To learn the basics about atherogenic dyslipidemia, see my previous article "Why you need to look beyond your LDL - “bad cholesterol” - level". 
Niacin is especially noteworthy because it is the most potent drug available for raising HDL levels.[1, 2] Besides boosting  HDL levels, niacin also markedly lowers triglyceride levels while reducing LDL to a smaller degree.[1]
The table below provides an overview of the effects of popular drugs and supplements on blood lipids.[3]

Drug / Supplement









↓ 5-25%


↑ 15-35%


↓ 20-50%


Fish oil



↓ 6% to ↑ 25%


↓ 5% to ↑ 7%


↓ 19-44%





↓ 18-55%


↑ 5-15%


↓ 7-30%





↓ 5% to ↑ 20%


↑ 10-20%


↓ 20-50%


Bile acid sequestrants



↓ 15-30%


↑ 3-5%


↑ 0-10%


Cholesterol absorption inhibitors



↓ 13-15%


↑ 3-5%


↓ 5-11%

As outlined in the table, niacin by far excels over statins – the most commonly prescribed cholesterol drug – in improving both HDL and triglyceride levels. Also, in contrast to statins, niacin more effectively reduces the number of atherogenic small LDL particles.[4, 5] In other words, statins result in less reductions in LDL particles than LDL cholesterol levels, while niacin results in greater reductions in LDL particles than LDL cholesterol levels. Niacin also shifts the LDL particle distribution toward a predominance of larger, less atherogenic particles.[6, 7] 
Like LDL, HDL particle size also matters. Larger HDL particles – HDL2 – seem to be more cardio-protective than smaller HDL3 particles [8, 9], and niacin effectively increases those anti-atherosclerotic larger HDL2 particles.[7, 10-15] Supplementing with 3 g immediate-release niacin for 3 weeks not only slashes triglyceride levels by 27% but also elevates HDL levels by 23% and specifically boosts HDL2 levels 6.5-fold.[10]

Unique benefit of niacin – reduction of Lipoprotein(a), a.k.a. Lp(a)

While being recognized as a cardiovascular risk factor for a long time [16], due to incomplete scientific evidence, screening for and treating elevated Lp(a) levels has not been done in general clinical practice. However, recently major advances have been made in understanding the causal role of elevated Lp(a) in premature cardiovascular disease.[17-21]
Elevated Lp(a) levels can potentially increase the risk of cardiovascular disease by increasing formation of blood clots (due to its prothrombotic/anti-fibrinolytic effects), and/or by accelerating atherogenesis as a result of deposition of Lp(a) cholesterol in the arterial walls.[21, 22]
What makes Lp(a) different from other risk factors is that it is relatively resistant to treatment by either lifestyle and drug intervention – even statins won’t affect Lp(a) significantly.[22, 23] The notable exception is niacin. Treatment with immediate-release niacin or extended release niacin reduces Lp(a) levels by a whopping 30-40%.[13, 24-27]

