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Purpose: The aim of this literature review is to examine evidence of time trends and birth cohort effects in depressive disorders and symptoms among US adolescents in peer-reviewed articles from January 2004 to April 2022. Methods: We conducted an integrative systematic literature review. Three reviewers participated at different stages of article review. Of the 2234 articles identified in three databases (Pubmed, ProQuest Central, Ebscohost), 10 met inclusion criteria (i.e., adolescent aged United States populations, included information about birth cohort and survey year, focused on depressive symptoms/disorders). Results: All 10 articles observed increases in depressive symptoms and disorders in adolescents across recent survey years with increases observed between 1991 and 2020. Of the 3 articles that assessed birth cohort trends, birth cohort trends were less prominent than time period trends. Proposed explanations for increases included social media, economic-related reasons, changes in mental health screening and diagnosis, declining mental health stigma, increased treatment, and, in more recent years, the COVID-19 pandemic. Conclusions: Multiple cross-sectional surveys and cohort studies documented rising prevalence of depressive symptoms and disorder among adolescents from 1991 to 2020. Mechanisms driving this increase are still unknown. Research to identify these mechanisms is needed to inform depression screening and intervention efforts for adolescents. [ABSTRACT FROM AUTHOR]

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 4th 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 20th 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. [ABSTRACT FROM AUTHOR]

Aging is a process of progressive change. To develop biological models of aging, longitudinal datasets with high temporal resolution are needed. Here we report a multi-omics longitudinal dataset for cultured primary human fibroblasts measured across their replicative lifespans. Fibroblasts were sourced from both healthy donors (n = 6) and individuals with lifespan-shortening mitochondrial disease (n = 3). The dataset includes cytological, bioenergetic, DNA methylation, gene expression, secreted proteins, mitochondrial DNA copy number and mutations, cell-free DNA, telomere length, and whole-genome sequencing data. This dataset enables the bridging of mechanistic processes of aging as outlined by the "hallmarks of aging", with the descriptive characterization of aging such as epigenetic age clocks. Here we focus on bridging the gap for the hallmark mitochondrial metabolism. Our dataset includes measurement of healthy cells, and cells subjected to over a dozen experimental manipulations targeting oxidative phosphorylation (OxPhos), glycolysis, and glucocorticoid signaling, among others. These experiments provide opportunities to test how cellular energetics affect the biology of cellular aging. All data are publicly available at our webtool: https://columbia-picard.shinyapps.io/shinyapp-Lifespan_Study/ Measurement(s) gene expression assay • DNA Methylation • Telomere Length • Seahorse Bioenergetics • mtDNA copy number • Whole Genome Sequencing • Cytokine • cell-free DNA • mtDNA sequencing • cell-free GDF15 • cell-free IL6 Technology Type(s) Illumina HiSeq. 4000 • Illumina epic array • Real Time PCR • Seahorse XFe96 • Real Time PCR • Luminex 200 • ELISA Factor Type(s) time grown in culture Sample Characteristic - Organism Homo sapiens Sample Characteristic - Environment cell culture Sample Characteristic - Location contiguous United States of America [ABSTRACT FROM AUTHOR]

Objectives: To investigate multiple dimensions of social relationships related to biomarkers of cardiometabolic health and how their associations vary by wealth in older adults. Methods: Growth curve models were used to investigate the longitudinal associations between measures of both positive and negative social relationships and cardiometabolic risk (CMR) over a 10-year period from 2006 to 2016 and the moderation of this association by wealth in the Health and Retirement Study (HRS). Results: Older adults with better social relationships had lower CMR on average. The protective effects of positive social relationships, however, waned at older ages, particularly for low-wealth individuals. Discussion: Our results suggest that good social relationships promote healthy aging by buffering against harmful cardiometabolic consequences of psychosocial stress, particularly among relatively wealthy individuals. Efforts to improve old age health would be more effective when focusing simultaneously on fostering social connections and boosting financial resources. [ABSTRACT FROM AUTHOR]

