PP37 Use of mendelian randomisation to assess whether smoking is causally associated with alcohol consumption

Abstract

Background Many studies have shown that tobacco and alcohol use co-occur, with many reporting that tobacco use is a risk factor for later alcohol use. Determining the causality of this relationship from conventional epidemiological studies is difficult due to problems of confounding or reverse causation. Mendelian randomisation utilises the properties of genetic variants to assess causality in the absence of these problems. Methods Using data from mothers in the Avon Longitudinal Study of Parents and Children (ALSPAC), we investigated observational associations between 1 continued smoking (binary variable: yes/no) and alcohol consumption (binary variable: less than one drink per week/ one or more drinks per week) during pregnancy and 2 cigarettes per day (continuous measure) in those who smoke and units of alcohol per week (continuous measure) before pregnancy. We also performed a Mendelian randomisation analysis using rs1051730 as the genetic instrument, as this variant has been shown to be associated with both heaviness of smoking in individuals who smoke and reduced ability to quit smoking during pregnancy. Results Observationally, we found evidence of an association between continuing to smoke and alcohol consumption during pregnancy (N = 1,411; OR = 1.87, 95% CI 1.36 to 2.58; P Conclusion Observationally, there are strong links between both smoking behaviours and alcohol consumption. However Mendelian randomisation analysis suggests that the associations between smoking and alcohol (both here and in previously reported research) are not causal. This finding should be followed up in larger samples using the Mendelian randomisation approach.