Niacin’s non-lipid effects - further health benefits

In addition to its pronounced beneficial effects on blood lipids, a growing body of evidence shows that niacin has multiple beneficial effects - that are unrelated to the improvements in lipids - on a range of tissues and cells in the body.[28-31]
Atherosclerosis is the main underlying process giving rise to the development of cardiovascular disease, and endothelial dysfunction is the forerunner of atherosclerosis.[32-36] The endothelium is a single layer of endothelial cells that lines the blood vessel lumen. Endothelial functions include the regulation of vascular tone and blood pressure, blood coagulation, nutrient and electrolyte uptake in all body tissues, and leukocyte trafficking (the recruitment of immune cells to sites of infection or tissue injury), as well as suppression of inflammation and oxidative stress.[37, 38]
Endothelial function is an integrated index of all atherogenic factors present in an individual, including both traditional and non-traditional factors, as well as unknown factors.[36] Leading cardiovascular scientists have highlighted the importance of a healthy endothelial function by suggesting that introducing endothelial function testing into clinical practice might enable innovation of individualized cardiovascular medicine.[36] Therefore, it is notable that niacin significantly improves endothelial function.[39] The protection against endothelial dysfunction by niacin is independent of its effects on blood lipids.[40] It should be underscored that the effect size is greater in studies administering higher doses of niacin (2000 mg/day or more), and in studies administering niacin for primary prevention of atherosclerosis and cardiovascular disease.[39] This suggests that niacin may be an especially good supplement for healthy people to take in order to prevent the early stages of atherosclerosis development.
Importantly, niacin supplementation not only increases HDL levels but markedly improves the endothelial-protective functions of HDL, which is potentially more important.[41] Specifically, niacin treatment improves the capacity of HDL to stimulate endothelial nitric oxide production, reduce superoxide production, and promote endothelial progenitor cell-mediated endothelial repair (i.e. it helps to heal blood vessel injuries and thereby keeps blood vessels working at their best capacity).[41]
Niacin supplementation also has anti-inflammatory effects [40, 42-46], as manifested by reduced levels of C-reactive protein [12] and lipoprotein-associated phospholipase A2 (Lp-PLA2).[12] Niacin also reduces oxidative stress.[47, 48] The anti-inflammatory and anti-oxidative effects of niacin treatment may contribute to plaque stabilization (i.e. making atherosclerotic plaque less prone to rupture) [46] and  prevention of atherosclerosis progression.[49] In line with this, experiments show that niacin indeed does reduce the progression of atherosclerosis.[46, 50]
In addition, niacin boosts levels of the protective peptide adiponectin.[44, 51-55] Because higher levels of adiponectin are associated with reduced inflammation, oxidative stress and metabolic dysregulation [56], as well as with a lower risk of coronary heart disease [57], its pronounced increase by niacin may bring about additional protection against atherosclerosis beyond niacin’s improvement in lipids.[54] Notably, it has been suggested that adiponectin may serve as therapeutic target for treatment of both the metabolic syndrome, diabetes, and heart disease.[58] In addition, women with the highest vs. lowest adiponectin levels have a 34% reduction in breast cancer risk.[59]

Niacin improves erectile function!

Niacin – at a dose of 1,500 mg/day – also can improve erectile function in men suffering from moderate to severe erectile dysfunction.[67] This makes sense, as niacin prevents the development and progression of atherosclerosis (see above), which negatively impacts the function of penile and cavernosal arteries.[68, 69] The earliest signal of endothelial damage in men with cardiovascular risk factors is the manifestation of erectile dysfunction.[69] The penis is a barometer of a man's endothelial function, so it is reasonable that cardiovascular risk factors may be direct causes of erectile dysfunction, and that erectile dysfunction may be the first early clinical presentation of cardiovascular risk factors.[69]

Niacin reduces heart attacks, strokes and mortality!

