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IJE Advance Access originally published online on July 19, 2006
International Journal of Epidemiology 2006 35(4):932-934; doi:10.1093/ije/dyl107
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Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2006; all rights reserved.

Commentary

Commentary: Genes as instruments for evaluation of markers and causes

Robert J Glynn

Division of Preventive Medicine, Brigham, Women's Hospital, 900 Commonwealth Avenue, Boston, MA 02215, USA. E-mail: rglynn@rics.bwh.harvard.edu

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

In this issue of the journal, Casas et al.1 provide important information on a genetic determinant of C-reactive protein (CRP) with little apparent relationship to risk of coronary heart disease (CHD). The implications of these relationships for our understanding of a possibly causal role of inflammation in CHD can shed light on the contributions of Mendelian randomization to causal inference in epidemiology. Mendelian randomization gives a focused evaluation of causality, but it relies on strong assumptions and may be of limited usefulness in the evaluation of CRP as a marker of inflammation when the genetic variant has a modest ability to predict the phenotype of interest.


   The mechanics of Mendelian randomization
 
Mendelian randomization capitalizes on the random allocation of a genetic variant that influences an intermediate phenotype such as CRP to evaluate the possibly confounded relationship of that phenotype with an outcome such as CHD. A variety of approaches have been used in actual . . . [Full Text of this Article]


   Strength of instruments, markers, and causes
 

   Disclosure
 

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