Re-examining the relationship between education and adult mental health in the UK: A research note.

Previous studies using variation in education arising from compulsory schooling laws have found no causal effects of education on mental health in the UK. We re-examine the relationship between education and mental health in the UK by taking a different approach: sibling fixed-effects with controls for polygenic scores (summary measures of genetic predisposition) for educational attainment and adult depressive symptoms. We find that higher educational attainment is associated with better adult mental health, that sibling controls reduce these associations by ~40-70% but important associations remain and find evidence for non-monotonic effects. We also find suggestive evidence that education partially "rescues" genetic predictors of poor mental health.

Genetic risks, adolescent health, and schooling attainment.

We provide new evidence on the effect of adolescent health behaviors/outcomes (obesity, depression, smoking, and attention deficit hyperactivity disorder [ADHD]) on schooling attainment using the National Longitudinal Study of Adolescent to Adult Health. We take two different approaches to deal with omitted variable bias and reverse causality. Our first approach attends to the issue of reverse causality by estimating the effect of health polygenic scores (PGSs) on schooling. Second, we estimate the effect of adolescent health using sibling fixed-effects models that control for unmeasured genetic and family factors shared by siblings. We use the PGSs as additional controls in the sibling fixed-effects models to reduce concerns about residual confounding from sibling-specific genetic differences. We find consistent evidence across both approaches that being genetically predisposed to smoking and smoking regularly in adolescence reduces schooling attainment. Estimates for depression are more imprecise, but also suggest that a high genetic risk of depression and adolescent depression reduce schooling attainment. We find mixed evidence for ADHD. Our estimates suggest that having a high genetic risk for ADHD reduces grades of schooling, but we do not find any statistically significant negative effects of ADHD. Finally, we find no consistent evidence for a detrimental effect of obesity on schooling attainment.

Does More Schooling Improve Health Outcomes and Health Related Behaviors? Evidence from U.K. Twins.

Several recent studies using instrumental variables based on changes in compulsory schoolleaving age laws have estimated the causal effect of schooling on health outcomes and health-related behaviors in the U.K. Despite using the same identification strategy and similar datasets, no consensus has been reached. We contribute to the literature by providing results for the U.K. using a different research design and a different dataset. Specifically, we estimate the effect of schooling on health outcomes (obesity and physical health) and health-related behaviors (smoking, alcohol consumption and exercise) for women through within-MZ twins estimates using the TwinsUK database. For physical health, alcohol consumption and exercise, the within-MZ twins estimates are uninformative about whether there is a causal effect. However, we find (1) that the significant association between schooling and smoking status is due to unobserved endowments that are correlated with schooling and smoking (2) there is some indication that more schooling reduces the body mass index for women, even once these unobserved endowments have been controlled for.

Heterogenous trajectories in physical, mental and cognitive health among older Americans: Roles of genetics and life course contextual factors.

We investigate the roles of genetic predispositions, childhood SES and adult educational attainment in shaping trajectories for three important components of the overall health of older adults -- BMI, depressive symptoms and cognition. We use the Health & Retirement Study (HRS) and group-based trajectory modeling (GBTM) to identify subgroups of people who share the same underlying trajectories ages 51-94 years. After identifying common underlying health trajectories, we use fractional multinomial logit models to estimate associations of (1) polygenic scores for BMI, depression, ever-smoked, education, cognition and subjective wellbeing, (2) childhood SES and (3) educational attainment with the probabilities of trajectory group memberships. While genetic predispositions do play a part in predicting trajectory group memberships, our results highlight the long arm of socioeconomic factors. Educational attainment is the most robust predictor-it predicts increased probabilities of belonging to trajectories with BMI in the normal range, low depressive symptoms and very-high initial cognition. Childhood circumstances are manifested in trajectories to a lesser extent, with childhood SES predicting higher likelihood of being on the low depressive symptoms and very-high initial cognition trajectories. We also find suggestive evidence that associations of educational attainment on the probabilities of being on trajectories with BMI in the normal range, low depressive symptoms and very-high initial cognition vary with genetic predispositions. Our results suggest that policies to increase educational attainment may improve population health by increasing the likelihood of belonging to "good" aging trajectories.