The landmark clinical trial of niacin - the Coronary Drug Project which was conducted in the pre-statin era - treated men with coronary heart disease with 3 g immediate-release niacin per day for 6.2 years.[60] 1119 men, aged 30-64 at baseline, were randomized to niacin and 2789 to placebo by the end of recruitment in March 1969. At the end of the study in 1975, the niacin-treated group had a significant reduced incidence of non-fatal heart attacks by 26% and a 24% reduced incidence of stroke, compared with placebo.[60] This despite that patients in the niacin group had nearly half as many cardiovascular surgery procedures than did the placebo-treated patients.[60] 
9 years after termination of the Coronary Drug Project study – and cessation of niacin treatment - a follow-up study reported that mortality among men who had been in the niacin group was significantly 11% lower than the mortality among men who had been in the placebo group.[61] This late benefit of niacin, occurring after discontinuation of its supplementation, may be a result of a translation into a mortality benefit over subsequent years after the early favorable effect of niacin in decreasing non-fatal heart attacks, and/or a result of the beneficial effects of niacin on lipids.[61]
Studies evaluating the impact of niacin in statin-naïve patients on atherosclerosis and cardiovascular disease have been universally favorable.[62] In a meta-analysis including 11 randomized controlled trials with 2682 patients in the niacin group and 3934 in the control group, niacin in doses of 1 to 3 g per day reduced major coronary heart disease events by 25%, stroke by 26%, and any cardiovascular event by 27%.[63] Another meta-analysis found that niacin treatment reduces risk of non-fatal heart attack by 28%, and stroke and transient ischemic attack by 24%.[64] A more recent meta-analysis included a total of 9,959 subjects (4,365 subjects allocated to receive niacin treatment and 5,596 allocated to placebo), for a mean duration of 2.7 years.[65] It was found that niacin treatment reduced overall cardiovascular events by 34% and major coronary heart disease events by 25%.[65]
Placing the results of these meta-analyses in context, the Cholesterol Treatment Trialists’ Collaboration - a meta-analysis of 21 trials including 129,526 subjects - reported 22% and 27% reductions in similar clinical endpoints in statin-treated subjects, compared with a control population.[66] Importantly, this clearly shows that long-term niacin treatment may confer similar reductions in heart disease risk and clinical events as statins.


Atherogenic dyslipidemia is a hallmark of metabolic disorders such as insulin resistance, metabolic syndrome, obesity and expanding waistlines, which are escalating in prevalence. I covered this in more detail in a previous article “Why you need to look beyond your LDL - “bad cholesterol” – level”.
Since 1950, clinical data have confirmed the overall safety and efficacy of niacin supplementation in preventing and treating atherogenic dyslipidemia and cardiovascular disease. Niacin is a unique cholesterol drug because it is the most potent available treatment to markedly increase HDL and reduce Lp(a) levels. In addition, niacin substantially improves the LDL and HDL particle distribution towards a more cardio-protective and less atherogenic profile. The beneficial effects of niacin also extend beyond lipids; it markedly improves endothelial (blood vessel) function and has strong anti-inflammatory and anti-oxidative effects.
It should be highlighted that the improvement in endothelial dysfunction by niacin is independent of its effects on blood lipids. Research shows that niacin may be an especially good supplement for healthy people to take in order to prevent the early stages of atherosclerosis development. But it is never too late; niacin also markedly reduces heart attacks, strokes and mortality in people with pre-existing heart disease. And here comes the kicker; comparative data shows that niacin works better than the most popular and widely prescribed drug today – statins!
And best of all, niacin is a vitamin – commonly known as vitamin B3. Thus it is not a pharmaceutically made synthetic drug that is foreign to the body and has with unknown side effects. Niacin is an essential vitamin that the body needs to function at its optimal. In higher doses, this remarkable vitamin acts as a broad spectrum cholesterol “drug”.
In my other article "Niacin Supplements - what you need to know about niacin products" you can find out more about vitamin doses and “drug doses" of niacin, and learn how to navigate the niacin supplement jungle and pick the right niacin product.

1.            Drexel, H., Statins, fibrates, nicotinic acid, cholesterol absorption inhibitors, anion-exchange resins, omega-3 fatty acids: which drugs for which patients? Fundam Clin Pharmacol, 2009. 23(6): p. 687-92.

2.            Carlson, L.A., Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review. J Intern Med, 2005. 258(2): p. 94-114.

3.            Gotto, A.M. and J.A. Farmer, Lipid management and cardiovascular risk reduction, in Metabolic Risk for Cardiovascular Disease, R.H. Eckel, Editor. 2011, Blackwell Publilshing Ltd.: American Heart Association. p. 156-180.

4.            Rosenson, R.S. and J.A. Underberg, Systematic review: Evaluating the effect of lipid-lowering therapy on lipoprotein and lipid values. Cardiovasc Drugs Ther, 2013. 27(5): p. 465-79.

