IJE Advance Access originally published online on July 26, 2006
International Journal of Epidemiology 2006 35(4):944-947; doi:10.1093/ije/dyl149
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Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2006; all rights reserved.
Commentary |
Commentary: Fibrinogen and coronary heart diseasetest of causality by Mendelian randomization by Keavney et al.
Department of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK
* Corresponding author. E-mail: tom.meade@lshtm.ac.uk
| The first 150 words of the full text of this article appear below. |
The theory of Mendelian randomization (MR) represents a relatively new and promising way of determining whether associations between risk factors and important clinical events such as myocardial infarction (MI) are of causal significance or not. But how does it work out in practice? A good deal of attention has been given to the relation between fibrinogen and MI. In this issue of the IJE, Keavney et al.1 conclude that usual fibrinogen concentrations do not materially influence coronary disease incidence and that their analysis provides strong evidence (our italics) that fibrinogen is not a major determinant of coronary risk. They acknowledge that in this case, the contribution of a common polymorphism to the level of fibrinogen is small, so the contribution of any polymorphism to MI risk is also likely to be small. So far, so good. But there are a number of other questions to be answered about
| Mendelian randomization |
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| Estimating the relationship between fibrinogen levels and MI risk |
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| Estimating the relationship between genotype and fibrinogen levels |
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| Estimating the relationship between genotype and MI risk |
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| Predicting the relationship between genotype and MI risk |
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| Conclusions |
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