Fish oil

The specific mechanism of action by which the fish oil EPA and DHA acids are capable of reducing serum triglyceride levels is not yet fully understood. Nevertheless, it is proposed that such omega-3-fatty acids may not be the preferred substrates of the enzyme diacylglycerol O-acyltransferase that participates in the generation of triglycerides; that they might interact with nuclear transcription factors that manage lipogenesis; or that their presence and increase in levels can cause cellular metabolism to subsequently shift toward a decrease in triglyceride synthesis and an increase in fatty acid oxidation. Moreover, the EPA and DHA acids are also believed to be able to promote apolipoprotein B degradation in the liver through the stimulation of an autophagic process. It may also be possible that these fish oil acids can accelerate the clearance of very-low-density lipoprotein (VLDL) particles and chylomicron. The combination of all these actions results in fewer VLDL particles being assembled and secreted, which is of considerable importance as VLDL particles are the major endogenous source of triglycerides.

Moreover, new paradigms of how inflammation is contained and dissipated involve various newly discovered chemical mediators, resolvins, and protectins. Such agents are believed to be directly involved in blocking neutrophil migration, infiltration, recruitment, as well as blocking T-cell migration and promoting T-cell apoptosis. Additionally, such protectins can also reduce tumor necrosis factor and interferon secretion. Of particular importance, however, is the fact that protectins and resolvins are exclusively derived from omega-3-fatty acids and that EPA is the substrate of the resolvins family and DHA can be converted to both resolvins and protectins. It is believed that these effects of such fish oil acids underlie the actions that fish oil have demonstrated on eliciting stability for vulnerable inflammatory plaques.

Finally, fish oil acids have demonstrated certain direct electrophysiological effects on the myocardium. In animal studies, it was shown that the ventricular fibrillation threshold could be increased in both animals fed or infused with omega-3-fatty acids. Further studies subsequently revealed that such fatty acids could reduce both sodium currents and L-type calcium currents on a cellular and ion channel level. It is consequently hypothesized that during ischemia, a reduction in the sodium ion current protects hyperexcitable tissue, and a reduction in the calcium ion current could reduce arrhythmogenic depolarizing currents - and that perhaps the use of EPA and DHA fish oil acids could facilitate such activity. For the time being, however, omega-3-fatty acids in pharmaceutical supplement form have not been shown to elicit such protection against heart conditions.