5.            Jafri, H., et al., Extended-release niacin reduces LDL particle number without changing total LDL cholesterol in patients with stable CAD. J Clin Lipidol, 2009. 3(1): p. 45-50.

6.            McKenney, J.M., et al., Effect of niacin and atorvastatin on lipoprotein subclasses in patients with atherogenic dyslipidemia. Am J Cardiol, 2001. 88(3): p. 270-4.

7.            Morgan, J.M., et al., Effects of extended-release niacin on lipoprotein subclass distribution. Am J Cardiol, 2003. 91(12): p. 1432-6.

8.            Pirillo, A., G.D. Norata, and A.L. Catapano, High-density lipoprotein subfractions--what the clinicians need to know. Cardiology, 2013. 124(2): p. 116-25.

9.            Morgan, J., et al., High-density lipoprotein subfractions and risk of coronary artery disease. Curr Atheroscler Rep, 2004. 6(5): p. 359-65.

10.          Shepherd, J., et al., Effects of nicotinic acid therapy on plasma high density lipoprotein subfraction distribution and composition and on apolipoprotein A metabolism. J Clin Invest, 1979. 63(5): p. 858-67.

11.          Blum, C.B., et al., High density lipoprotein metabolism in man. J Clin Invest, 1977. 60(4): p. 795-807.

12.          Kuvin, J.T., et al., Effects of extended-release niacin on lipoprotein particle size, distribution, and inflammatory markers in patients with coronary artery disease. Am J Cardiol, 2006. 98(6): p. 743-5.

13.          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.

14.          Koh, Y., et al., Responses of blood lipids and lipoproteins to extended-release niacin and exercise in sedentary postmenopausal women. J Gerontol A Biol Sci Med Sci, 2010. 65(9): p. 924-32.

15.          Goldberg, A., et al., Multiple-dose efficacy and safety of an extended-release form of niacin in the management of hyperlipidemia. Am J Cardiol, 2000. 85(9): p. 1100-5.

16.          Cantin, B., et al., Is lipoprotein(a) an independent risk factor for ischemic heart disease in men? The Quebec Cardiovascular Study. J Am Coll Cardiol, 1998. 31(3): p. 519-25.

17.          Man, L.C., E. Kelly, and D. Duffy, Targeting lipoprotein (a): an evolving therapeutic landscape. Curr Atheroscler Rep, 2015. 17(5): p. 502.

18.          Kassner, U., et al., Lipoprotein(a) - An independent causal risk factor for cardiovascular disease and current therapeutic options. Atheroscler Suppl, 2015. 18: p. 263-7.

19.          Jacobson, T.A., Lipoprotein(a), cardiovascular disease, and contemporary management. Mayo Clin Proc, 2013. 88(11): p. 1294-311.

20.          Kostner, K.M., W. Marz, and G.M. Kostner, When should we measure lipoprotein (a)? Eur Heart J, 2013. 34(42): p. 3268-76.

21.          Tsimikas, S. and J.L. Hall, Lipoprotein(a) as a potential causal genetic risk factor of cardiovascular disease: a rationale for increased efforts to understand its pathophysiology and develop targeted therapies. J Am Coll Cardiol, 2012. 60(8): p. 716-21.

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.          Berglund, L., Diet and drug therapy for lipoprotein (a). Curr Opin Lipidol, 1995. 6(1): p. 48-56.

24.          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.

25.          Capuzzi, D.M., et al., Efficacy and safety of an extended-release niacin (Niaspan): a long-term study. Am J Cardiol, 1998. 82(12A): p. 74U-81U; discussion 85U-86U.

26.          Morgan, J.M., D.M. Capuzzi, and J.R. Guyton, A new extended-release niacin (Niaspan): efficacy, tolerability, and safety in hypercholesterolemic patients. Am J Cardiol, 1998. 82(12A): p. 29U-34U; discussion 39U-41U.

