestry of the respondents. Finally, rather than conducting a traditional cross-sectional genome-wide association study (GWAS) of body mass index (BMI), we opted to utilize the extensive publicly available genome-wide information to conduct a weighted GWAS of longitudinal BMI while accounting for both family and ethnic variation.

Psychosocial stress is well known to be positively associated with subsequent depressive symptoms. Cortisol response to stress may be one of a number of biological mechanisms that links psychological stress to depressive symptoms, although the precise causal pathway remains unclear. Activity of the x-linked serotonin 5-HTR2C receptor has also been shown to be associated with depression and with clinical response to antidepressant medications. We recently demonstrated that variation in a single nucleotide polymorphism on the HTR2C gene, rs6318 (Ser23Cys), is associated with different cortisol release and short-term changes in affect in response to a series of stress tasks in the laboratory. Based on this observation, we decided to examine whether rs6318 might moderate the association between psychosocial stress and subsequent depressive symptoms. In the present study we use cross-sectional data from a large population-based sample of young adult White men (N = 2,366) and White women (N = 2,712) in the United States to test this moderation hypothesis. Specifically, we hypothesized that the association between self-reported stressful life events and depressive symptoms would be stronger among homozygous Ser23 C females and hemizygous Ser23 C males than among Cys23 G carriers. In separate within-sex analyses a genotype-by-life stress interaction was observed for women (p = .022) but not for men (p = .471). Homozygous Ser23 C women who reported high levels of life stress had depressive symptom scores that were about 0.3 standard deviations higher than female Cys23 G carriers with similarly high stress levels. In contrast, no appreciable difference in depressive symptoms was observed between genotypes at lower levels of stress. Our findings support prior work that suggests a functional SNP on the HTR2C gene may confer an increased risk for depressive symptoms in White women with a history of significant life stress.

Background: Influenza vaccination remains below the federally targeted levels outlined in Healthy People 2020. Compared to non-Hispanic whites, racial and ethnic minorities are less likely to be vaccinated for influenza, despite being at increased risk for influenza-related complications and death. Also, vaccinated minorities are more likely to receive influenza vaccinations in office-based settings and less likely to use non-medical vaccination locations compared to non-Hispanic white vaccine users., Objective: To assess the number of "missed opportunities" for influenza vaccination in office-based settings by race and ethnicity and the magnitude of potential vaccine uptake and reductions in racial and ethnic disparities in influenza vaccination if these "missed opportunities" were eliminated., Design: National cross-sectional Internet survey administered between March 4 and March 14, 2010 in the United States., Participants: Non-Hispanic black, Hispanic and non-Hispanic white adults living in the United States (N = 3,418)., Main Measures: We collected data on influenza vaccination, frequency and timing of healthcare visits, and self-reported compliance with a potential provider recommendation for vaccination during the 2009-2010 influenza season. "Missed opportunities" for seasonal influenza vaccination in office-based settings were defined as the number of unvaccinated respondents who reported at least one healthcare visit in the Fall and Winter of 2009-2010 and indicated their willingness to get vaccinated if a healthcare provider strongly recommended it. "Potential vaccine uptake" was defined as the sum of actual vaccine uptake and "missed opportunities.", Key Results: The frequency of "missed opportunities" for influenza vaccination in office-based settings was significantly higher among racial and ethnic minorities than non-Hispanic whites. Eliminating these "missed opportunities" could have cut racial and ethnic disparities in influenza vaccination by roughly one half., Conclusions: Improved office-based practices regarding influenza vaccination could significantly impact Healthy People 2020 goals by increasing influenza vaccine uptake and reducing corresponding racial and ethnic disparities.

To estimate the number of physician-reported influenza vaccination reminders during the 2010-2011 influenza season, the first influenza season after universal vaccination recommendations for influenza were introduced, we interviewed 493 members of the Physicians Consulting Network. Patient vaccination reminders are a highly effective means of increasing influenza vaccination; nonetheless, only one quarter of the primary care physicians interviewed issued influenza vaccination reminders during the first year of universal vaccination recommendations, highlighting the need to improve office-based promotion of influenza vaccination.

