4.7 Article

Dietary intake of PUFAs and colorectal polyp risk

Journal

AMERICAN JOURNAL OF CLINICAL NUTRITION
Volume 95, Issue 3, Pages 703-712

Publisher

ELSEVIER SCIENCE INC
DOI: 10.3945/ajcn.111.024000

Keywords

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Funding

  1. National Cancer Institute [P50CA 95103, R01CA97386, R01CA143288, K07CA114029]
  2. Survey and Biospecimen Shared Resource [P30CA68485]

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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 E-2 metabolite, which is a biomarker of prostaglandin E-2 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 alpha-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 E-2 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 E-2. This trial was registered at clinical-trials.gov as NCT00625066. Am J Clin Nutr 2012;95:703-12.

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