Resilience, Accelerated Aging and Persistently Poor Health: Diverse Trajectories of Health in Malawi.

Individuals age at vastly different rates resulting in significant within-population heterogeneity in health and aging outcomes. This diversity in health and aging trajectories has rarely been investigated among low-income aging populations that have experienced substantial hardships throughout their lifecourses. Utilizing 2006-2018 data from the Malawi Longitudinal Study of Families and Health (MLSFH) and estimating group-based trajectory models (GBTM), our analyses identified three distinct lifecourse health trajectories: (1) comparatively good initial mental and physical health that persisted throughout the lifecourse ("resilient aging"); (2) relatively good initial mental and physical health that started to deteriorate during mid-adulthood ("accelerated aging"); and (3) poor initial mental and physical health that further declined over the lifecourse ("aging with persistently poor health"). For both physical and mental health, men were more likely to enjoy resilient aging than women. Predictors other than gender of trajectory membership sometimes confirmed, and sometimes contradicted, hypotheses derived from high-income country studies. Our analyses highlight the long arm of early life conditions and gender in determining aging trajectories and show that a non-trivial sub-population is characterized by aging with persistently poor health. The study uncovers widening gaps in health outcomes between those who age with resilience and those who experience accelerated aging.

What is driving the relationship between height and cognition? Evidence from the Twins Early Development Study.

Taller children tend to have better cognitive ability, and the relationship between height and cognition has been proposed as an explanation for the height-wage labor market premium. Height-cognition associations may arise due to social factors that favor taller individuals or be driven by "common factors" that are correlated with height and cognition. Indeed, there is now evidence of a genetic correlation between height and cognition that provides specific evidence for this concern. We examine whether genetic factors explain the relationship by estimating associations between childhood height and cognition in the Twins Early Development Study. We find that height is associated with better cognition even after controlling for genetic and environmental factors shared by twins. The association between height and cognition within fraternal twin pairs is also robust to controlling for individual genetic predictors of height and cognition. These results suggest that genetic factors are not solely responsible for driving the relationship between height and cognition.

Higher educational attainment is associated with longer telomeres in midlife: Evidence from sibling comparisons in the UK Biobank.

Prior studies have established that higher educational attainment is associated with a longer telomere length (TL), a marker of cellular aging. However, it is unclear whether extant associations are causal, since they are likely confounded by unobserved genetic, early-life and family background factors that are correlated with education and TL. We leverage sibling differences in TL, education and measured genetics (polygenic scores for educational attainment and TL) to estimate associations between educational attainment and TL in midlife for European ancestry individuals in the UK Biobank, while controlling for unobserved confounders shared by siblings. After controlling for genetics and shared background between siblings, we find suggestive evidence that high school graduates have longer telomeres than high school dropouts, but we find no differences in TL between high school dropouts and college graduates.

The impact of BMI on mental health: Further evidence from genetic markers.

We estimate the effect of BMI on mental health for young adults and elderly individuals using data from the National Longitudinal Study of Adolescent Health and the Health & Retirement Study. To tackle confounding due to unobserved factors, we exploit variation in a polygenic score (PGS) for BMI within two related econometric methods that differ in the assumptions they employ. First, we use the BMI PGS as an IV and adjust for PGSs for other factors (depression and educational attainment) that may invalidate this IV. We find a large statistically significant effect of BMI on mental health for the elderly: a 5 kg/m2 increase in BMI (a difference equivalent to moving from overweight to obese) increases the probability of depression by 29 %. In contrast, for young adults the IV estimates are statistically and economically insignificant. We show that IV estimates likely have to be interpreted as identifying a weighted average of effects of BMI on mental health mostly for compliers on the upper quantiles of the BMI distribution. Second, we use the BMI PGS as an "imperfect" IV and estimate an upper bound on the average treatment effect for the population. The estimated upper bounds are consistent with the conclusions from the IV estimates.

