Role of obesity in smoking behaviour: Mendelian randomisation study in UK BiobankBMJ 2018; 361 doi: https://doi.org/10.1136/bmj.k1767 (Published 16 May 2018) Cite this as: BMJ 2018;361:k1767
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I read the Mendelian randomisation (MR) study performed by Carreras-Torres et al. investigating the effect of obesity on smoking behaviour with great interest. The authors concluded that their ‘results strongly suggest that higher adiposity influences smoking behaviour’. When exploring the ‘mechanistic basis of the association between the genetic instrument of body mass index and smoking habits by separately analysing SNPs clustering in neuronal pathways’, the authors found that restricting the analysis to non-neuronal SNPs attenuated the MR odds ratio for the effect of body mass index on being an ever smoker.
Furthermore, for cigarettes smoked per day, this was to the extent that a ‘weaker or null association was observed using the non-neuronal-body mass index score’. The authors point out in the Discussion section ‘that associations of body mass index with measures of tobacco exposure appeared to be primarily driven by SNPs clustering in neuronal pathways’ and further that this ‘suggests a common biological basis for addictive behaviours’, with ‘overweight smokers maintaining smoking at higher rates as a result of genetically predisposed compulsive behaviour.’ Such a ‘common biological basis’ that is ‘a result of a genetically predisposed compulsive behaviours’ would suggest that the findings of the MR analyses at least in part relate to pleiotropy of the instruments used, rather than a true influence of adiposity on smoking behaviour. This contradicts the conclusions of the paper.
Competing interests: No competing interests