Trial reportThe American journal of clinical nutrition2024
Fatty acid desaturase insertion-deletion polymorphism rs66698963 predicts colorectal polyp prevention by the n-3 fatty acid eicosapentaenoic acid: a secondary analysis of the seAFOod polyp prevention trial.
Trial report in The American journal of clinical nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Effect of icosapent ethyl treatment on colorectal tissue marine ω-3 polyunsaturated fatty acid levels among patients with a history of adenoma: a prospective, single-arm clinical trial.The American journal of clinical nutrition · 2026Trial
- Fatty Acid Heterogeneity in Colorectal Cancer: From Food Matrices to Targeted Interventions.Cancers · 2026Review
- The relationship between elongation of very long-chain fatty acids (ELOVL) 2 polymorphism rs953413 and blood n-3 HUFA levels: a secondary analysis of EPA treatment in the seAFOod polyp prevention trial.Genes & nutrition · 2026Article
- Hypothesis: the rs66698963 insertion-deletion alters the AA/EPA ratio and cardiovascular disease risk.Lipids in health and disease · 2026Review
- Revisiting Bill Lands' Hypotheses: HUFA Balance, Immuno-Metabolic Regulation, and Conflicting Clinical Evidence.Nutrients · 2026Review
- The Impact of Specialized Pro-Resolving Mediators on Disease Activity and the Risk of Associated Colorectal Carcinoma in Inflammatory Bowel Disease.Current gastroenterology reports · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA fatty acid desaturase (FADS) insertion-deletion (Indel) polymorphism (rs66698963) influences the expression of FADS1, which controls the synthesis of n-6 highly unsaturated fatty acid (HUFA) arachidonic acid (AA). The anti-inflammatory activity of the n-3 HUFA eicosapentaenoic acid (EPA) may be explained by competition with AA for proinflammatory lipid mediator synthesis. A precision medicine approach based on stratification by FADS Indel genotype could identify individuals, who benefit from greatest disease risk reduction by n-3 HUFAs.
objectivesWe tested the hypothesis that the FADS insertion (I) allele predicts colorectal polyp risk reduction in a secondary analysis of the randomized, placebo-controlled, 2×2 factorial seAFOod polyp prevention trial of EPA 2000 mg daily and aspirin 300 mg daily for 12 mo (ISRCTN05926847).
methodsParticipant Indel genotype was determined by polymerase chain reaction (PCR) blind to trial outcomes. Colorectal polyp outcomes were included in negative binomial (polyp number) and logistic (polyp detection rate [PDR; percentage with one or more polyps]) regression models comparing each active intervention with its placebo. Presence of ≥1 Indel I allele and an interaction term (I allele × active intervention) were covariates.
resultsIn 528 participants with colonoscopy and FADS Indel data, EPA use irrespective of Indel genotype, was not associated with reduced colorectal polyp number (incidence rate ratio [IRR]: 0.92; 95% confidence interval: 0.74, 1.16), mirroring original seAFOod trial analysis. However, the presence of ≥1 I allele identified EPA users with a significant reduction in colorectal polyp number (IRR: 0.50 [0.28, 0.90]), unlike aspirin, for which there was no interaction. Similar findings were obtained for the PDR.
conclusionsThe FADS Indel I allele identified individuals, who displayed colorectal polyp prevention by EPA with a similar effect size to aspirin. Assessment of rs66698963 as a biomarker of therapeutic response to n-3 HUFAs in other populations and healthcare settings is warranted. The seAFOod polyp prevention trial and STOP-ADENOMA study were registered at International Standard Randomised Controlled Trial Number registry as ISRCTN05926847.
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