Autistic adults are more likely to drink hazardously (in a way that increases their risk of adverse health events) or not at all than non-autistic people. However, we do not know whether genetics play a role in this. The relationship between factors that may be related to health outcomes (exposures) and the outcomes themselves are often estimated without taking the role of genetics into account. This means that estimates of the relationship between the exposure and outcome may be incorrect. Both autism and alcohol use are heritable, in that they are transmissible from parent to offspring. There is some evidence that a genetic difference in the susceptibility candidate 2 gene (AUTS2) is related to alcohol use, but studies on this are limited and we do not know whether there are other genetic differences relating to autism that are also related alcohol use. We can calculate a measure of the propensity for a trait due to an individual’s genes (known as a polygenic risk score or PRS), using data from genome-wide association studies (GWAS). In GWAS, specific genetic differences have been found to be related behaviours of interest. PRS can also be used to better understand the cause of certain traits. Looking at the relationship between polygenic risk for autism and alcohol use will help our understanding of whether autism directly causes alcohol use, or genetics play a role in the link between the two. This could potentially help us estimate the relationship more accurately in future research.
