Why Fish Oil Fails to Prevent or Improve CVD: A 21st Century Analysis

In May 2013, The Risk and Prevention Study Collaborative Group (Italy) released a conclusive negative finding regarding fish oil for those patients with high risk factors but no previous myocardial infarction. Fish oil failed in all measures of CVD prevention—both primary and secondary. This study was so conclusive that Eric Topol, MD, editorin-chief of Medscape and Medscape’s Heartwire for cardiologists, issued a new directive to patients to stop taking fish oil, i.e., long-chain EFA metabolites of EPA/DHA. Fish oil’s failure is shown to be consistent with known physiology and biochemistry: there should never have been any expectation of success. To the contrary, true EFAs, linoleic acid and alpha-linolenic acid, termed Parent Essential Oils (PEOs), fulfill fish oil’s failed promise. Fish oil supplements contain supra-physiologic amounts of EPA/DHA. Recommendations are often paramount to pharmacologic overdose. Unlike fish oil, which failed to decrease 19 markers of inflammation, PEOs do decrease inflammation. The first screening experiment comparing fish oil with Parent EFA oils, the seminal IOWA experiment utilizing pulse wave velocity, demonstrated unequivocally that fish oil contributes to hardening of the arteries, aging subjects by nearly 4 years (P < 0.0001). To the contrary, PEOs increase arterial compliance, making subjects’ arteries “biologically younger” (increased arterial compliance) by more than 11 years compared to subjects taking fish oil fish (P < 0.001).