Does education attenuate the genetic risk of obesity? Evidence from U.K. Twins.

More education is associated with a lower body mass index (BMI) and likelihood of being obese. Obesity and BMI also have a strong genetic basis. Given these observations, we investigate whether more education can reduce obesity by attenuating the underlying genetic risk of being obese, through gene-environment (GxE) interactions. We estimate associations between (i) education, (ii) a genetic risk score (GRS) and (iii) GxE interactions between education and the GRS through Ordinary least Squares (OLS) and twins fixed-effect regressions using data on female twins from the TwinsUK database. OLS estimates show that there are significant associations of education and genetics. Female twins with a university education are 14.3 percentage points less likely to be obese compared to twins with less than compulsory education, and a 1 standard deviation increase in the GRS increases the likelihood of being obese by 5.2 percentage points. The GxE interactions are statistically insignificant, suggesting that the marginal association of the GRS with obesity does not differ by educational attainment. When controlling for confounding through twins fixed-effects, we find a smaller role of genetics. The association of the GRS with obesity decreases to 0.040. Associations of educational attainment are substantially reduced and insignificant. GxE interactions also remain insignificant. Overall, we find little evidence of any GxE interactions.

Gene-environment interactions between education and body mass: Evidence from the UK and Finland.

More education is associated with a lower body mass index (BMI) and likelihood of being overweight. However, since a large proportion of the variation in body mass is due to genetic makeup, it has been hypothesized that education may moderate the genetic risk. We estimate main associations between (i) education, (ii) genetic risk, and (iii) interactions between education and genetic risk on BMI and the probability of being overweight in the UK and Finland. The estimates show that education is negatively associated with BMI and overweightness, and genetic risk is positively associated. However, the interactions between education and genetic risk are small and statistically insignificant.

Decomposing racial differences in adolescent smoking in the U.S.

Despite declining smoking rates in the U.S., a substantial fraction of adolescents still smoke. In addition, there are notable racial differences in adolescent smoking. We use Add Health data and apply a nonlinear decomposition method to determine the extent to which racial differences in observable characteristics account for (i) the racial smoking gaps in adolescent smoking (ages 12-18) and (ii) racial gaps in the probability of becoming a smoker in young adulthood (ages 18-24), conditional on being a non-smoker in adolescence. The model includes a host of explanatory factors, including individual, family socioeconomics, smoke exposure, school characteristics, and county crime rate. Of the 19 (9) percentage-point gap in white-black (white-Hispanic) smoking in adolescence, these factors together account for 22-28% (39-77%) of the smoking gap; and of the 18 (13) percentage-point gap in white-black (white-Hispanic) smoking up-take in young adulthood, these factors together account for 26-50% (48-100%) of the gap, depending on which set of coefficients are used for the decomposition. The biggest drivers of racial smoking gaps in adolescence are differences in friends' smoking and school peer smoking, while only school peer smoking contributes to the explained portion of racial gaps in smoking up-take in young adulthood.

Schooling has smaller or insignificant effects on adult health in the US than suggested by cross-sectional associations: new estimates using relatively large samples of identical twins.

Numerous theoretical reasons have been posited about why more schooling might improve health. Adult health outcomes and behaviors generally are significantly associated with schooling. However, such associations do not necessarily imply that schooling has causal effects on health outcomes and behaviors. Causal estimates based on schooling variation from policies and from within-MZ (monozygotic) twins have reached mixed conclusions. This study contributed new estimates of cross-sectional associations and within-MZ causal effects using three relatively large US twins samples. The estimates suggested that schooling was significantly associated with numerous health outcomes and behaviors. However, with within-MZ twins control for unobserved factors, schooling was no longer associated with most indicators of better health (with the exception of self-reported health), while it continued to be associated with outcomes such as fertility and spousal schooling. Similar patterns were observed for spousal schooling.