BMJ  2005;330:1076-1079 (7 May), doi:10.1136/bmj.330.7499.1076

Education and debate

What can mendelian randomisation tell us about modifiable behavioural and environmental exposures?

¹ Department of Social Medicine, University of Bristol, Bristol BS8 2PR

Using genetic variants as a proxy for modifiable environmental factors that are associated with disease can circumvent some of the problems of observational studies

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

Introduction

Epidemiologists look for modifiable causes of common diseases to improve population health. However, epidemiological studies may identify spurious "causes." For example, the epidemiological findings that hormone replacement therapy protects against coronary heart disease,^w1 carotene prevents lung cancer,^w2 and vitamin E and vitamin C reduce risk of cardiovascular disease^w3 have all been refuted by randomised controlled trials and have raised concerns about the value of epidemiological studies.¹ The misleading findings were probably due to confounding by behavioural, physiological, and socioeconomic factors related both to exposures and to disease end points.^{2 3} One solution to these problems is mendelian randomisation.^{4 5}

What is mendelian randomisation?

Mendelian randomisation is a recent development in genetic epidemiology^{6 7} based on Mendel's second law that inheritance of one trait is independent of inheritance of other traits. It uses common genetic polymorphisms that are known to influence exposure patterns (such as propensity to drink alcohol) or have effects equivalent to those produced by modifiable . . . [Full text of this article]

Scope of mendelian randomisation

Understanding effects of health related behaviours
Understanding effects of modifying physiological factors
Swinging the lead or toxic jobs?
Intrauterine environment and health

Limitations of mendelian randomisation

Conclusion

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