Nicotinic acid is a form of water-soluble vitamin B3. Vitamin B3 was discovered in 1937 by American biochemist Conrad Elvehjem, and as a result cured pellagra, a disease caused by niacin deficiency that causes horrible skin lesions, diarrhea, dementia, and even death. This compound is now commonly marketed as niacin and is the third of eight presently known B vitamins.
Originally found as a molecule in yeast and meat, as said niacin was first called nicotinic acid. This is because if you oxidize nicotine, it produces nicotinic acid. However, people associated nicotine as a toxic chemical in tobacco, and so the name niacin was adopted, which stands for: NIcotinic ACid + vitamIN. For the purposes of this article, we will refer to nicotinic acid as niacin from now on.
Niacin in nature
Foods rich in niacin include chicken, tuna, turkey, peanuts, coffee, kidney beans, pork, and bacon. Meats are generally the highest in niacin content by a large margin; however, this may not be practical for dietary reasons. Thankfully, niacin is readily available as a supplement, and even better – it is cheap. When taking niacin, you should be aware that it can cause a hot burning or itchy flush like sensation. This is completely harmless and its severity can be reduced by starting at a low dose (100 mg), taking an aspirin or white willow extract before and drinking water.
A word of caution should be made here: there are two versions of nicotinic acid available, a regular- and a slow-release type. The slow release version is sometimes called delayed action, no flush, non flush, or persistent release. Slow-release nicotinic acid is not recommended for regular supplementation, as it carries the risk of liver damage. Only take slow-release nicotinic acid when directed to do so by a qualified physician, and only for the stated duration.
Potential health benefits
Niacin is essential for the normal function of the nervous system and the maintenance of healthy skin and mucous membranes. Niacin helps the body convert food (carbohydrates) into fuel (glucose), which the body uses to produce energy. A common sign of niacin deficiency is therefore fatigue. As a precursor of nicotinamide adenine dinucleotide (NAD), niacin can increase levels of NAD in cells. NAD is involved in the repair of DNA[2-3] and recently the mechanism of how NAD repairs DNA was discovered.
In the metabolism, NAD is a coenzyme involved in redox reactions, helping to move electrons from one reaction to another. NAD is found in two forms in cells: NAD+ is an oxidizing agent – it accepts electrons from other molecules and becomes reduced. This reaction forms NADH, which is then used as a reducing agent to donate electrons. These electron transfer reactions are the primary function of NAD, but NAD is involved in other cellular processes too. NAD is also associated with the sirtuins, which are closely linked to longevity in mammals.
Niacin is able to increase levels of good high-density lipoprotein (HDL) cholesterol that helps to remove the bad low-density lipoprotein (LDL) cholesterol[6-7]. This has historically led to niacin being used to control cholesterol levels in patients at risk of heart disease, hypercholesterolemia, or hyperlipidemia. It inhibits production of very-low-density lipoprotein (VLDL) in the liver and consequently its byproduct, LDL.
VLDL transports both triglycerides and cholesterol. Once in the circulation, VLDL is broken down, releasing triglycerides for energy use by cells or for storage in the adipose fat tissue. Once triglycerides are released from VLDL, its composition changes, and it changes into intermediate-density lipoprotein (IDL). Later, when the amount of cholesterol increases, IDL becomes LDL.
Niacin can raise HDL by as much as 30-35 percent. This effect is caused by a reduction of cholesterol transfer from HDL to VLDL and delayed clearance of HDL. The drug also lowers total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides, and lipoprotein. Whilst some studies dispute that niacin reduces risk factor for stroke or heart attack, a number of clinical trials have been conducted that suggest otherwise.
The CLAS study – a two-part, randomized, placebo-controlled, angiographic trial testing – combined colestipol-niacin therapy in 162 subjects . Two-year results (CLAS-I) showed a decreased progression of atherosclerosis and an increased regression. A subgroup of 103 subjects were treated for four years (CLAS-II). Changes in blood lipid, lipoprotein-cholesterol, and apolipoprotein levels were maintained, and at four years significantly more drug-treated subjects demonstrated non-progression (52% drug- vs 15% placebo-treated) and regression (18% drug- vs 6% placebo-treated) in native coronary artery lesions.
Significantly fewer drug-treated subjects developed new lesions in native coronary arteries (14% drug- vs 40% placebo-treated) and bypass grafts (16% drug- vs 38% placebo-treated). These results confirm the CLAS-I findings and indicate that regression can continue for at least four years.