Biological aging is a proposed mechanism through which social determinants drive health disparities. We conducted proof-of-concept testing of 8 DNA-methylation (DNAm) and blood-chemistry quantifications of biological aging as mediators of disparities in healthspan between Black and White participants in the 2016 wave of the Health and Retirement Study (n = 9,005). We quantified biological aging from 4 DNAm "clocks" (Horvath, Hannum, PhenoAge, and GrimAge clock), a DNAm pace-of-aging measure (DunedinPoAm), and 3 blood-chemistry measures (PhenoAge, Klemera-Doubal method biological age, and homeostatic dysregulation). We quantified Black-White disparities in healthspan from cross-sectional and longitudinal data on physical performance tests, self-reported limitations in activities of daily living, and physician-diagnosed chronic diseases, self-rated health, and survival. DNAm and blood-chemistry quantifications of biological aging were moderately correlated (Pearson's r = 0.1–0.4). The GrimAge clock, DunedinPoAm, and all 3 blood-chemistry measures were associated with healthspan characteristics (e.g. mortality effect-size hazard ratios were 1.71–2.32 per standard deviation of biological aging) and showed evidence of more advanced/faster biological aging in Black participants than in White participants (Cohen's d = 0.4–0.5). These measures accounted for 13%–95% of Black-White differences in healthspan-related characteristics. Findings suggest that reducing disparities in biological aging can contribute to building health equity. [ABSTRACT FROM AUTHOR]

Objective: Experience of stressful life events is associated with risk of depression. Yet many exposed individuals do not become depressed. A controversial hypothesis is that genetic factors influence vulnerability to depression following stress. This hypothesis is often tested with a "diathesis-stress" model, in which genes confer excess vulnerability. The authors tested an alternative formulation of this model: genes may buffer against depressogenic effects of life stress.Method: The hypothesized genetic buffer was measured using a polygenic score derived from a published genome-wide association study of subjective well-being. The authors tested whether married older adults who had higher polygenic scores were less vulnerable to depressive symptoms following the death of their spouse compared with age-matched peers who had also lost their spouse and who had lower polygenic scores. Data were analyzed from 8,588 non-Hispanic white adults in the Health and Retirement Study (HRS), a population-representative longitudinal study of older adults in the United States.Results: HRS adults with higher well-being polygenic scores experienced fewer depressive symptoms during follow-up. Those who survived the death of their spouses (N=1,647) experienced a sharp increase in depressive symptoms following the death and returned toward baseline over the following 2 years. Having a higher well-being polygenic score buffered against increased depressive symptoms following a spouse's death.Conclusions: The effects were small, and the clinical relevance is uncertain, although polygenic score analyses may provide clues to behavioral pathways that can serve as therapeutic targets. Future studies of gene-environment interplay in depression may benefit from focus on genetics discovered for putative protective factors. [ABSTRACT FROM AUTHOR]

Background: Adverse childhood experiences (ACEs; e.g. abuse, neglect, and parental loss) have been associated with increased risk for later-life disease and dysfunction using adults’ retrospective self-reports of ACEs. Research should test whether associations between ACEs and health outcomes are the same for prospective and retrospective ACE measures. Methods: We estimated agreement between ACEs prospectively recorded throughout childhood (by Study staff at Study member ages 3, 5, 7, 9, 11, 13, and 15) and retrospectively recalled in adulthood (by Study members when they reached age 38), in the population-representative Dunedin cohort (N = 1,037). We related both retrospective and prospective ACE measures to physical, mental, cognitive, and social health at midlife measured through both objective (e.g. biomarkers and neuropsychological tests) and subjective (e.g. self-reported) means. Results: Dunedin and U.S. Centers for Disease Control ACE distributions were similar. Retrospective and prospective measures of adversity showed moderate agreement (r = .47, p < .001; weighted Kappa = .31, 95% CI: .27–.35). Both associated with all midlife outcomes. As compared to prospective ACEs, retrospective ACEs showed stronger associations with life outcomes that were subjectively assessed, and weaker associations with life outcomes that were objectively assessed. Recalled ACEs and poor subjective outcomes were correlated regardless of whether prospectively recorded ACEs were evident. Individuals who recalled more ACEs than had been prospectively recorded were more neurotic than average, and individuals who recalled fewer ACEs than recorded were more agreeable. Conclusions: Prospective ACE records confirm associations between childhood adversity and negative life outcomes found previously using retrospective ACE reports. However, more agreeable and neurotic dispositions may, respectively, bias retrospective ACE measures toward underestimating the impact of adversity on objectively measured life outcomes and overestimating the impact of adversity on self-reported outcomes. Associations between personality factors and the propensity to recall adversity were extremely modest and warrant further investigation. Risk predictions based on retrospective ACE reports should utilize objective outcome measures. Where objective outcome measurements are difficult to obtain, correction factors may be warranted. [ABSTRACT FROM AUTHOR]

