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Abstract
Decreases in global cardiovascular disease (CVD) mortality and morbidity in recent decades can be partly attributed to cholesterol reduction through statin use. n-3 long chain polyunsaturated fatty acids are recommended by some authorities for primary and secondary CVD prevention, and for triglyceride reduction. The residual risk of CVD that remains after statin therapy may potentially be reduced by n-3 long chain polyunsaturated fatty acids. However, the effects of concomitant use of statins and n-3 long chain polyunsaturated fatty acids are not well understood. Pleiotropic effects of statins and n-3 long chain polyunsaturated fatty acids overlap. For example, cytochrome P450 enzymes that metabolize statins may affect n-3 long chain polyunsaturated fatty acid metabolism and vice versa. Clinical and mechanistic study results show both synergistic and antagonistic effects of statins and n-3 long chain polyunsaturated fatty acids when used in combination.
Highlights
Cardiovascular diseases (CVDs) are the leading cause of global mortality, accounting for 32% of the 56 million deaths in 2015 [1]
The aim of this review is to explore the interrelationship between statins and n-3 long chain (LC) polyunsaturated fatty acids (PUFAs) in the context of CVD
Overlapping or even counteractive effects of combined treatment with statins and n-3 LC PUFAs may be confounding outcomes of clinical trials. Both statins and n-3 LC PUFAs are recommended for CVD prevention
Summary
Cardiovascular diseases (CVDs) are the leading cause of global mortality, accounting for 32% of the 56 million deaths in 2015 [1]. CVDs contribute to mortality, but cause a considerable disease burden in healthy life years lost [4]. Reductions in cardiovascular risk factors such as smoking have contributed to half the drop in mortality, whereas the other half can be attributed to medical therapies that include the use of medications such as statins, niacin and fibrates in both primary and secondary prevention [5]. Statins are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and are currently considered standard of care in both primary and secondary prevention of CVD. Their main mode of action is to lower circulating cholesterol, mainly low-density lipoprotein (LDL)
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