A new study out today has found increasing education by 3.6 years – similar to the length of a university undergraduate degree – could reduce the risk of heart disease by a third. A decrease of this magnitude is similar to short-term use of a cholesterol-lowering medication.
Coronary heart disease refers to the build up of plaque in the blood vessels supplying the heart. Over time, this build up may lead to the blockage of one or more blood vessels, depriving the heart of oxygen, and producing a heart attack. Coronary heart disease is the most common cause of death in Australia and worldwide.
While education has previously been associated with better health outcomes, there has been limited evidence that education actually causes these health effects, rather than just being linked by association. The suggestion has been that actual benefits may derive from variables associated with both education and risk of heart disease, such as socioeconomic status.
To demonstrate that exposure to A causes outcome B, scientists traditionally rely on randomised controlled trials. In randomised controlled trials, subjects are randomly placed into a group receiving exposure A, or a group that does not (typically some sort of placebo or sham treatment).
This randomisation process ensures the groups are equal on average across all variables at the beginning of the trial, except for the exposure variable. When the groups are compared at the end of the trial, any difference between the groups can therefore be attributed to the effect of the exposure.
But due to the obvious ethical dilemmas posed by restricting education for a group of people, a randomised trial is not feasible in this situation.
The closest reflection of such an experiment was the staggered introduction of an additional year of schooling in Sweden, between 1949 and 1962. Comparing health outcomes by region, the extra year of school decreased all causes of early death after the age of 40.
But in this new study, scientists turned to nature, and the genes we randomly inherit from our parents. They used a technique called Mendelian randomisation, which utilises the random transmission of genes from parents to offspring, to mimic a randomised controlled trial.
More than 160 genetic variants have been shown to be associated with years of education in dozens of studies involving more than 500,000 men and women. We don’t know exactly how these genes predict how many years of education someone will have, but we know that people with these genes on average will go on to more education.
The researchers used genes to randomly classify participants into high or low education groups. Participants in the genetically high and low education groups should have been equal across all other variables because of this randomisation. Thus, any difference between the groups in terms of risk of coronary heart disease should be due to the effect of education.
Individuals who had randomly received more genetic variants associated with longer education from their parents were also less likely to suffer from heart disease. This observation suggested that increased number of years in education causally decreased risk of heart disease.
The reduced heart disease risk brought about through increased years of education seemed to be mediated by better lifestyle choices – less smoking, healthier diet choices and lower cholesterol levels.
One of the limitations of such a study is that genes linked to educational attainment were associated with other traits such as self-discipline, which would have an effect on other things such as smoking and diet. So a difference in risk of heart disease between the groups might be due to the effect of one of these other variables rather than an effect of education.
If education decreased the risk of heart disease, then the effect of this should be similar across all the different genes used in the study. If, however, another variable besides education were responsible for the association, then the apparent effect of education on heart disease should vary across the different genes used in the study.
As the authors found a relatively consistent effect of education on risk of heart disease across all genes in the study, it appeared their results were robust and their assumptions valid. Importantly, the authors’ conclusions were also supported by the results from previous observational epidemiological studies and quasi-experiments like the Swedish study.
This study alone may not carry sufficient weight to prompt calls for extending the number of years at school mandated by governments. But it does add more robust evidence that more years in the classroom could lead to reduced risk of heart disease, and subsequently longer life.