Social relationships have long been held to have powerful effects on health and survival, but it remains unclear whether such associations differ by function and domain of relationships over time and what biophysiological mechanisms underlie these links. This study addressed these gaps by examining the longitudinal associations of persistent relationship quality across a ten year span with a major indicator of immune function. Specifically, we examined how perceived social support and social strain from relationships with family, friends, and spouse at a prior point in time are associated with subsequent risks of inflammation, as assessed by overall inflammation burden comprised of five markers (C-reactive protein, interleukin-6, fibrinogen, E-selectin, and intracellular adhesion molecule-1) in a national longitudinal study of 647 adults from the Midlife Development in the United States (1995-2009). Results from multivariate regression analysis show that (1) support from family, friends, and spouse modestly protected against risks of inflammation; (2) family, friend, and total social strain substantially increased risks of inflammation; and (3) the negative associations of social strain were stronger than the positive associations of social support with inflammation. The findings highlight the importance of enriched conceptualizations, measures, and longitudinal analyses of both social and biological stress processes to elucidate the complex pathways linking social relationships to health and illness., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Background: Little is known about the interaction between genetic and behavioural factors during lifecycle risk periods for obesity and how associations vary across race/ethnicity., Objective: The objective of this study was to examine joint associations of adiposity-related single-nucleotide polymorphisms (SNPs) and moderate to vigorous physical activity (MVPA) with body mass index (BMI) in a diverse adolescent cohort., Methods: Using data from the National Longitudinal Study of Adolescent Health (n = 8113: Wave II 1996; ages 12-21, Wave III; ages 18-27), we assessed interactions of 41 well-established SNPs and MVPA with BMI-for-age Z-scores in European Americans (EA; n = 5077), African-Americans (AA; n = 1736) and Hispanic Americans (HA; n = 1300)., Results: Of 97 assessed, we found nominally significant SNP-MVPA interactions on BMI-for-age Z-score in EA at GNPDA2 and FTO and in HA at LZTR2/SEC16B. In EA, the estimated effect of the FTO risk allele on BMI-for-age Z-score was lower (β = -0.13; 95% confidence interval [CI]: 0.08, 0.18) in individuals with ≥5 vs. <5 (β = 0.24; CI: 0.16, 0.32) bouts of MVPA per week (P for interaction 0.02). Race/ethnicity-pooled meta-analysis showed nominally significant interactions for SNPs at TFAP2B, POC5 and LYPLAL1., Conclusions: High MVPA may attenuate underlying genetic risk for obesity during adolescence, a high-risk period for adult obesity., (© 2013 The Authors. Pediatric Obesity © 2013 International Association for the Study of Obesity.)

This study uses data from the Framingham Heart Study to examine the relevance of the gene-environment interaction paradigm for genome-wide association studies (GWAS). We use completed college education as our environmental measure and estimate the interactive effect of genotype and education on body mass index (BMI) using 260,402 single-nucleotide polymorphisms (SNPs). Our results highlight the sensitivity of parameter estimates obtained from GWAS models and the difficulty of framing genome-wide results using the existing gene-environment interaction typology. We argue that SNP-environment interactions across the human genome are not likely to provide consistent evidence regarding genetic influences on health that differ by environment. Nevertheless, genome-wide data contain rich information about individual respondents, and we demonstrate the utility of this type of data. We highlight the fact that GWAS is just one use of genome-wide data, and we encourage demographers to develop methods that incorporate this vast amount of information from respondents into their analyses.

A huge literature shows that teen mothers face a variety of detriments across the life course, including truncated educational attainment. To what extent is this association causal? The estimated effects of teen motherhood on schooling vary widely, ranging from no discernible difference to 2.6 fewer years among teen mothers. The magnitude of educational consequences is therefore uncertain, despite voluminous policy and prevention efforts that rest on the assumption of a negative and presumably causal effect. This study adjudicates between two potential sources of inconsistency in the literature—methodological differences or cohort differences—by using a single, high-quality data source: namely, The National Longitudinal Study of Adolescent Health. We replicate analyses across four different statistical strategies: ordinary least squares regression; propensity score matching; and parametric and semiparametric maximum likelihood estimation. Results demonstrate educational consequences of teen childbearing, with estimated effects between 0.7 and 1.9 fewer years of schooling among teen mothers. We select our preferred estimate (0.7), derived from semiparametric maximum likelihood estimation, on the basis of weighing the strengths and limitations of each approach. Based on the range of estimated effects observed in our study, we speculate that variable statistical methods are the likely source of inconsistency in the past. We conclude by discussing implications for future research and policy, and recommend that future studies employ a similar multimethod approach to evaluate findings.

