We use unique longitudinal data to document an economically and statistically significant positive correlation between the facial attractiveness of male high school graduates and their subsequent ...labor market earnings. There are only weak links between facial attractiveness and direct measures of cognitive skills and no link between facial attractiveness and mortality. Even after including a lengthy set of characteristics, including IQ, high school activities, proxy measures for confidence and personality, family background, and additional respondent characteristics in an empirical model of earnings, the attractiveness premium is present in the respondents' mid-30s and early 50s. Our findings are consistent with attractiveness being an enduring, positive labor market characteristic.
Women’s opportunities have been profoundly altered over the past century by reductions in the social and structural constraints that limit women’s educational attainment. Do social constraints ...manifest as a suppressing influence on genetic indicators of potential, and if so, did equalizing opportunity mean equalizing the role of genetics? We address this with three cohort studies: the Wisconsin Longitudinal Study (WLS; birth years 1939 to 1940), the Health and Retirement Study, and the National Longitudinal Study of Adolescent Health (Add Health; birth years 1975 to 1982). These studies include a “polygenic score” for educational attainment, providing a novel opportunity to explore this question. We find that within the WLS cohort, the relationship between genetics and educational outcomes is weaker for women than for men. However, as opportunities changed in the 1970s and 1980s, and many middle-aged women went back to school, the relationship between genetic factors and education strengthened for women as they aged. Furthermore, utilizing the HRS and Add Health, we find that as constraints limiting women’s educational attainment declined, gender differences in the relationship between genetics and educational outcomes weakened. We demonstrate that genetic influence must be understood through the lens of historical change, the life course, and social structures like gender.
Low muscle strength is an important heritable indicator of poor health linked to morbidity and mortality in older people. In a genome-wide association study meta-analysis of 256,523 Europeans aged 60 ...years and over from 22 cohorts we identify 15 loci associated with muscle weakness (European Working Group on Sarcopenia in Older People definition: n = 48,596 cases, 18.9% of total), including 12 loci not implicated in previous analyses of continuous measures of grip strength. Loci include genes reportedly involved in autoimmune disease (HLA-DQA1 p = 4 × 10
), arthritis (GDF5 p = 4 × 10
), cell cycle control and cancer protection, regulation of transcription, and others involved in the development and maintenance of the musculoskeletal system. Using Mendelian randomization we report possible overlapping causal pathways, including diabetes susceptibility, haematological parameters, and the immune system. We conclude that muscle weakness in older adults has distinct mechanisms from continuous strength, including several pathways considered to be hallmarks of ageing.
We undertook a genome-wide association study (GWAS) of parental longevity in European descent UK Biobank participants. For combined mothers' and fathers' attained age, 10 loci were associated (p<5*10
...), including 8 previously identified for traits including survival, Alzheimer's and cardiovascular disease. Of these, 4 were also associated with longest 10% survival (mothers age ≥90 years, fathers ≥87 years), with 2 additional associations including
intronic variants (coding for the adrenocorticotropic hormone receptor). Mother's age at death was associated with 3 additional loci (2 linked to autoimmune conditions), and 8 for fathers only. An attained age genetic risk score associated with parental survival in the US Health and Retirement Study and the Wisconsin Longitudinal Study and with having a centenarian parent (
=1,181) in UK Biobank. The results suggest that human longevity is highly polygenic with prominent roles for loci likely involved in cellular senescence and inflammation, plus lipid metabolism and cardiovascular conditions. There may also be gender specific routes to longevity.
As the population ages and the prevalence of dementia increases, unpacking robust and persistent associations between educational attainment and later life cognitive functioning is increasingly ...important. We do know, from studies with robust causal designs, that policies that increase years of schooling improve later life cognitive functioning. Yet these studies don't illuminate why older adults with greater educational attainment have relatively preserved cognitive functioning. Studies focused on why, however, have been hampered by methodological limitations and inattention to some key explanations for this relationship. Consequently, we test explanations encompassing antecedent factors, specifically family environments, adolescent IQ, and genetic factors, as well as adult mediating mechanisms, specifically health behaviors and health. We employ the Wisconsin Longitudinal Study, which includes 80 years of prospectively collected data on a sample of 1 in every 3 high school graduates, and a selected sibling, from the class of 1957. Sibling models, and the inclusion of prospectively collected early and midlife covariates, allows us to address the explanatory and methodological limitations of the prior literature to better unpack the relationship between education and later life cognitive functioning. We find little evidence that early life genetic endowments and environments, or midlife health and health behaviors, explain the relationship. Adolescent cognition, however, does matter; higher educational attainment, linked to antecedent adolescent cognitive functioning, helps protect against lower levels of cognitive functioning in later life. Both adolescent cognition and education, however, independently associate with later life cognitive functioning at relatively similar magnitudes. Educational attainment's relationship to later life cognitive functioning is not simply a function of adolescent cognitive functioning.
•The education and late life cognition relationship is not well understood.•Genetic factors influencing education do not influence late life cognition.•Adolescent cognition influences late life cognition, in part, via education.•Education's influence is independent of adolescent cognition.•Midlife health and health behaviors do not mediate these relationships.
