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International Journal of Epidemiology, Volume 33, Number 1, pp. 26-29
IJE vol.33 no.1 © International Epidemiological Association 2004; all rights reserved.


Reprints and Reflections

Commentary: Development of Mendelian randomization: from hypothesis test to ‘Mendelian deconfounding’

Martin D Tobin, Cosetta Minelli, Paul R Burton and John R Thompson

University of Leicester, Department of Epidemiology and Public Health, 22–28 Princess Road West, Leicester LE1 6TP, UK. E-mail: mt47@leicester.ac.uk

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

In his letter to the Lancet in 1986, reprinted in this issue of the International Journal of Epidemiology (IJE), Katan described the idea of using data from genetic studies to test for a relationship between a quantitative intermediate phenotype and a disease in a way that is not distorted by confounding or reverse causality.1 Following the application of these ideas by other authors2–5 interest in the concept has grown, although it is still not widely understood. This important and novel method has the potential to improve the way that the quantitative phenotypes that underlie common diseases are investigated, so better informing public health interventions that alter the level of the phenotype in order to reduce the risk of disease.4

Katan described how evidence of the effect of the apolipoprotein E (APOE) genotype on cancer risk could be used to test the hypothesis that ‘a naturally low cholesterol favours . . . [Full Text of this Article]


    Applications of Mendelian randomization to learn about phenotype–disease relationships
 

    ORK/{Delta}IP
 

    Developing the concept: from hypothesis testing to Mendelian deconfounding
 

    The future
 

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