Clinical Prevention of Sudden Cardiac Death by n-3 Polyunsaturated Fatty Acids and Mechanism of Prevention of Arrhythmias by n-3 Fish Oils
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This review will be limited specifically to the beneficial prevention by the n-3 polyunsaturated fatty acids (PUFAs) of arrhythmic deaths, including sudden cardiac death, which annually causes some 300 000 deaths in the United States and millions more worldwide. We will also show that the growing body of positive clinical studies is supported by what has been learned in animal and laboratory studies regarding the mechanism by which n-3 PUFAs prevent cardiac arrhythmias.
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The Essential PUFAs
Figure 1 shows the 2 essential classes of PUFAs, the n-6 (ω6) and n-3 (ω3) classes. Both classes are “essential” because we cannot make them in our bodies. They must come in our diets, and they are essential for normal growth, development, and optimal function of brain, heart, and probably other systems. The parent fatty acid of the n-6 class, linoleic acid (C18:2n-6; LA) has 18 carbon atoms in its acyl chain, and the first C=C double bond is 6 carbons back from the methyl end of the fatty acid, hence the “n-6” appellation. In the bodies of animals, including humans, LA can be elongated and desaturated through a series of enzymatic steps to form arachidonic acid (C20:4n-6; AA). AA is the source of the n-6 eicosanoids that result from oxygenation of AA by cyclooxygenase, lipoxygenase, and epoxygenase enzymes to form prostaglandins, leukotrienes, lipoxines, and P-450 compounds, which in many instances are potent cell messengers.
In the chloroplast of green plants, algae, and phytoplankton, LA can be further desaturated in the n-3 position to yield α-linolenic acid (C18:3 n-3; ALA), the 18-carbon parent fatty acid of the n-3 class. ALA can be further elongated and desaturated by the same enzymes that convert n-6 LA to AA to form the 20-carbon n-3 analog of AA, namely, eicosapentaenoic acid …