Incarceration is a disruptive event that is experienced by a considerable proportion of the United States population. Research has identified social factors that predict incarceration risk, but scholars have called for a focus on the ways that individual differences combine with social factors to affect incarceration risk. Our study is an initial attempt to heed this call using whole-genome data. We use data from the Health and Retirement Study (HRS) (N = 6716) to construct a genome-wide measure of genetic propensity for aggressive behavior and use it to predict lifetime incarceration risk. We find that participants with a higher genetic propensity for aggression are more likely to experience incarceration, but the effect is stronger for males than females. Importantly, we identify a gene-environment interaction (G × E)—genetic propensity is reduced, substantively and statistically, to a non-significant predictor for males raised in homes where at least one parent graduated high school. We close by placing these findings in the broader context of concerns that have been raised about genetics research in criminology. • Socio-genomics offers insight into gene-environment interplay. • We construct a genome-wide measure of genetic propensity for aggressive behavior. • Males with higher genetic propensity were more likely to experience incarceration. • But gene-environment interaction (G × E) was observed • Genetic propensity was not predictive for males raised in high education homes. [ABSTRACT FROM AUTHOR]

Purpose: Household economic adversity during adolescence is hypothesized to be a risk factor for poor mental health later in life. To test this hypothesis, we conducted a quasi-experimental analysis of an economic shock, the Great Recession of 2007-2009. We tested if going through adolescence during the Great Recession was associated with increased risk of major depressive episodes (MDE) and mental health treatment in young adulthood with potential moderation by household poverty to explore differences by economic adversity., Methods: We analyzed data on young adults age 18-29 years from the 2005-2019 National Survey on Drug Use and Health (N = 145,394). We compared participants who were adolescents during the recession to those followed-up prior to the recession. Regression analysis tested effect modification by household poverty status., Results: Adolescent exposure to the Great Recession was associated with higher likelihood of MDE during young adulthood (aOR = 1.30, 95% CI = 1.23, 1.37); there was no relationship with mental health treatment. Effects on MDE were stronger among those in households with higher incomes compared to those living in poverty., Conclusion: Findings support the hypothesis that exposure to the Great Recession during adolescence may have increased risk for MDE, but raise questions about whether the mechanism of this association is economic distress., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

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.