27.          Guyton, J.R., et al., Effectiveness of once-nightly dosing of extended-release niacin alone and in combination for hypercholesterolemia. Am J Cardiol, 1998. 82(6): p. 737-43.

28.          Digby, J.E., N. Ruparelia, and R.P. Choudhury, Niacin in cardiovascular disease: recent preclinical and clinical developments. Arterioscler Thromb Vasc Biol, 2012. 32(3): p. 582-8.

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

30.          Lukasova, M., et al., Nicotinic acid (niacin): new lipid-independent mechanisms of action and therapeutic potentials. Trends Pharmacol Sci, 2011. 32(12): p. 700-7.

31.          Kamanna, V.S., S.H. Ganji, and M.L. Kashyap, Recent advances in niacin and lipid metabolism. Curr Opin Lipidol, 2013. 24(3): p. 239-45.

32.          Hadi, H.A., C.S. Carr, and J. Al Suwaidi, Endothelial dysfunction: cardiovascular risk factors, therapy, and outcome. Vasc Health Risk Manag, 2005. 1(3): p. 183-98.

33.          Bonetti, P.O., L.O. Lerman, and A. Lerman, Endothelial dysfunction: a marker of atherosclerotic risk. Arterioscler Thromb Vasc Biol, 2003. 23(2): p. 168-75.

34.          Landmesser, U. and H. Drexler, The clinical significance of endothelial dysfunction. Curr Opin Cardiol, 2005. 20(6): p. 547-51.

35.          Reriani, M.K., L.O. Lerman, and A. Lerman, Endothelial function as a functional expression of cardiovascular risk factors. Biomark Med, 2010. 4(3): p. 351-60.

36.          Matsuzawa, Y. and A. Lerman, Endothelial dysfunction and coronary artery disease: assessment, prognosis, and treatment. Coron Artery Dis, 2014. 25(8): p. 713-24.

37.          Goveia, J., P. Stapor, and P. Carmeliet, Principles of targeting endothelial cell metabolism to treat angiogenesis and endothelial cell dysfunction in disease. EMBO Mol Med, 2014. 6(9): p. 1105-20.

38.          Schulz, E., et al., Nitric oxide, tetrahydrobiopterin, oxidative stress, and endothelial dysfunction in hypertension. Antioxid Redox Signal, 2008. 10(6): p. 1115-26.

39.          Sahebkar, A., Effect of niacin on endothelial function: a systematic review and meta-analysis of randomized controlled trials. Vasc Med, 2014. 19(1): p. 54-66.

40.          Wu, B.J., et al., Evidence that niacin inhibits acute vascular inflammation and improves endothelial dysfunction independent of changes in plasma lipids. Arterioscler Thromb Vasc Biol, 2010. 30(5): p. 968-75.

41.          Sorrentino, S.A., et al., Endothelial-vasoprotective effects of high-density lipoprotein are impaired in patients with type 2 diabetes mellitus but are improved after extended-release niacin therapy. Circulation, 2010. 121(1): p. 110-22.

42.          Digby, J.E., et al., Anti-inflammatory effects of nicotinic acid in human monocytes are mediated by GPR109A dependent mechanisms. Arterioscler Thromb Vasc Biol, 2012. 32(3): p. 669-76.

43.          Chai, J.T., J.E. Digby, and R.P. Choudhury, GPR109A and vascular inflammation. Curr Atheroscler Rep, 2013. 15(5): p. 325.

44.          Digby, J.E., et al., Anti-inflammatory effects of nicotinic acid in adipocytes demonstrated by suppression of fractalkine, RANTES, and MCP-1 and upregulation of adiponectin. Atherosclerosis, 2010. 209(1): p. 89-95.

45.          Wu, B.J., et al., Niacin inhibits vascular inflammation via the induction of heme oxygenase-1. Circulation, 2012. 125(1): p. 150-8.

