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International Journal of Epidemiology, Volume 33, Number 1, pp. 17-21
IJE vol.33 no.1 © International Epidemiological Association 2004; all rights reserved.

Reprints and Reflections

Commentary: Mendelian randomization and gene–environment interaction

Paul Brennan

International Agency for Research on Cancer, 150 cours Albert Thomas, 69008 Lyon, France. Email: brennan@iarc.fr

The first 150 words of the full text of this article appear below.

Genetic association studies for non-familial diseases typically focus on a particular candidate gene and one or more environmental exposures (gene–environment interaction). The long term rationale of such studies appears to be that an accumulation of knowledge regarding susceptibility genes will allow us to identify high risk population subgroups. This in turn may subsequently allow the development of intervention strategies aimed at such high risk groups including modification of lifestyle habits and increased surveillance for those at most risk. However, the feasibility of this strategy is uncertain and indeed it may ultimately prove to be unfeasible, especially if there is a strong stochastic component inherent in the development of individual cases of a particular disease.

An alternative rationale for conducting genetic susceptibility studies is to use genetics to test specific hypotheses regarding the role of non-genetic exposures. The concept of ‘Mendelian randomization’ has recently been discussed in some detail in the . . . [Full Text of this Article]


   Example 1: Isothiocyanate (ITC) consumption and lung cancer
 

   Example 2: Acetaldehyde exposure and head and neck cancer
 

   Summary and implications
 

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