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Diet and Colorectal Adenomatous Polyps
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
Include no more than 300 words of text, three authors, and five references
Type with double-spacing
Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
TO THE EDITOR:
The study by Neugut and colleagues [1] represents an important advance in our understanding of the role of diet in the multistep progression to colorectal cancer.
The investigators state that three casecontrol studies have explored the association of adenomatous polyps with diet. I would like to draw their attention to a study by Kune and colleagues [2] that compared 49 patients who had one or more histologically confirmed adenomatous polyps larger than 1 cm in diameter with a community control group. Those with adenomatous polyps were found to have a low fiber and vegetable intake (P = 0.04); in men, a high intake of beef (P = 0.04), milk drinks (P = 0.01), and beer (P = 0.05) was noted. The authors concluded that both dietary factors and alcohol consumption may play a role in the development of colorectal adenomatous polyps and that these factors are similar to dietary risk factors for colorectal cancer.
Furthermore, dietary modifications have been shown to affect the proliferation rate of colonic mucosal cells [3]. Another study [4] has shown that modification of fat intake in humans can affect cell proliferation, as measured by mucosal cell thymidine uptake and ornithine decarboxylase activity. An interesting recent report [5] showed that fecal diglycerides, normally present in the colonic lumen, enhance mitogenesis in adenoma and carcinoma cells but have no effect on normal colonic mucosa. This finding may indicate that the carcinogenic effect of dietary factors may depend, at least in part, on an inherited predisposition that makes the normal mucosa susceptible to the carcinogenic effects of the diet.
Ajay Anand
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
Include no more than 300 words of text, three authors, and five references
Type with double-spacing
Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright 2004 by the American College of Physicians