46.          Holzhauser, E., et al., Nicotinic acid has anti-atherogenic and anti-inflammatory properties on advanced atherosclerotic lesions independent of its lipid-modifying capabilities. J Cardiovasc Pharmacol, 2011. 57(4): p. 447-54.

47.          Ganji, S.H., et al., Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells. Atherosclerosis, 2009. 202(1): p. 68-75.

48.          Huang, H., et al., Niacin reverses migratory macrophage foam cell arrest mediated by oxLDL in vitro. PLoS One, 2014. 9(12): p. e114643.

49.          Lipszyc, P.S., et al., Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect. Open Cardiovasc Med J, 2013. 7: p. 90-8.

50.          Lukasova, M., et al., Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells. J Clin Invest, 2011. 121(3): p. 1163-73.

51.          Westphal, S., et al., Extended-release niacin raises adiponectin and leptin. Atherosclerosis, 2007. 193(2): p. 361-5.

52.          Plaisance, E.P., et al., Increased total and high-molecular weight adiponectin after extended-release niacin. Metabolism, 2008. 57(3): p. 404-9.

53.          Plaisance, E.P., et al., Niacin stimulates adiponectin secretion through the GPR109A receptor. Am J Physiol Endocrinol Metab, 2009. 296(3): p. E549-58.

54.          Westphal, S., et al., Adipokines and treatment with niacin. Metabolism, 2006. 55(10): p. 1283-5.

55.          Fraterrigo, G., et al., Relationship between Changes in Plasma Adiponectin Concentration and Insulin Sensitivity after Niacin Therapy. Cardiorenal Med, 2012. 2(3): p. 211-217.

56.          Lim, S., M.J. Quon, and K.K. Koh, Modulation of adiponectin as a potential therapeutic strategy. Atherosclerosis, 2014. 233(2): p. 721-8.

57.          Zhang, H., et al., Adiponectin levels and risk of coronary heart disease: a meta-analysis of prospective studies. Am J Med Sci, 2013. 345(6): p. 455-61.

58.          Fisman, E.Z. and A. Tenenbaum, Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease? Cardiovasc Diabetol, 2014. 13: p. 103.

59.          Macis, D., A. Guerrieri-Gonzaga, and S. Gandini, Circulating adiponectin and breast cancer risk: a systematic review and meta-analysis. Int J Epidemiol, 2014. 43(4): p. 1226-36.

60.          Clofibrate and niacin in coronary heart disease. JAMA, 1975. 231(4): p. 360-81.

61.          Canner, P.L., et al., Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin. J Am Coll Cardiol, 1986. 8(6): p. 1245-55.

62.          Villines, T.C., et al., Niacin: the evidence, clinical use, and future directions. Curr Atheroscler Rep, 2012. 14(1): p. 49-59.

63.          Bruckert, E., J. Labreuche, and P. Amarenco, Meta-analysis of the effect of nicotinic acid alone or in combination on cardiovascular events and atherosclerosis. Atherosclerosis, 2010. 210(2): p. 353-61.

64.          Duggal, J.K., et al., Effect of niacin therapy on cardiovascular outcomes in patients with coronary artery disease. J Cardiovasc Pharmacol Ther, 2010. 15(2): p. 158-66.

65.          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.

66.          Cholesterol Treatment Trialists, C., et al., Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet, 2010. 376(9753): p. 1670-81.

67.            Ng, C.F., et al., Effect of niacin on erectile function in men suffering erectile dysfunction and dyslipidemia. J Sex Med, 2011. 8(10): p. 2883-93.

68.            Sullivan, M.E., S.R. Keoghane, and M.A. Miller, Vascular risk factors and erectile dysfunction. BJU Int, 2001. 87(9): p. 838-45.

69.            Kendirci, M., S. Nowfar, and W.J. Hellstrom, The impact of vascular risk factors on erectile function. Drugs Today (Barc), 2005. 41(1): p. 65-74.