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                |  2012/01/25 | 
               
               
                | AJCN – PUFAs and Reduction of Colorectal Polyp Risk   | 
               
               
                
                    Murff HJ, Shrubsole MJ, Cai Q, et al. Dietary intake of PUFAs and colorectal polyp risk. Am J Clin Nutr. 2012 Jan 25.   
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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 α-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 clinicaltrials.gov as NCT00625066. 
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                | Source: 
								http://www.ncbi.nlm.nih.gov/pubmed/22277551
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