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Randomized Controlled Trial
. 2019 May;28(3):188-195.
doi: 10.1097/CEJ.0000000000000455.

Effects of fish oil supplementation on eicosanoid production in patients at higher risk for colorectal cancer

Affiliations
Randomized Controlled Trial

Effects of fish oil supplementation on eicosanoid production in patients at higher risk for colorectal cancer

Maya N White et al. Eur J Cancer Prev. 2019 May.

Abstract

Fish oil supplementation may represent a potential chemopreventive agent for reducing colorectal cancer risk. The mechanism of action of fish oil is unknown but presumed to be related to eicosanoid modification. The purpose of this study was to evaluate the effects of fish oil supplementation on the levels of urinary and rectal eicosanoids. We conducted a randomized, double-blind, controlled trial of 2.5 g of fish oil per day compared with olive oil supplementation over a 6-month period. Study participants had a history of colorectal adenomas. Randomization was stratified based on the gene variant rs174535 in the fatty acid desaturase 1 enzyme (FADS1), which affects tissue levels of arachidonic acid. A total of 141 participants were randomized. Urinary prostaglandin E2 metabolite (PGE-M) was measured at baseline, 3, and 6 months and rectal prostaglandin E2 (PGE2) at baseline and 6 months. Repeated-measures linear regression was used to determine the effect of the intervention on each outcome measure. Overall, fish oil supplementation was found to reduce urinary PGE-M production compared with olive oil (P=0.03). Fish oil did not reduce rectal PGE2 overall; however, it did significantly reduce PGE2 in the subgroup of participants not using aspirin or NSAIDs (P=0.04). FADS1 genotype did not seem to modify effects of fish oil on PGE2 production. We conclude that fish oil supplementation has a modest but beneficial effect on eicosanoids associated with colorectal carcinogenesis, particularly in those not taking aspirin or NSAIDs.

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Conflict of interest statement

Conflicts of Interests

Disclosure of potential conflict of interest: The authors report no conflict of interests to disclose.

Figures

Figure 1
Figure 1
Flow diagram of trial recruitment and retention
Figure 2
Figure 2
Concentrations of Urinary PGEM at baseline, 3-months, and 6-months aLinear regression comparing baseline to 3-month values adjusted for baseline value, genotype, and sample batch, bLinear regression comparing baseline to 6-month values adjusted for baseline value of urinary PGEM, genotype, and sample batch; cRepeated measures analysis of variance adjusted for genotype and sample batch
Figure 3
Figure 3
Figure 3a–d: Changes in Rectal Eicosanoids after 6-Months of n-3 LCPUFA Supplementation Linear regression comparing baseline to 6-month values adjusted for baseline value of rectal eicosanoid, genotype, and sample batch. Panel a: Changes in mean log transformed rectal biopsy PGE2 concentrations; Panel b: Changes in mean log transformed rectal biopsy PGE3 concentrations; Panel c: Changes in mean log transformed rectal biopsy PGD2 concentrations; and Panel d: Changes in mean log transformed rectal biopsy PGD3 concentrations
Figure 4
Figure 4
Figure 4a–b: Changes in red blood cell phospholipid fatty acid content based on study arm
Figure 4
Figure 4
Figure 4a–b: Changes in red blood cell phospholipid fatty acid content based on study arm

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