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Niacin - vitamin B3 - elevates HDL levels (the "good" cholesterol) more than popular medications

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Low HDL-C levels are an independent risk factor for development of coronary heart disease (CHD).[1] At all levels of total cholesterol, HDL-C shows a strong inverse association with incidence of CHD. Every 1 mg/dl increase in HDL is associated with a 2-3% decrease cardiovascular risk.[1]

Among men and women aged 49-82 years, who were free of CHD at baseline, after a follow up of 12 yr, the participants with high HDL-C levels (over 60 mg/dL) had half the risk of cardiovascular events compared with participants with low HDL-C levels (below 40 mg/dL).[2] Another large study of 4,500 subjects aged 16-65 years, found after a follow-up of 6 years that individuals with HDL-C levels below <35 mg/dl were at 4 times higher heart disease risk than those with HDL-C levels over 35 mg/dl.[3]

The prevalence of low HDL levels in apparently healthy US adults is 35% in men (defined as below 40 mg/dL or 1.03 mmol/) and 39% of women (below 50 mg/dL or 1.29 mmol/L).[4] Among patients with established cardiovascular disease, 20% to 60% have low HDL levels.[5-7] Furthermore, low HDL levels are part of the criteria for the metabolic syndrome [8] and are highly prevalent among patients with diabetes, affecting more than 50% of men and 66% of women who are diabetic.[9, 10]

Statins are the most commonly used medications for heart disease. However, while statin is the most effective medication to reduce LDL (the "bad" cholesterol) levels, there remains an unacceptably high residual risk in patients who have been on statin treatment. Even after intensive statin treatment that has achieved very low LDL levels, morbidity and mortality rates among statin-treated patients still remain approximately two thirds to three quarters of those found in patients who were getting placebo.[11, 12] This large residual risk clearly indicates that LDL only modestly impacts atherosclerosis at best. Therefore, medical research is investigating HDL elevating treatments with the aim to reduce residual risk, and prevent development of cardiovascular diesase in the first place.

Niacin (aka nicotinic acid) is another name for vitamin B3. In high dosages of 3-4 g per day, niacin very effectively increases HDL levels by up to 35%.[13] In this regard, niacin strikingly outperforms statins, which raise HDL by only around 5%.[11] A recent study compared head-to-head the HDL elevating efficacy of low dose niacin (750-1500 mg/day) with statin and fibrate (two commonly used lipid medications).


200 patients with low HDL levels were randomly assigned for treatment either with: 

First 6 weeks

atorvastatin 10 mg/day

fenofibrate 160 mg/day

niacin-extended release (ER) 750 mg/day 

Final 6 weeks

atorvastatin 20 mg/day

fenofibrate 320 mg/day

niacin-extended release (ER) 1,500 mg/day

After 6 weeks of treatment, the dosages of the medications were doubled and the patients were finally assessed after 12 weeks for their lipid values. 


Niacin therapy 750 mg and 1.5 g/day resulted in a significant rise in HDL by 8.1% and 12.4% respectively. 

Fenofibrate 160 and 320 mg/day also resulted in a significant rise in HDL by 3.8% and 6.2%, respectively. 

However, atorvastatin 10 and 20 mg/day did not significantly impact HDL levels. 

By increasing HDL, niacin was found to be most effective in reduction of 10-year heart disease risk percentage, followed by fenofibrate, while atorvastatin had no effect.


This study shows that a moderately high dose of niacin (vitamin B3) is more effective in elevating protective HLD levels than popular cardiovascular disease medications. By increasing HDL levels, niacin is a safe and effective way to reduce the cumulative heart disease risk among people with low HDL levels. Niacin also beneficially impacts a number of other important heart disease risk factors (which will be covered in upcoming articles).[14]

The take home message is that high dose vitamin therapies, which are safe, can be far more effective than medications which often come with serious side effects. Decades of clinical data have confirmed the overall safety of niacin therapy.[15, 16] A review of the U.S. Food and Drug Administration (FDA) Adverse Event Reporting System found niacin (in the form of nicotinic acid) to be associated with a lower rate of serious adverse events (defined as resulting in hospitalization or death), liver toxicity, and muscle destruction (rhabdomyolysis) compared with that of several other commonly used lipid-altering drugs including simvastatin, pravastatin, atorvastatin, gemfibrozil, and fenofibrate.[16]

It is notable that niacin is the only available agent that significantly reduces levels of Lp(a) [Lipoprotein(a)][17-19], an established heart disease risk factor.[20-24] Statins either don't impact Lp(a) levels [25, 26] or actually increase Lp(a) levels.[27] Thus, it is possible that Lp(a) contributes to the residual risk seen after statin treatments.[28] Support for this comes from the finding that Lp(a) is not correlated with other well-recognized risk factors for early heart attack (myocardial infarction), such as LDL and old age, and is under separate metabolic control than other cardiovascular risk factors (like apolipoprotein B).[29]

SIDE NOTE          

Elevated Lp(a) levels constitute an independent risk factor for early heart attack even in young adults under 45 years of age.[29] Therefore, niacin holds tremendous potential as a primary prevention supplement/medication for the younger generation in order to prevent development of future heart disease. More in this in upcoming posts...