Policy Points The Paycheck Plus randomized controlled trial tested a fourfold increase in the Earned Income Tax Credit (EITC) for single adults without dependent children over 3 years in New York and Atlanta. In New York, the intervention improved economic, mental, and physical health outcomes. In Atlanta, it had no economic benefit or impact on physical health and may have worsened mental health. In Atlanta, tax filing and bonus receipt were lower than in the New York arm of the trial, which may explain the lack of economic benefits. Lower mental health scores in the treatment group were driven by disadvantaged men, and the study sample was in good mental health., Context: The Paycheck Plus experiment examined the effects of an enhanced Earned Income Tax Credit (EITC) for single adults on economic and health outcomes in Atlanta, GA and New York City (NYC). The NYC study was completed two years prior to the Atlanta study and found mental and physical benefits for the subgroups that responded best to the economic incentives provided. In this article, we present the findings from the Atlanta study, in which the uptake of the treatment (tax filings and EITC bonus) were lower and economic and health benefits were not observed., Methods: Paycheck Plus Atlanta was an unblinded randomized controlled trial that assigned n = 3,971 participants to either the standard federal EITC (control group) or an EITC supplement of up to $2,000 (treatment group) for three tax years (2017-2019). Administrative data on employment and earnings were obtained from the Georgia Department of Labor and survey data were used to examine validated measures of health and well-being., Findings: In Atlanta, the treatment group had significantly higher earnings in the first project year but did not have significantly higher cumulative earnings than the control group overall (mean difference = $1,812, 95% CI = -150, 3,774, p = 0.07). The treatment group also had significantly lower scores on two measures of mental health after the intervention was complete: the Patient Health Questionnaire 8 (mean difference = 0.19, 95% CI = 0.06, 0.32, p = 0.005) and the Kessler 6 (mean difference = 0.15, 95% CI = 0.03, 0.27, p = 0.012). Secondary analyses suggested these results were driven by disadvantaged men, but the study sample was in good mental health., Conclusions: The EITC experiment in Atlanta was not associated with gains in earnings or improvements in physical or mental health., (© 2023 The Authors. The Milbank Quarterly published by Wiley Periodicals LLC on behalf of The Milbank Memorial Fund.)

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.

Purpose: In the United States, adolescent depression increased beginning in 2008-2010, coinciding with the Great Recession. We investigated whether this time of changing economic circumstances impacted adolescent depression and treatment., Methods: We analyzed data for adolescents aged 12-17 years from the 2004-2019 National Survey on Drug Use and Health (N = 256,572). Adolescents' past-year major depressive episodes (MDEs) were measured by self-reported symptoms. MDE treatment included seeing a health professional or receiving MDE medication. We tested how MDE and MDE treatment changed from pre-Great Recession (2004 to Fall 2007) to post-Great Recession (Winter 2007-2019) using interrupted time-series segmented regression models, accounting for seasonality and autocorrelation and testing for moderation by household poverty., Results: The Great Recession was not associated with an immediate increase in MDE prevalence (β:-0.77 [i.e., quarter-year change in prevalence], 95% confidence interval (CI): -2.23, 0.69). However, the increase in MDE prevalence accelerated following the Great Recession (β: 0.29, 95% CI: 0.13, 0.44). The Great Recession was not associated with immediate or long-term changes in adolescent MDE treatment (immediate β: -2.87, 95% CI: -7.79, 2.04; long-term β: 0.03, 95% CI: -0.46, 0.51). Effects were similar for households by poverty status., Discussion: The Great Recession was not associated with increased adolescent depression prevalence, although there was an acceleration in the trend of adolescent MDE following the recession. The prevalence of MDE treatment remained stable. Adolescent depression prevention efforts should be heightened as prevalence increases, including actively engaging caregivers as family supports to alleviate potential negative implications of economic distress for adolescent MDE., (Copyright © 2023 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.)

