Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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 ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Fallon, U. B
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fallon, U. B
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Journal of Epidemiology 2003;32:67-70
© International Epidemiological Association 2003

Special Theme: Genetic Epidemiology

Commentary: Colon cancer, folate and genetic status

Una B Fallon

Department of Social Medicine, University of Bristol, Canynge Hall, Whiteladies Rd, Bristol BS8 2PR, UK. E-mail: una.fallon@bristol.ac.uk

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

Colon cancer is the third most common cancer worldwide.1 Vastly different rates between countries,2 migrants quickly assuming the rates of the host country,3 and major changes in rates within populations over short periods of time, suggest that environmental and lifestyle factors are important in its aetiology. Ecological studies have shown that fat,4 meat,2 fibre, and fruit and vegetable consumption5 vary consistently with rates of colon cancer across countries. However, large prospective cohort studies6 and secondary prevention trials of recurrent adenomas7–9 have not demonstrated robust consistent associations, particularly with fibre and fruit and vegetable intake. Identifying specific constituents of food amenable to preventive interventions is difficult using traditional epidemiological methods. Case-control studies are subject to recall and selection bias. Cohort studies have problems with residual confounding, poorly understood interactions, and co-linearity of nutrients and vitamins, making it impossible to identify their separate effects. Primary prevention trials are possible,10 but likely to . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 CarcinogenesisHome page
K. Matsuo, H. Ito, K. Wakai, K. Hirose, T. Saito, T. Suzuki, T. Kato, T. Hirai, Y. Kanemitsu, H. Hamajima, et al.
One-carbon metabolism related gene polymorphisms interact with alcohol drinking to influence the risk of colorectal cancer in Japan
Carcinogenesis, December 1, 2005; 26(12): 2164 - 2171.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
M. F. Rudd, G. S. Sellick, R. Allinson, E. Matutes, D. Catovsky, and R. S. Houlston
MTHFR Polymorphisms and Risk of Chronic Lymphocytic Leukemia
Cancer Epidemiol. Biomarkers Prev., December 1, 2004; 13(12): 2268 - 2270.
[Abstract] [Full Text] [PDF]

Home page
 Int J EpidemiolHome page
G. Davey Smith and S. Ebrahim
'Mendelian randomization': can genetic epidemiology contribute to understanding environmental determinants of disease?
Int. J. Epidemiol., February 1, 2003; 32(1): 1 - 22.
[Abstract] [Full Text] [PDF]