A component of the STOP-ADENOMA study, the seAFOod polyp prevention trial enrolled participants in the English Bowel Cancer Screening Programme aged 55-73 deemed at high risk, i.e., at baseline they had an increase in the size and/or number of adenomas. Over 700 participants received either placebo, 300mg aspirin per day, 2g EPA per day, or both aspirin and EPA for 12 months. In the Lancet article, neither treatment reduced the primary outcome, the adenoma detection rate (ADR, the proportion of participants with any adenoma). This is in contrast to the chemopreventative efficacy EPA has shown for familial adenomatous polyposis.
However, this more recent publication was stratified by one specific polymorphism in the fatty acid desaturase (FADS) gene, rs66698963, previously shown to influence levels of arachidonic acid (AA). An insertion-deletion polymorphism, AA levels have been observed to be as much as 50% greater among people who are insertion homozygotes compared to deletion homozygotes. In this trial, EPA supplementation among people with at least one insertion allele reduced the incidence rate of adenomas by 50%. No benefit was observed among people without the insertion allele, and no difference was observed when aspirin use was stratified by genotype. Several hypotheses exist for the gene-nutrient interaction observed with EPA, including competition with AA as a substrate for cyclooxygenase (COX), or otherwise interferes with FADS1 expression, thereby inhibiting the production of pro-inflammatory tumorigenic signals.