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?
George Davey Smith, professor1,
Shah Ebrahim, head of department1
1 Department of Social Medicine, University of Bristol, Bristol BS8 2PR
Correspondence to: G Davey Smith zetkin@bristol.ac.uk
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
Limitations of mendelian randomisation
Conclusion

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