1.         Gordon, D.J., et al., High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation, 1989. 79(1): p. 8-15.

2.         Castelli, W.P., et al., Incidence of coronary heart disease and lipoprotein cholesterol levels. The Framingham Study. JAMA, 1986. 256(20): p. 2835-8.

3.         Assmann, G., et al., High-density lipoprotein cholesterol as a predictor of coronary heart disease risk. The PROCAM experience and pathophysiological implications for reverse cholesterol transport. Atherosclerosis, 1996. 124 Suppl: p. S11-20.

4.         Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation, 2002. 106(25): p. 3143-421.

5.         Sviridov, D. and P.J. Nestel, Genetic factors affecting HDL levels, structure, metabolism and function. Curr Opin Lipidol, 2007. 18(2): p. 157-63.

6.         Asztalos, B.F., et al., High-density lipoprotein subpopulation profile and coronary heart disease prevalence in male participants of the Framingham Offspring Study. Arterioscler Thromb Vasc Biol, 2004. 24(11): p. 2181-7.

7.         Asztalos, B.F., et al., Value of high-density lipoprotein (HDL) subpopulations in predicting recurrent cardiovascular events in the Veterans Affairs HDL Intervention Trial. Arterioscler Thromb Vasc Biol, 2005. 25(10): p. 2185-91.

8.         Alberti, K.G., et al., Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation, 2009. 120(16): p. 1640-5.

9.         Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA, 2001. 285(19): p. 2486-97.

10.       Jacobs, M.J., et al., Prevalence and control of dyslipidemia among persons with diabetes in the United States. Diabetes Res Clin Pract, 2005. 70(3): p. 263-9.

11.       LaRosa, J.C., J. He, and S. Vupputuri, Effect of statins on risk of coronary disease: a meta-analysis of randomized controlled trials. JAMA, 1999. 282(24): p. 2340-6.

12.       Boden, W.E., M.S. Sidhu, and P.P. Toth, The therapeutic role of niacin in dyslipidemia management. J Cardiovasc Pharmacol Ther, 2014. 19(2): p. 141-58.

13.       McKenney, J., New perspectives on the use of niacin in the treatment of lipid disorders. Arch Intern Med, 2004. 164(7): p. 697-705.

14.       Florentin, M., et al., Pleiotropic effects of nicotinic acid: beyond high density lipoprotein cholesterol elevation. Curr Vasc Pharmacol, 2011. 9(4): p. 385-400.

15.       Lavigne, P.M. and R.H. Karas, The current state of niacin in cardiovascular disease prevention: a systematic review and meta-regression. J Am Coll Cardiol, 2013. 61(4): p. 440-6.

16.       Alsheikh-Ali, A.A. and R.H. Karas, The safety of niacin in the US Food and Drug Administration adverse event reporting database. Am J Cardiol, 2008. 101(8A): p. 9B-13B.

17.       Carlson, L.A., A. Hamsten, and A. Asplund, Pronounced lowering of serum levels of lipoprotein Lp(a) in hyperlipidaemic subjects treated with nicotinic acid. J Intern Med, 1989. 226(4): p. 271-6.

18.       Scanu, A.M. and R. Bamba, Niacin and lipoprotein(a): facts, uncertainties, and clinical considerations. Am J Cardiol, 2008. 101(8A): p. 44B-47B.

19.       Pan, J., et al., Niacin treatment of the atherogenic lipid profile and Lp(a) in diabetes. Diabetes Obes Metab, 2002. 4(4): p. 255-61.

20.       Malaguarnera, M., et al., Lipoprotein(a) in cardiovascular diseases. Biomed Res Int, 2013. 2013: p. 650989.

21.       Rhoads, G.G., et al., Lp(a) lipoprotein as a risk factor for myocardial infarction. JAMA, 1986. 256(18): p. 2540-4.

22.       Nordestgaard, B.G., et al., Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J, 2010. 31(23): p. 2844-53.

23.       Anuurad, E., et al., Lipoprotein(a): a unique risk factor for cardiovascular disease. Clin Lab Med, 2006. 26(4): p. 751-72.

24.       Erqou, S., et al., Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA, 2009. 302(4): p. 412-23.

25.       Thiery, J., et al., Serum lipoprotein Lp(a) concentrations are not influenced by an HMG CoA reductase inhibitor. Klin Wochenschr, 1988. 66(10): p. 462-3.

26.       Illingworth, D.R., et al., Comparative effects of lovastatin and niacin in primary hypercholesterolemia. A prospective trial. Arch Intern Med, 1994. 154(14): p. 1586-95.

27.       Kostner, G.M., et al., HMG CoA reductase inhibitors lower LDL cholesterol without reducing Lp(a) levels. Circulation, 1989. 80(5): p. 1313-9.

28.       Cai, A., et al., Lipoprotein(a): a promising marker for residual cardiovascular risk assessment. Dis Markers, 2013. 35(5): p. 551-9.

29.       Sandkamp, M., et al., Lipoprotein(a) is an independent risk factor for myocardial infarction at a young age. Clin Chem, 1990. 36(1): p. 20-3.

Last modified on Tuesday, 13 May 2014 01:08

Medical Writer & Nutritionist

MSc Nutrition

University of Stockholm & Karolinska Institute, Sweden 

   Baylor University, TX, USA

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