4.7 Article

The causal effects of education on adult health, mortality and income: evidence from Mendelian randomization and the raising of the school leaving age

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OXFORD UNIV PRESS
DOI: 10.1093/ije/dyad104

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Raising Of School Leaving Age (ROSLA); instrumental variable analysis; education; genomic confounding

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Previous studies have tried to determine whether education causes differences in later health outcomes or whether other factors ultimately cause differences in education and subsequent outcomes. This study compared two natural experiments: a policy reform raising the school leaving age in the UK in 1972 and Mendelian randomization. The results showed consistent positive effects of education on various outcomes, including diabetes, stroke, heart attack, mortality, smoking, income, grip strength, height, body mass index (BMI), intelligence, alcohol consumption, and sedentary behavior, but a negative impact on moderate exercise.
Background On average, educated people are healthier, wealthier and have higher life expectancy than those with less education. Numerous studies have attempted to determine whether education causes differences in later health outcomes or whether another factor ultimately causes differences in education and subsequent outcomes. Previous studies have used a range of natural experiments to provide causal evidence. Here we compare two natural experiments: a policy reform, raising the school leaving age in the UK in 1972; and Mendelian randomization. Methods We used data from 334 974 participants of the UK Biobank, sampled between 2006 and 2010. We estimated the effect of an additional year of education on 25 outcomes, including mortality, measures of morbidity and health, ageing and income, using multivariable adjustment, the policy reform and Mendelian randomization. We used a range of sensitivity analyses and specification tests to assess the plausibility of each method's assumptions. Results The three different estimates of the effects of educational attainment were largely consistent in direction for diabetes, stroke and heart attack, mortality, smoking, income, grip strength, height, body mass index (BMI), intelligence, alcohol consumption and sedentary behaviour. However, there was evidence that education reduced rates of moderate exercise and increased alcohol consumption. Our sensitivity analyses suggest that confounding by genotypic or phenotypic confounders or specific forms of pleiotropy are unlikely to explain our results. Conclusions Previous studies have suggested that the differences in outcomes associated with education may be due to confounding. However, the two independent sources of exogenous variation we exploit largely imply consistent causal effects of education on outcomes later in life.

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