We aim to explore if parental smoking causes offspring to smoke more. Estimating the effect of social transmissibility of traits is methodologically difficult because people relatives generally share similar genetics and environmental exposures. This can make issues around confounding difficult to control for.
Children inherit a random half of each parent’s genetic liability. Mendelian randomisation (MR) is a study design in epidemiology which leverages this to analogise with a randomised controlled trial (RCT). In an RCT some people are randomised to an exposure, and then followed up over a period of time. In an MR study people are randomised to a genetic variant which increases their liability to an exposure at conception, and then recruited into a study some time after birth.
Although understanding the effects of second-hand smoking has important public health implications, it would be unethical to randomise someone to exposure to second hand smoking because of the definite harm on the individual who would have to smoke, and the probable harm on the person exposure to second-hand smoking.
Here we aim to explore an extension of MR to explore the social transmissibility of traits, and specifically whether parental smoking influences their children to smoke. Although we only inherit half of each of our parent’s genetic variants, the other half can still influence us via our parents. For example, if a parent has a variant which causes them to smoke, this variant in effect exposes their child to second-hand smoking. Thus, randomly not inheriting a smoking variant, is analogous to being randomised to second-hand smoking. Our research here will build on theoretical and simulation research already conducted to demonstrating the theoretical utility of this approach.