The HATS study looked at niacin plus simvastatin and antioxidant-vitamin therapy alone and together compared with a placebo, in patients with coronary disease and low HDL cholesterol levels. The anti-oxidant therapy was composed of vitamin E, 1000 mg of vitamin C, 25 mg of natural beta-carotene, and 100 μg of selenium. Simvastatin plus niacin provided marked a clinical and angiographically measurable benefits on coronary artery blockages compared with antioxidant vitamin therapy and the placebo.
However, more recent studies suggest that niacin increases blood glucose levels. Thus, it has been suggested that it may contribute to new-onset diabetes. A meta-analysis was made of 11 randomized trials conducted to confirm whether or not a link exists between niacin therapy and new-onset diabetes.
The trials were found by a search of the Cochrane database and EMBASE between the years 1975-2014. Inclusion criteria consisted of randomized controlled trials on niacin and its cardiovascular effects with 50 or more non-diabetic participants. This was conducted as a 2-armed study with a total of 26,340 participants; of these, 13,121 were assigned to the niacin therapy group and 13,219 were assigned to the control group.
Of the 26,340 total participants analyzed, 725 in the niacin group and 646 in the control group developed new-onset diabetes. The use of niacin was shown to be associated with a moderately increased risk of developing diabetes compared to a placebo.
Thus, there is some evidence to suggest that niacin supplementation could increase an individual’s risk of developing diabetes. This should be taken into consideration when weighing the pros and cons of beginning therapy with niacin. However, the cardiovascular benefits of niacin therapy may outweigh the risk of developing diabetes. You should consult your physician before taking niacin and it should not be used if you are already a diabetic.
This article is only a very brief summary, and is not intended as an exhaustive guide and is based on the interpretation of research data, which is speculative by nature. This article is not a substitute for consulting your physician about which supplements may or may not be right for you. We do not endorse supplement use or any product or supplement vendor and all discussion here is for scientific interest.
 Rader, J. I., Calvert, R. J., & Hathcock, J. N. (1992). Hepatic toxicity of unmodified and time-release preparations of niacin. The American journal of medicine, 92(1), 77-81.
 Kennedy, D. O. (2016). B vitamins and the brain: Mechanisms, dose and efficacy—A review. Nutrients, 8(2), 68.
 Kirkland, J. B. (2012). Niacin requirements for genomic stability. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 733(1), 14-20.
 Li, J., Bonkowski, M. S., Moniot, S., Zhang, D., Hubbard, B. P., Ling, A. J., … & Aravind, L. (2017). A conserved NAD+ binding pocket that regulates protein-protein interactions during aging. Science, 355(6331), 1312-1317.
 Brown G, Albers JJ, Fisher LD, et al. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. N Engl J Med. 1990;323:1289–98.
 Kamanna VS, Kashyap ML. Mechanism of action of niacin on lipoprotein metabolism. Curr Atheroscler Rep. 2000;2:36–46.
 Cashin-Hemphill L, Mack WJ, Pogoda JM, et al. Beneficial effects of colestipol-niacin on coronary atherosclerosis. A 4-year follow-up. JAMA. 1990;264:3013–7.
 Grundy, S. M., Mok, H. Y. L., Zech, L., & Berman, M. (1981). Influence of nicotinic acid on metabolism of cholesterol and triglycerides in man. Journal of lipid research, 22(1), 24-36.
 Illingworth, D. R., Stein, E. A., Mitchel, Y. B., Dujovne, C. A., Frost, P. H., Knopp, R. H., … & Greguski, R. A. (1994). Comparative effects of lovastatin and niacin in primary hypercholesterolemia: a prospective trial. Archives of internal medicine, 154(14), 1586-1595.
 Cashin-Hemphill, L., Mack, W. J., Pogoda, J. M., Sanmarco, M. E., Azen, S. P., & Blankenhorn, D. H. (1990). Beneficial effects of colestipol-niacin on coronary atherosclerosis: a 4-year follow-up. Jama, 264(23), 3013-3017.
 Brown, B. G., Zhao, X. Q., Chait, A., Fisher, L. D., Cheung, M. C., Morse, J. S., … & Frohlich, J. (2001). Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. New England Journal of Medicine, 345(22), 1583-1592.
 Goldie, C., Taylor, A. J., Nguyen, P., McCoy, C., Zhao, X. Q., & Preiss, D. (2016). Niacin therapy and the risk of new-onset diabetes: a meta-analysis of randomised controlled trials. Heart, 102(3), 198-203.