Niacin is a vitamin B3 which is essential to proper cell functioning. It is involved in energy metabolism as part of reduction/oxidation coenzymes, metabolism of amino acids, as well as in detoxification reactions for drugs and other substances. It also represents an important therapeutic option for several conditions.
Lack of niacin can result in a disease called pellagra. This condition was common throughout human history, namely among impoverished people whose diet consisted almost entirely of corn products. Such diet lacked adequate amounts of niacin, triggering in turn symptoms such as diarrhea, inflamed mucous membranes, skin sores, weakness, irritability and mental delusions.
Niacin is a colorless, water-soluble derivative of pyridine, with a carboxyl group found at the 3-position. It comes in several forms – namely nicotinic acid (pyridine-3-carboxylic acid) and nicotinamide (nicotinic acid amide), but there are also some other derivatives that exhibit the biological activity of nicotinamide as well (such as inositol hexanicotinate).
Due to the same biochemical activity, the terms niacin, vitamin B3, nicotinic acid or nicotinamide are often used interchangeably. In the human body, nicotinic acid and its derivative nicotinamide are converted to NAD and NADP. These chemicals are coenzymes necessary for hundreds of oxidation-reduction redox reactions, which are essential sources of energy for a myriad of cellular functions.
NAD is necessary for DNA synthesis, and it is also involved in transferring chemical components to proteins. Such transfers can be catalyzed by the structures called PARPs (poly-ADP-ribose-polymerases), which regulate the transfer of ADP-ribose units from NAD to proteins. An ongoing research explores all the functions of niacin, PARPs and their mutual interplay in health and disease.
Niacin has a plethora of beneficial effects for the human organism, especially regarding the metabolism of cholesterol and lipoproteins. There is a lot of evidence on how niacin improves lipid profiles and reduces vascular disease, which prompted its use in the treatment of cardiovascular diseases.
It has been repeatedly shown that niacin lowers triglycerides and low density lipoproteins (LDL, one of the “bad” cholesterols) and raises high density lipoproteins (HDL, also known as the “good” cholesterol), with a subsequent effect on plaque and thickness of arterial walls. It also decreases the plasma concentration of lipoprotein A, which plays an independent role in the development of coronary heart disease.
Much of the aforementioned changes take place in the liver and influence the way this organ handles cholesterol, triglyceride and lipoprotein metabolism. Niacin inhibits a specific liver enzyme involved in the synthesis of triglycerides, thus resulting in lower levels of triglycerides. It also lowers the expression of another liver chemical (beta-chain of ATP synthase), which increases HDL levels by decreasing its breakdown.
Some studies have reported several non-lipoprotein mediated effects of niacin with an effect on atherosclerosis progression and risk. In addition to the favorable lipoprotein modulating effects of niacin, study of the pharmacology and mechanisms of action of have revealed anti-inflammatory effects in macrophages, adipocytes and vascular endothelium.
Niacin also lowers the expression of cytokines involved in the building up of cholesterol-filled plaque in arterial walls. Restraint of immune cell infiltration of the vessel wall mediated by GPR109A (a receptor for niacin and the commensal metabolite butyrate) also retards atherogenesis in the absence of significant lipid changes.