Genetic variants identified in genome-wide association studies of educational attainment have been linked with a range of positive life course development outcomes. However, it remains unclear ...whether school environments may moderate these genetic associations. We analyze data from two biosocial surveys that contain both genetic data and follow students from secondary school through mid- to late life. We test if the magnitudes of the associations with educational and occupational attainments varied across the secondary schools that participants attended or with characteristics of those schools. Although we find little evidence that genetic associations with educational and occupational attainment varied across schools or with school characteristics, genetic associations with any postsecondary education and college completion were moderated by school-level socioeconomic status. Along similar lines, we observe substantial between-school variation in the average level of educational attainment students achieved for a fixed genotype. These findings emphasize the importance of social context in the interpretation of genetic associations. Specifically, our results suggest that though existing measures of individual genetic endowment have a linear relationship with years of schooling that is relatively consistent across school environments, school context is crucial in connecting an individual’s genotype to his or her likelihood of crossing meaningful educational thresholds.
Abstract
Ever since releasing genotype data in 2017, the WLS continually expands resources available to users interested in genetic research. Key advantages to the WLS data for genetics research ...include its sibling sample and nearly full life course longitudinal study design. In 2021, we now have state-of-the-art polygenic scores available in multiple domains, such as health, cognition, fertility, personality, risk behaviors and attitudes, and life satisfaction. The scores cover phenotypes spanning from adventurousness, through educational attainment, to age at which voice deepened. Additionally, the genotype data was re-imputed in 2021 to the superior Haplotype Reference Consortium reference panel and the WLS expects to obtain copy number variants data next year. In addition to genetic data, we have a set of novel microbiome data on a subset of participants that allows researchers to study relationships between environments and gut microbial composition.
Despite decades of research on unintended pregnancies, we know little about the health implications for the women who experience them. Moreover, no study has examined the implications for women whose ...pregnancies occurred before Roe v. Wade was decided--nor whether the mental health consequences of these unintended pregnancies continue into later life. Using the Wisconsin Longitudinal Study, a 60-year ongoing survey, we examined associations between unwanted and mistimed pregnancies and mental health in later life, controlling for factors such as early life socioeconomic conditions, adolescent IQ, and personality. We found that in this cohort of mostly married and White women, who completed their pregnancies before the legalization of abortion, unwanted pregnancies were strongly associated with poorer mental health outcomes in later life.
There is a robust consensus, most recently articulated in the 2020 Lancet Commission, that the roots of dementia can be traced to early life, and that the path to prevention may start there as well. ...Indeed, a growing body of research demonstrates that early life disadvantage may influence the risk for later life dementia and cognitive decline. A still understudied risk, however, is early life rural residence, a plausible pathway given related economic and educational disadvantages, as well as associations between later life rural living and lower levels of cognitive functioning.
We aim to examine whether living in rural environments during early life has long term implications for cognitive health in later life.
We employed the Wisconsin Longitudinal Study, which tracked 1 in every 3 high school graduates from the class of 1957, from infancy to ∼age 72. The data include a rich array of prospectively collected early life data, unique among existing studies, as well as later life measures of cognitive functioning.
We found a robust relationship between early life rural residence, especially living on a farm, and long-term risk for reduced cognitive performance on recall and fluency tasks. Controls for adolescent cognitive functioning, APOEɛ2 and APOEɛ4, as well as childhood and adult factors, ranging from early life socioeconomic conditions to later life health and rural and farm residency, did not alter the findings.
Rural living in early life is an independent risk for lower levels of cognitive functioning in later life.
Background
Exposure to ambient air pollution is an emerging risk factor for dementia, yet air pollution levels are found to vary by neighborhood affluence and across rural/urban settings. In this ...study, we leverage data from the Wisconsin Longitudinal Study (WLS) to evaluate the effects of ambient air pollution exposure on the rate of memory decline in late life, while accounting for both local (neighborhood) and regional (urbanization) residency characteristics.
Method
Annualized rate of change for both immediate and delayed recall trials of a 10‐item word list were calculated between 2010‐1 (baseline) and 2021‐2 (follow‐up) data collection waves. Yearly averages of geocoded regional air pollution data were obtained for 5 pollutants at baseline: particulate matter > 2.5um (PM2.5), ozone (O3), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO). Principal component analysis was performed to reduce multicollinearity among the 5 pollutants in subsequent analyses. Annualized rate of change in memory measures were regressed on resultant pollutant factor scores, additionally controlling for baseline age, adolescent IQ, education, health conditions (heart disease, stroke, hypertension, diabetes), neighborhood‐level deprivation, ApolipoproteinE‐4 (ApoE‐4) status, and sex.
Result
3,601 WLS participants were included in analyses, with a mean age of 70.4±3.4 years at baseline and 80.1±3.4 years at follow‐up. PCA yielded a 2‐factor solution classifying air pollutants into distinct urban (PM2.5, NO2, and CO2) versus rural (SO2 and O3) composites. Linear regression analysis revealed that greater annualized decline in delayed recall was predicted by higher exposure to urban air pollutants (but not rural), adolescent IQ, older age at baseline, and a history of heart disease. Air pollution exposure did not predict annualized change in immediate recall.
Conclusion
Using longitudinal data from the WLS cohort, we find that higher levels of urban ambient air pollutant exposure predicted a more precipitous decline in delayed memory across late life. This finding remained significant after controlling for relevant confounders including neighborhood disadvantage, adolescent IQ, and ApoE‐4 status. Although the effect size of pollution exposure on the rate of memory decline was small, it remains a modifiable risk factor and stands to inform public policies to optimize late life cognition.
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