Dietary Supplements in Dyslipidemia
1. Neuronutrition Associates 6618 Sitio Del Rio Suite D102 Austin, TX 78730
Received: March 4, 2018 | Accepted: May 23, 2018 | Published: May 24, 2018
OBM Integrative and Complementary Medicine 2018, Volume 3, Issue 2 doi:10.21926/obm.icm.1802008
Academic Editor: Srinivas Nammi
Special Issue: Herbal Medicines for the Treatment of Metabolic Syndrome
Recommended citation: Gutierrez E, Elyaman Y. Dietary Supplements in Dyslipidemia. OBM Integrative and Complementary Medicine 2018;3(2):008; doi:10.21926/obm.icm.1802008.
© 2018 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.
Dietary Supplements in Dyslipidemia
While dietary and lifestyle intervention should be the primary treatment for dyslipidemia, there may be a role for recommending specific dietary supplements. This report focuses on four commonly used supplements that have demonstrated efficacy.
1. Red Yeast Rice- is a fermented rice product containing monacolin K, an HMG- CoA reductase inhibitor. It has been found to lower total cholesterol, low-density lipoprotein (LDL), and in one study, decrease mortality in patients with cardiovascular disease [1,2,3]. Even though monacolin K is the active ingredient in lovastatin, the lipid lowering effect of Red Yeast Rice is greater than equivalent doses of lovastatin, suggesting other active ingredients. The source is extremely important ensuring that every batch is citrinin (a potentially nephrotoxic mycotoxin) free . Red yeast rice dosages of 600-1,200mg/day are most widely studied but some data suggests 2,400-4,800mg/day .
2. Omega 3 Fatty Acids- both docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have been widely studied for the treatment of heart disease and hyperlipidemia [6,7]. Newer data supports EPA only formulations significantly reduce lipid peroxidation and cholesterol formation at a dose of 1,800mg/day [8,9]. Not only has it been found to lower triglyceride and LDL levels, but it has demonstrated possible plaque regression and improvement in unstable angina when given with a statin vs statin therapy alone.
3. Niacin- or (B3), is a water-soluble vitamin that has been shown to be effective in dyslipidemia. Negative effects of niacin found in the HPS2-THRIVE study may have been due to the addition of laropiprant (a prostaglandin D2 receptor antagonist) and should not be attributed to niacin alone . Also of note, the nicotinamide or “flush free” form of niacin does not have lipid lowering properties and should not be used in place of nicotinic acid. Recommending baby aspirin 30 minutes prior to dosing, slow titration, and using an extended release formula may decrease the common side effect of flushing. Dosages range from 500-4,000mg/day . Caution is advised in diabetic and hyperuricemia patients since niacin can increase both serum uric acid and glucose.
4. Berberine- is an isoquinoline plant alkaloid that has several therapeutic benefits including cholesterol and glucose lowering properties [12,13,14]. Preliminary data suggests it to be a potential proprotein convertase subtilisin-like kexin type 9 (PCSK9) inhibitor. PCSK9 is a serine protease that degrades hepatic LDL receptors increasing serum LDL . The recommended dose is 1-4g per day.
Clinicians must be judicious in their use of prescribing dietary supplements, taking into account comorbid conditions and closely monitoring laboratory values pre and post treatment to ensure safety and efficacy.
Dietary supplements lack the same regulatory rigor as prescription medications in the United States, therefore specific product and brand recommendations are imperative for clinicians to give to their patients so that product potency, purity, and quality can be assured . Recommendations should include pharmaceutical grade supplements that have third party product testing and verification through organizations such as Good Manufacturing Practice Certification or the National Sanitation Foundation.
Dr. Emily Gutierrez, DNP, C-PNP, PMHS, IFM-CP and Dr. Yousef Elyaman, MD, IFM-CP. These are the only two authors on this manuscript, with Dr. Gutierrez being lead author and contributor.
The authors have declared that no competing interests exist.
- Lu Z, Kou W, Du B, Wu Y, Zhao S, Brusco OA, et al. Effect of Xuezhikang, an extract from red yeast Chinese rice, on coronary events in a Chinese population with previous myocardial infarction. Am J Cardiol. 2008; 101: 1689-1693. [CrossRef]
- Mortensen S, Leth A, Agner E, Rohde M. Dose-related decrease of serum coenzyme Q10 during treatment with HMG-CoA reductase inhibitors. Mol Aspects Med. 1997; 18: 137-144. [CrossRef]
- Horton JD, Cohen JC, Hobbs HH. Molecular biology of PCSK9: its role in LDL metabolism. Trends Biochem Sci. 2007; 32: 71-77. [CrossRef]
- Gordon RY, Cooperman T, Obermeyer W, Becker DJ. Marked variability of monacolin levels in commercial red yeast rice products: buyer beware! Arch Intern Med. 2010; 170: 1722-1727. [CrossRef]
- Patrick L, Uzick M. Cardiovascular disease: C-reactive protein and the inflammatory disease paradigm: HMG-CoA reductase inhibitors, alpha-tocopherol, red yeast rice, and olive oil polyphenols. A review of the literature. Altern Med Rev. 2001; 6: 248-271.
- Bays HE, Ballantyne CM, Kastelein JJ, Isaacsohn JL, Braeckman RA, Soni PN. Eicosapentaenoic acid ethyl ester (AMR101) therapy in patients with very high triglyceride levels (from the multi-center, placebo-controlled, randomized, double-blInd, 12-week study with an open-label extension [MARINE] trial). Am J Cardiol. 2011; 108: 682-690. [CrossRef]
- Mason RP, Jacob RF. Eicosapentaenoic acid inhibits glucose-induced membrane cholesterol crystalline domain formation through a potent antioxidant mechanism. BBA- Biomembranes. 2015; 1848: 502-509. [CrossRef]
- Watanabe T, Miyamoto T, Miyasita T, Shishido T, Arimoto T, Takahashi H, et al. Combination therapy of eicosapentaenoic acid and pitavastatin for coronary plaque regression evaluated by integrated backscatter intravascular ultrasonography (CHERRY study)—Rationale and design. J Cardiol. 2014; 64: 236-239. [CrossRef]
- Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet. 2007; 369: 1090-1098. [CrossRef]
- Houston M, Guarneri, M, Kahn. J.ISIFMC* Position Paper on the HPS2-Thrive Study. Int J Hum Nutr Funct Med. 2014; 2: 15-32.
- Available from: http://naturaldatabase.therapeuticresearch.com/homeaspx.
- Kong W, Wei J, Abidi P, Lin M, Inaba S, Li C, et al. Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins. Nat Med. 2004; 10: 1344. [CrossRef]
- Pirillo A, Catapano AL. Berberine, a plant alkaloid with lipid-and glucose-lowering properties: From in vitro evidence to clinical studies. Atherosclerosis. 2015; 243: 449-461. [CrossRef]
- Barbagallo CM, Cefalù AB, Noto D, Averna MR. Role of nutraceuticals in hypolipidemic therapy. Front Cardiovasc Med. 2015; 2: 22. [CrossRef]
- Schulz R, Schlüter K-D, Laufs U. Molecular and cellular function of the proprotein convertase subtilisin/kexin type 9 (PCSK9). Basic Res Cardiol. 2015; 110: 4. [CrossRef]
- Senate and house of representatives of the United States of America. Dietary supplement health and education act of 1994. America: Public law 103-417rd congress; 1994. Available from: https://ods.od.nih.gov/About/DSHEA_Wording.aspx.