Objectives: To examine the association between socioeconomic status (SES) and C-reactive protein (CRP) to understand how SES may increase the risk of cardiovascular disease and thus identify targets for prevention measures., Methods: Path models were used to examine direct and indirect associations of four indices of SES (objective early life built environment ratings, parental and participant education, and income) with CRP measured during early adulthood using data from the National Longitudinal Adolescent Health Study (n = 11,371; mean age = 29 years, range = 24-32 years; 53.8% women, 28.0% black participants). The present study examined potential mediation of the association of SES with CRP by way of body mass index (BMI), smoking, and alcohol consumption within white and black men and women., Results: BMI was a mediator of the relation between parent education and CRP for white men (path coefficient [γ] = -0.05, p < .001) and women (γ = -0.05, p < .001). Smoking mediated the income-CRP (γ = -0.01, p < .01) and the education-CRP (γ = -0.07, p < .001) relation for white men. BMI mediated the relation between all measures of SES and CRP for white women (γ values between -0.02 and -0.05; p values < .01). None of the risk factors mediated the SES-CRP relation in black participants., Conclusions: These findings indicate that the association of SES with CRP is influenced by both the timing and type of SES measure examined. In addition, race and sex play a role in how potential mediators are involved with the SES-CRP relationship, such that BMI and smoking were mediators in white men, whereas BMI was the sole mediator in white women.

Background: Few data exist on race-related differences in acute aortic dissection patients., Methods: We evaluated black (n = 189, 14%) or white (n = 1165, 86%) patients (mean age 62.8 ± 15.3 years; 36.4% women) enrolled in 13 US centers participating in the International Registry of Acute Aortic Dissection. We excluded patients of other racial descent., Results: Type B acute aortic dissection was more frequent in the black cohort (52.4% vs 39.3%, P = .001). Black patients were younger (mean age 54.6 ± 12.8 years vs 64.2 ± 15.2 years, P <.001) and more likely to have a history of cocaine abuse (12% vs 1.6%, P <.001), hypertension (89.7% vs 73.9%, P <.001), and diabetes (13.2% vs 6.4%, P = .001). Conversely, they were less likely to have bicuspid aortic valve (1.8% vs 5.8%, P = .029), iatrogenic dissection (0.5% vs 4.5%, P = .010), and prior aortic dissection repair (7.7% vs 12.8%, P = .047). Presenting features were similar except for more abdominal pain (44.6% vs 30.6%, P <.001) and left ventricular hypertrophy on echocardiogram (44.2% vs 20.1%, P <.001) in blacks. Management was similar. Hypotension/shock/tamponade was less common (7.6% vs 20.1%, P <.001), whereas acute kidney failure was more common (41.0% vs 21.7%, P <.001) in blacks. Mortality was similar in-hospital (14.3% vs 19.1%, P = .110, odds ratio 0.704, 95% confidence interval 0.457-1.085) and at 3 years postdischarge, as evaluated by Kaplan-Meier survival analysis (22.0% vs 14.3%, P = .224, SE = 0.062 and 0.018)., Conclusions: Our study shows differences in type, etiology, and presentation of blacks and whites with acute aortic dissection, yet similar mortality for these cohorts., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background: The rise in adolescent obesity has become a public health concern, especially because of its impact on disadvantaged youth. This article examines the role of disadvantage at the family-, peer-, school-, and neighborhood-level, to determine which contexts are related to obesity in adolescence and young adulthood., Methods: We analyzed longitudinal data from Waves I (1994-1995), II (1996), and III (2001-2002) of the National Longitudinal Study of Adolescent Health, a nationally representative population-based sample of adolescents in grades 7-12 in 1995 who were followed into young adulthood. We assessed the relationship between obesity in adolescence and young adulthood, and disadvantage (measured by low parent education in adolescence) at the family-, peer-, school-, and neighborhood-level using multilevel logistic regression., Results: When all levels of disadvantage were modeled simultaneously, school-level disadvantage was significantly associated with obesity in adolescence for males and females and family-level disadvantage was significantly associated with obesity in young adulthood for females., Conclusions: Schools may serve as a primary setting for obesity prevention efforts. Because obesity in adolescence tracks into adulthood, it is important to consider prevention efforts at this stage in the life course, in addition to early childhood, particularly among disadvantaged populations., (© 2013, American School Health Association.)

