(02-03-12) Dietary intake of PUFAs and colorectal polyp risk

1,2,3,4
1. Harvey J Murff,
2. Martha J Shrubsole,
3. Qiuyin Cai,
4. Walter E Smalley,
5. Qi Dai,
6. Ginger L Milne,
7. Reid M Ness, and
8. Wei Zheng
+Author Affiliations
1. 1From the Divisions of General Internal Medicine (HJM), Public Health and Epidemiology, Vanderbilt Epidemiology Center (MJS, QC, QD, and WZ), Gastroenterology (WES and RMN), and Clinical Pharmacology (GLM), and the Department of Preventive Medicine (WES), Vanderbilt University School of Medicine, Nashville, TN; the Geriatric Research Education and Clinical Care, Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN (HJM, MJS, QD, and WZ); and the Vanderbilt Ingram Cancer Center, Nashville, TN (HJM, MJS, QC, WES, QD, RMN, and WZ).
+Author Notes
? ↵2 The contents of this article are solely the responsibility of the authors and do not necessarily represent the official views of the National Cancer Institute or the NIH.
? ↵3 Supported by the National Cancer Institute (grants P50CA 95103, R01CA97386, R01CA143288, and K07CA114029). Surveys and sample collection and processing for this study were conducted by the Survey and Biospecimen Shared Resource, which is supported in part by grant P30CA68485.
? ↵4 Address correspondence to HJ Murff, Vanderbilt Epidemiology Center, Institute of Medicine and Public Health, Sixth Floor, Suite 600, 2525 West End Avenue, Nashville, TN 37203-1738. E-mail: [email protected].
Abstract
Background: Marine-derived n−3 (omega-3) PUFAs may reduce risk of developing colorectal cancer; however, few studies have investigated the association of n−3 PUFA intakes on colorectal polyp risk.
Objective: The objective of this study was to examine the associations of dietary PUFA intake on risk of colorectal adenomatous and hyperplastic polyps.
Design: This was a colonoscopy-based case-control study that included 3166 polyp-free control subjects, 1597 adenomatous polyp cases, and 544 hyperplastic polyp cases. Dietary PUFA intake was calculated from food-frequency questionnaires and tested for association by using unconditional logistic regression. The urinary prostaglandin E2 metabolite, which is a biomarker of prostaglandin E2 production, was measured in 896 participants by using liquid chromatography and tandem mass spectrometry.
Results: n−6 PUFAs were not associated with adenomatous or hyperplastic polyps in either men or women. Marine-derived n−3 PUFAs were associated with reduced risk of colorectal adenomas in women only, with an adjusted OR of 0.67 (95% CI: 0.47, 0.97) for the highest quintile of intake compared with the lowest quintile of intake (P-trend = 0.01). Dietary intake of ?-linolenic acid was associated with an increased risk of hyperplastic polyps in men (P-trend = 0.03), which was not seen in women. In women, but not in men, dietary intake of marine-derived n−3 PUFAs was negatively correlated with urinary prostaglandin E2 production (r = −0.18; P = 0.002).
Conclusion: Higher intakes of marine-derived n−3 PUFAs are associated with lower risk of adenomatous polyps in women, and the association may be mediated in part through a reduction in the production of prostaglandin E2. This trial was registered atclinicaltrials.gov as NCT00625066.

Source: Am J Clin Nutr March 2012 vol. 95 no. 3 703-712

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