A Higher Dietary Ratio of Long-Chain Omega-3 to Total Omega-6 Fatty Acids for Prevention of COX-2-Dependent Adenocarcinomas Article

Full Text via DOI: 10.1080/01635581.2014.956262 PMID: 25356937 Web of Science: 000344863600002
International Collaboration

Cited authors

  • DiNicolantonio, James J.; McCarty, Mark F.; Chatterjee, Subhankar; Lavie, Carl J.; O'Keefe, James H.


  • Compelling evidence that daily low-dose aspirin decreases risk for a number of adenocarcinomas likely reflects the fact that a modest but consistent inhibition of cyclooxygenase-2 (COX-2) activity can have a meaningful protective impact on risk for such cancers. The cancer-promoting effects of COX-2 are thought to be mediated primarily by prostaglandin E2 (PGE2), synthesized from arachidonic acid. The long-chain omega-3s eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), abundant in many fatty fish, can interfere with the availability of arachidonate to COX-2 by multiple complementary mechanisms; moreover, the PGE3 produced by COX-2 from EPA is a competitive inhibitor of the receptors activated by PGE2. These considerations have given rise to the hypothesis that a high dietary intake of EPA/DHA, relative to omega-6 (from which arachidonate is generated), should lessen risk for a number of adenocarcinomas by impeding PGE2 production and activity-while not posing the risk to vascular health associated with COX-2-specific nonsteroidal antiinflammatory agents. Analyses that focus on studies in which the upper category of fish consumption (not fried or salt-preserved) is 2 or more servings weekly, and on studies that evaluate the association of long-term fish oil supplementation with cancer risk yields a number of findings that are consistent with the hypothesis. Further studies of this nature may help to clarify the impact of adequate regular intakes of long-chain omega-3 on cancer risk, and perhaps provide insight into the dose-dependency of this effect.

Publication date

  • 2014

Published in


International Standard Serial Number (ISSN)

  • 0163-5581

Start page

  • 1279

End page

  • 1284


  • 66


  • 8