Objective: To measure support for seasonal influenza vaccination requirements among US healthcare personnel (HCP) and its associations with attitudes regarding influenza and influenza vaccination and self-reported coverage by existing vaccination requirements., Design: Between June 1 and June 30, 2010, we surveyed a sample of US HCP ([Formula: see text]) recruited using an existing probability-based online research panel of participants representing the US general population as a sampling frame., Setting: General community., Participants: Eligible HCP who (1) reported having worked as medical doctors, health technologists, healthcare support staff, or other health practitioners or who (2) reported having worked in hospitals, ambulatory care facilities, long-term care facilities, or other health-related settings., Methods: We analyzed support for seasonal influenza vaccination requirements for HCP using proportion estimation and multivariable probit models., Results: A total of 57.4% (95% confidence interval, 53.3%-61.5%) of US HCP agreed that HCP should be required to be vaccinated for seasonal influenza. Support for mandatory vaccination was statistically significantly higher among HCP who were subject to employer-based influenza vaccination requirements, who considered influenza to be a serious disease, and who agreed that influenza vaccine was safe and effective., Conclusions: A majority of HCP support influenza vaccination requirements. Moreover, providing HCP with information about the safety of influenza vaccination and communicating that immunization of HCP is a patient safety issue may be important for generating staff support for influenza vaccination requirements.

Purpose: This study examined trends in body mass index (BMI) during the transition from adolescence to young adulthood by gender and race, using national data from the United States spanning for >40 years from 1959 and 2002. Although past research has investigated BMI trends separately in childhood/adolescence and adulthood, this study uniquely focused on the transition to adulthood (12-26 years) to identify the emergence of the obesity epidemic during this critical life-stage., Methods: Longitudinal and cross-sectional data were obtained from four nationally representative surveys: National Health and Nutrition Examination Survey, National Longitudinal Study of Adolescent Health, National Health Interview Survey, and National Longitudinal Surveys of Youth (NLSY79 and NLSY97). The analysis tracked age trends in BMI by time, which allowed for the examination of how BMI changed during the transition to adulthood and whether the patterns of change varied by period. Data best suited for trend analysis were identified. Age trends in BMI by gender and race were graphed and regression analysis was used to test for significant differences in the trends using the National Health and Nutrition Examination Survey and National Longitudinal Study of Adolescent Health., Results: BMI increased sharply in the adolescent ages, beginning in the 1990s and among young adults around 2000. This age pattern of BMI increase was more dramatic among females and blacks, particularly black females., Conclusions: BMI increased during the transition to adulthood and these increases have grown larger over time. Obesity prevention efforts should focus on this high-risk transition period, particularly among minority populations., (Copyright © 2011 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.)

Background: In the United States, where coronary heart disease (CHD) is the leading cause of mortality, CHD risk assessment is a priority and accurate blood pressure (BP) measurement is essential., Methods: Hypertension estimates in the National Longitudinal Study of Adolescent Health (Add Health), Wave IV (2008)-a nationally representative field study of 15,701 participants aged 24-32-was referenced against NHANES (2007-2008) participants of the same age. We examined discordances in hypertension, and estimated the accuracy and reliability of blood pressure in the Add Health study., Results: Hypertension rates (BP: ≥ 140/90 mm Hg) were higher in Add Health compared with NHANES (19% vs. 4%), but self-reported history was similar (11% vs. 9%) among adults aged 24-32. Survey weights and adjustments for differences in participant characteristics, examination time, use of antihypertensive medications, and consumption of food/caffeine/cigarettes before blood pressure measurement had little effect on between-study differences in hypertension estimates. Among Add Health participants interviewed and examined twice (full and abbreviated interviews), blood pressure was similar, as was blood pressure at the in-home and in-clinic examinations conducted by NHANES III (1988-1994). In Add Health, there was minimal digit preference in blood pressure measurements; mean bias never exceeded 2 mm Hg; and reliability (estimated as intraclass correlation coefficients) was 0.81 and 0.68 for systolic and diastolic BPs, respectively., Conclusions: The proportion of young adults in NHANES reporting a history of hypertension was twice that with measured hypertension, whereas the reverse was found in Add Health. Between-survey differences were not explained by digit preference, low validity, or reliability of Add Health blood pressure data, or by salient differences in participant selection, measurement context, or interview content. The prevalence of hypertension among Add Health Wave IV participants suggests an unexpectedly high risk of cardiovascular disease among US young adults and warrants further scrutiny.