Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:2105
doi: 10.1161/01.ATV.0000041233.48898.F1
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, X. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, X. L.
Related Collections
Right arrow Risk Factors
Right arrow Epidemiology
Right arrow Genetics of cardiovascular disease
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:2105.)
© 2002 American Heart Association, Inc.


Letters to the Editor

Genetic Association Studies

Xing Li Wang

Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Tex


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

I am delighted to see that Arteriosclerosis, Thrombosis, and Vascular Biology has taken the lead in initiating an open discussion about genetic association studies in such a prominent manner. As correctly pointed out in the editorial by Dr Hegele,1 the number of publications has exponentially increased in the last decade. Despite the intrinsic problems with this approach, this exponential growth also demonstrates the popularity of this type of study. Anyone who follows the literature in genetic association studies will recognize, as Dr Hegele does, that none of the polymorphisms reported so far has been consistently associated with any phenotypic trait, either a single quantitative trait such as triglyceride level or a complex trait such as atherosclerosis. A typical example is the polymorphisms in endothelial NO synthase,2 which has been associated with various vascular diseases in some studies but not in others. Among many reasons for such inconsistent association studies, the importance of controlling for environmental influence should be specifically emphasized because it can modify the phenotypic effect of a given genotype and potentially alter the direction of the association.3,4 However, we should also not deny the fact that these association studies have stimulated many mechanistic investigations, often from a biochemically unconventional angle, which have the potential for novel findings. While I agree with most criteria set out by Dr Hegele1 and Drs Almasy and MacCluer,5 particularly multi-locus approaches and haplotype analyses, one must be aware that not many research groups have the resources to satisfy them all. This is particularly . . . [Full Text of this Article]