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Marine omega-3s for the prevention of arrhythmias
Omega-3s have been theorised to increase membrane fluidity by reducing compression of the acyl chains of membrane phospholipid fatty acids, which can lead to a reduction in the ‘spring-like’ tension on membrane ion channels. This spring-like tension can reduce the ability of ions to freely move in and out of the ion channel and hence reduce its conductance. This is known as the ‘Andersen membrane spring-like tension hypothesis’ and is just one way marine omega-3s may prevent arrhythmias.1 This theory states that the phospholipid cell membrane curves near the ion protein channel in order for the hydrophobic domains of the cell membrane to match up. The hydrophobic length of ion channel proteins is slightly less than the hydrophobic length of the acyl chains in the phospholipid bilayer, which causes a slight bend in the membrane, and this bend compresses the ion channel decreasing the space that ions can freely move in and out of the channel. However, supplementing with fish oil can prevent or reduce this compression increasing the movement of ions in and out of the channel.1 Other antiarrhythmic benefits of omega-3s include eicosapentaenoic acid (EPA)’s ability to be a competitive substrate for the enzymes that metabolise arachidonic acid (AA) to proinflammatory eicosanoids, which is partly how marine omega-3s reduce inflammation.2 EPA metabolites are also antiarrhythmic, whereas almost all metabolites from AA (and linoleic acid) are proarrhythmic.3
Dietary omega-3s are mainly consumed as triglycerides, which are absorbed as free fatty acids and monoglycerides. These fats then get rapidly resynthesised in the intestine and liver back to triglycerides with subsequent integration into chylomicrons, very low-density lipoprotein and low-density lipoprotein (LDL) (LDL can actually deliver omega-3s to tissues via LDL receptors). The omega-3 polyunsaturated fatty acids (PUFAs) can also be liberated from lipoproteins via lipoprotein and hepatic …
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