Links

Tools

Export citation

Search in Google Scholar

Establishing the causal impact of tobacco use on health outcomes using Mendelian randomisation: The CARTA consortium. Assessing causal links between smoking and vitamin D using a Mendelian randomisation approach.

This paper is available in a repository.
This paper is available in a repository.

Full text: Download

Question mark in circle
Preprint: policy unknown
Question mark in circle
Postprint: policy unknown
Question mark in circle
Published version: policy unknown

Abstract

There is a widening perception that many factors (lifestyle and others e.g., acute/chronic inflammation) may causally lower vitamin D levels. Observationally, smoking tends to be associated with lower vitamin D levels. Smokers also have increased fracture risk and decreased bone mass suggesting a potential causal effect of smoking on vitamin D. It has also been suggested that tobacco smoke chemicals may influence vitamin D metabolism and function. However, determining a causal link between smoking and lower vitamin D is problematic in conventional epidemiological studies due to confounding by other lifestyle factors. We performed a Mendelian randomisation analysis, using data on 32,823 individuals from the Consortium for Causal Analysis Research in Tobacco and Alcohol to investigate the causal nature of the associations of smoking with vitamin D levels. Associations between a smoking related variant (rs1051730/rs16969968) and serum vitamin D (25(OH)D) were assessed by linear regression stratified by smoking status (categorised as never, former, current, ever (former and current), and non (never and former)) and adjusted for age, sex, and geographic region, and additionally for body mass index (BMI). Observational associations between smoking status and vitamin D were assessed by linear regression, adjusted for age, sex, and month of data collection and additionally for geographic region, socio-economic status and BMI. Results from individual studies were meta-analysed. Interactions between smoking status and genotype were assessed using the Cochran Q statistic. We discuss the implications of these results for furthering understanding of the causal effect of smoking on vitamin D. This will inform the development of relevant public health messages and campaigns, and also potentially aid the development of novel treatments for disease outcomes. This is a work in progress and we anticipate that results will be available within a month.