Effects of Omega-3 Fatty Acids on Major Adverse Cardiovascular Events

Lipid Lowering Drugs: Present Status and Future Developments

“…This evidence is of extreme importance considering that CVD risk is eight-fold higher among those with ASCVD than those without it [125]. However, considering that the global market for omega-3 fatty acids has reached $4.1 billion and is expected to double by 2025, the neutral effects reported in the STRENGTH and VITAL (Vitamin D and Omega-3 Trial) studies should be a reminder that the widespread use of over-the-counter mixed omega-3 products lacks evidence for clinical utility [126].…”

Changes in lipoprotein particle subclasses, standard lipids, and apolipoproteins after supplementation with n-3 or n-6 PUFAs in abdominal obesity: A randomized double-blind crossover study

“…Therefore, we have reported results for each intervention in each period, as recommended for crossover studies [101], and conducted a secondary analysis of betweentreatment differences in follow-up scores, which are less biased by potential carryover effects than change scores [101,148e150]. However, in the absence of a 3 Â 3 crossover design including a placebo control intervention assumed to have neutral effects on the primary outcomes, a challenge described elsewhere [47,71,151,152], we were not able to provide placebo-adjusted treatment effect estimates for both the n-3 and n-6 interventions.…”

“…This inverse relationship has been partially attributed to changes in blood fat fractions [37,39], primarily reduced TAG levels after n-3 intake [29,40e43], and lower cholesterol levels after n-6 intake [30,31,44]. However, effects on CVD morbidity, mortality, and intermediate outcomes, including lipids and lipoproteins, have not been consistent across studies for n-3 [33,35,45e47], nor for n-6 [36,38,48e51], and it remains controversial whether dietary or supplemental PUFAs reduce cardiometabolic risk [44,47,52]. It is well established that increasing intakes or biomarker levels of marine n-3 PUFAs lower circulating concentrations of TAGs in a dose-dependent manner [29,40e42,53e59].…”

Mechanistic Insights from REDUCE-IT STRENGTHen the Case Against Triglyceride Lowering as a Strategy for Cardiovascular Disease Risk Reduction

“…Explanations include differences in formulation, on-treatment achieved levels of EPA, negating or "diluting" effects of DHA, type of placebo used in the study, and patient profile. 19 Indeed, EPA and DHA differ in their effects on membrane structure, rates of lipid oxidation, inflammatory biomarkers as well as tissue distributions (Figure 1). 20 In endothelial cells, EPA, unlike DHA, reversed endothelial dysfunction with small dense LDL exposure and increased nitric oxide release, a potent inhibitor of platelet aggregation and leukocyte adhesion.…”