Background and Objectives: Exposure to socioeconomic disadvantage is associated with early-onset cognitive aging. Biological aging, the progressive loss of system integrity that occurs as we age, is proposed as a modifiable process mediating this health inequality. We examined whether socioeconomic disparities in cognitive aging in mid-to late-life adults is explained by accelerated biological aging similarly across race, ethnicity, and sex/gender., Methods: Data were from a prospective cohort study of the US Health and Retirement Study DNA methylation substudy. Socioeconomic status (SES) was measured from years of education and household wealth at baseline. The extent and pace of biological aging were quantified using 3 DNA methylation measures: PhenoAge, GrimAge, and DunedinPoAm. Cognitive aging was measured from repeated longitudinal assessments of immediate and delayed word recall. Latent growth curve modeling estimated participants' level of memory performance and rate of decline over 2-11 follow-up assessments spanning 2-20 years. Multiple-group models were estimated to assess whether the relationship between SES and memory trajectories was mediated by biological aging across racial-ethnic by sex/gender subgroups., Results: Data from a total of 3,997 adults aged 50-100 years were analyzed. Participants with lower SES had a lower memory performance, had a faster decline, and exhibited accelerated biological aging (SES effect size associations [β] ranged from 0.08 to 0.41). Accelerated biological aging was associated with decreased memory performance and faster memory decline (effect size range 0.03-0.23). SES-biological aging associations were the strongest for White men and women and weakest for Latinx women. The relationship between biological aging measures and memory was weaker for Black participants compared with that for White and Latinx people. In mediation analysis, biological aging accounted for 4%-27% of the SES-memory gradient in White participants. There was little evidence of mediation in Black or Latinx participants., Discussion: Among a national sample of mid-to late-life adults, DNA methylation measures of biological aging were variably associated with memory trajectories and SES across White, Black, and Latinx mid-to late-life adults. These results challenge the assumption that DNA methylation biomarkers of aging that were developed in primarily White people can equivalently quantify aging processes affecting cognition in Black and Latinx mid-to late-life adults., (© 2022 American Academy of Neurology.)

Objectives: Spousal death is a common late-life event with health-related sequelae. Evidence linking poor mental health to disease suggests the hypothesis that poor mental health following death of a spouse could be a harbinger of physical health decline. Thus, identification of bereavement-related mental health symptoms could provide an opportunity for prevention., Methods: We analyzed data from N = 39,162 individuals followed from 1994 to 2016 in the U.S. Health and Retirement Study; N = 5,061 were widowed during follow-up. We tested change in mental and physical health from prebereavement through the 5 years following spousal death., Results: Bereaved spouses experienced an increase in depressive symptoms following their spouses' deaths but the depressive shock attenuated within 1 year. Bereaved spouses experienced increases in disability, chronic-disease morbidity, and hospitalization, which grew in magnitude over time, especially among older respondents. Bereaved spouses were at increased risk of death compared to nonbereaved respondents. The magnitude of depressive symptoms in the immediate aftermath of spousal death predicted physical-health decline and mortality risk over 5 years of follow-up., Discussion: Bereavement-related depressive symptoms indicate a risk for physical health decline and death in older adults. Screening for depressive symptoms in bereaved older adults may represent an opportunity for intervention to preserve healthy life span., (© The Author(s) 2020. 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.)

Americans have significantly poorer health outcomes and shorter longevity than citizens of other industrialized nations. Poverty is a major driver of these poor health outcomes in the United States. Innovative anti-poverty policies may help reduce economic malaise thereby increasing the health and longevity of the most vulnerable Americans. However, there is no consensus framework for studying the health impacts of anti-poverty social policies. In this paper, we describe a case study in which leading global experts systematically: (1) developed a conceptual model that outlines the potential pathways through which a social policy influences health, (2) fits outcome measures to this conceptual model, and (3) estimates an optimal time frame for collection of the selected outcome measures. This systematic process, called the Delphi method, has the potential to produce estimates more quickly and with less bias than might be achieved through expert panel discussions alone. Our case study is a multi-component randomized-controlled trial (RCT) of a workforce policy called MyGoals for Healthy Aging., Competing Interests: The authors declare no conflict of interest.

