Abstract

Long-chain omega 3 fatty acids EPA and DHA entered the nutrition and cardiovascular pharmacology fields quite recently, after the now famous studies of Bang and Dyrberg were published in the second half of the XX century. These molecules have a wide spectrum of activities, whose precise nature is often difficult to classify. For example they can be derived from food (in particular from appropriate diets) and yet they sometimes need to be taken as supplements: some of their favorable effects on the cardiovascular system, on the other hand, can only be obtained following pharmacological treatments that supply up to ten-twenty times the amounts usually present in Western diets. The triple connotation of EPA and DHA (food components, supplements, and drugs) translates into the positive effects that have been attributed to their regular consumption. It is not rare to read scientific papers in which a hypotriglyceridemic action is ascribed to “dietary” doses, whereas only pharmacological treatment can achieve this result. Yet, even at appropriate doses omega 3 fatty acids have been recently criticized. Some trials and a meta-analysis did negate the cardioprotective activities of omega 3 fatty acids that had been previously reported by, e.g., the famous GISSI-Prevenzione study carried out in Italy in the ’90s. The review by Connye N. Kuratko, Coleen C. Nolan, and Norman Salem Jr. published in this issue of Nutrafoods delivers an in-depth analysis of these complex issues and provides readers with information necessary to interpret the manifold physiological and functional actions of omega 3 fatty acids. Indeed, their effects recently extended to areas that are being now explored. As an example, in addition to the anti-arrhythmic activities and those on triglyceridemia and heart rate control, actions on inflammation and on endothelial function have been explored. In addition, recent data suggest that omega 3 fatty acids stabilize atherosclerotic plaques via increased fibrous cap thickness and reduction of inflammatory infiltration. How can we reconcile this increasing knowledge of omega 3-mediated cardioprotective mechanisms with the disappointing results stemming from clinical trials of pharmacological use we mentioned above? One potential answer can be found after careful analysis of how randomized, double-blind, placebocontrolled studies are carried out. In these protocols the drug at study is added “on top” of an established “best treatment”. In fact, this model may underestimate the effects of a compound added to pharmacological treatment, especially if the tested molecule (as in the case of omega 3 fatty acids) shares effects such as anti-inflammation, amelioration of endothelial function, plaque stabilization with established therapeutic agents, i.e. statins.

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