People who score higher on intelligence tests tend to have larger brains. Twin studies suggest the same genetic factors influence both brain size and intelligence. This has led to the hypothesis that genetics influence intelligence partly by contributing to the development of larger brains. We tested this hypothesis using four large imaging genetics studies (combined N = 7965) with polygenic scores derived from a genome-wide association study (GWAS) of educational attainment, a correlate of intelligence. We conducted meta-analysis to test associations among participants' genetics, total brain volume (i.e., brain size), and cognitive test performance. Consistent with previous findings, participants with higher polygenic scores achieved higher scores on cognitive tests, as did participants with larger brains. Participants with higher polygenic scores also had larger brains. We found some evidence that brain size partly mediated associations between participants' education polygenic scores and their cognitive test performance. Effect sizes were larger in the population-based samples than in the convenience-based samples. Recruitment and retention of population-representative samples should be a priority for neuroscience research. Findings suggest promise for studies integrating GWAS discoveries with brain imaging to understand neurobiology linking genetics with cognitive performance., (© The Author(s) 2018. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

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.

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.

Multi-locus profiles of genetic risk, so-called "genetic risk scores," can be used to translate discoveries from genome-wide association studies into tools for population health research. We developed a genetic risk score for obesity from results of 16 published genome-wide association studies of obesity phenotypes in European-descent samples. We then evaluated this genetic risk score using data from the Atherosclerosis Risk in Communities (ARIC) cohort GWAS sample (N = 10,745, 55% female, 77% white, 23% African American). Our 32-locus GRS was a statistically significant predictor of body mass index (BMI) and obesity among ARIC whites [for BMI, r = 0.13, p<1 × 10(-30); for obesity, area under the receiver operating characteristic curve (AUC) = 0.57 (95% CI 0.55-0.58)]. The GRS predicted differences in obesity risk net of demographic, geographic, and socioeconomic information. The GRS performed less well among African Americans. The genetic risk score we derived from GWAS provides a molecular measurement of genetic predisposition to elevated BMI and obesity.[Supplemental materials are available for this article. Go to the publisher's online edition of Biodemography and Social Biology for the following resource: Supplement to Development & Evaluation of a Genetic Risk Score for Obesity.].

The authors examined the role of food insecurity in the etiology of children's cognitive and mental health problems. Data from a prospective longitudinal study of 1,116 United Kingdom families with twins (sample constructed in 1999-2000) were used to test associations among household food insecurity; income; maternal personality; household sensitivity to children's needs; and children's cognitive, behavioral, and emotional development. Food-insecure children had lower IQs and higher levels of behavioral and emotional problems relative to their peers. After differences in household income, the personalities of children's mothers, and the sensitivity of household organization to children's needs were accounted for, food-insecure children had moderately higher levels of emotional problems relative to food-secure children (β = 0.22, P = 0.02). Differences in children's cognitive development were accounted for by household income, and differences in their behavioral development were accounted for by their mothers' personalities and their households' sensitivity to children's needs. Results suggest that food insecurity was associated with school-aged children's emotional problems but not with their cognitive or behavioral problems after accounting for differences in the home environments in which children were reared. Mothers' personality and household sensitivity to children's needs may present challenges to improving outcomes of children with food insecurity.

Objectives: To estimate the prevalence of major eye diseases and low vision or blindness in a national sample of male US Union Army veterans from 1890 to 1910 and to compare these prevalence rates with contemporary rates for the same diseases and visual status., Design: Longitudinal histories of 16,022 white Union Army veterans receiving disability pensions from 1890 to 1910 were developed from pension board examination records. Prevalence rates of trachoma, corneal opacities, cataract, diseases of the retina and optic nerve, and low vision or blindness were calculated in 1895 and 1910. Changes in prevalence by age were examined., Results: By 1910, 11.9% of veterans had low vision or were blind in both eyes. Prevalence of cataract increased with age, resulting in 13.1% of veterans having had cataract in one or both eyes. Rates of trachoma were 3.2% in 1895 and 4.8% in 1910. Rates of corneal opacity were 3.0% and 5.1%, respectively. Glaucoma was rarely diagnosed from 1890 to 1910, but diseases of the optic nerve were reported in 2.0% of veterans in 1895 and 3.6% in 1910., Conclusions: This study documents substantial reductions in the prevalence of low vision or blindness and changes in the composition of eye diseases from an era in which there were few effective therapies for eye diseases to the present.