Niacinamide (nicotinamide) is one of the two principal forms of the B‐complex vitamin niacin (see Niacin). The term niacin is used as a collective term to refer to both nicotinamide and nicotinic acid, the other principal form of niacin, or the term is used synonymously with nicotinic acid. Nicotinamide and nicotinic acid have identical vitamin activities, but they have very different pharmacological activities. 

Niacinamide is a component of two related coenzymes—nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). The principle function of these enzymes is to facilitate oxidation and reducing reactions in the form of dehydrogenases. 

Nicotinamide, via its major metabolite NAD++ (nicotinamide adenine dinucleotide), is involved in a wide range of biological processes including the production of energy, the synthesis of fatty acids, cholesterol and steroids, signal transduction, and the maintenance of the integrity of the genome. Nicotinic acid, in pharmacological doses, is used as an antihyperlipidemic agent. It also causes vasodilatation of cutaneous blood vessels resulting in the so‐called niacin flush. Nicotinamide in pharmacological doses does not have antihyperlipidemic activity, nor does it cause a niacin‐flush. There is evidence, however, that pharmacological doses of nicotinamide may help prevent type 1 diabetes mellitus. Pyrazinamide, an important drug in the treatment of tuberculosis, is an analogue of and shares the same biochemical mechanism with nicotinamide. 

Although niacinamide shares some characteristics of niacin, it has unique nutritional and pharmacological properties of its own. The niacinamide form of B3 is literally required in hundreds of enzymatic reactions in the human body. Research has demonstrated its remarkable benefits for arthritis, asthma, diabetes, heart disease, stress, stroke, and recently as an anti‐aging nutrient. 

The traditional medical use of both forms of B3 is to treat the vitamin deficiency syndrome known as pellagra, a disease that occurs frequently among people who subsisted mainly on corn (maize). After the Spanish introduced corn to Europe, a condition began to be observed which was first called ‘Mal de la Rosa’ (redness of the rose) because of the red skin lesions frequently seen — one of the hallmarks of pellagra. In Italy, the condition was called pellagra, which meant rough skin. The name Pellagra was introduced into medical literature in 1771 by Frapoli. 

Full‐blown pellagra is a chronic wasting disease associated with dermatitis, dementia and diarrhea (the three Ds). Early symptoms include weakness, lassitude, anorexia, and indigestion. Mental changes include fatigue, insomnia, and apathy, which precede encephalopathy, characterized by confusion, disorientation, hallucination, loss of memory and frank organic psychosis. 

Niacinamide is usually absorbed only in the small intestine, while nicotinic acid is absorbed in the stomach as well. Both niacinamide and nicotinic acid are present in blood plasma and are converted to the coenzyme form in the blood cells, kidney, brain and liver. Although niacinamide can be converted to nicotinic acid, there is no direct conversion back to niacinamide. Niacinamide is water soluble, and the body does not store a significant amount. Most of niacinamide is present in the tissues in the form of nicotinamide as NAD and NADP. Niacinamide converts twice as readily to NAD/NADP as does niacin. Tryptophan metabolism provides about two thirds of the nicotinamide the body utilizes (Fig. 1). A non‐redox function involves transfer of the coenzyme to macromolecules that attach to ribosomes in mitochondria and in the nucleus where it affects the activity of DNA. The non‐redox function is thought to account for the rapid turnover of NAD in the body.

Benefits of Niacinamide: 

Nicotinamide, unlike nicotinic acid, does not have significant effects on lipids, but it has been shown to be useful for some with type 1 (insulin‐dependent) diabetes. There is preliminary evidence showing that it might help individuals with generalized granuloma annular and osteoarthritis. There is little evidence that it is helpful in rheumatoid arthritis, schizophrenia or tinnitus. It has been suggested that it might aid in some cancer therapies. 

Nicotinamide is being investigated as an agent for the possible prevention or delaying of the onset of type 1 diabetes mellitus (insulin‐dependent diabetes mellitus or IDDM). The rationale for using nicotinamide in the prevention of type 1 diabetes mellitus is derived from human and animal studies as well as in vitro investigations. 

Nicotinamide has been found to prevent diabetes in alloxan‐ and streptozotocin‐treated mice and rats and in non‐obese diabetic (NOD) mice. In vitro studies have shown that nicotinamide can prevent macrophage‐ orinterleukin‐1beta‐induced beta‐cell damage. An intervention study in New Zealand using nicotinamide treatment showed a 50 reduction in the development of IDDM over a five‐year period. However, the use of nicotinamide in connection with diabetes is at best experimental. 

Nicotinamide has been shown to have antioxidant activity. In vitro, it has been found to inhibit protein oxidation and lipid peroxidation. It has also been found to inhibit reactive oxygen species‐induced apoptosis, to inhibit phagocytic generation of reactive oxygen species, to scavenge reactive oxygen species and to inhibit the oxidative activity of nitric oxide. Nicotinamide has demonstrated a number of anti‐inflammatory activities. Nicotinamide has been shown to inhibit lipopolysaccharide‐induced TNF‐alpha in mice, in a dosedependent manner. It is thought that this inhibition of TNF‐alpha is mediated via inhibition, at the gene transcription level, of NF‐Kappa B, which in turn inhibits TNFalpha. Nicotinamide has also been shown to decrease the production of IL‐12 and TNFalpha in cultures of whole blood from prediabetic and diabetic subjects and also in healthy subjects. 

Dosage and Administration: 

Typical supplemental dosage ranges from 20 to 100 milligrams daily. Pre‐ and postnatal vitamin/mineral supplements typically deliver a dose of 20 milligrams daily. Most people need more especially if illness is present related to circulatory or cardiovascular issues including elevated cholesterol. The correct dosage for Cholest, Niacinamide B3 and NAC are on the labels. A patient may be tested monthly by their health provider for dosage change. 

“Our new Cholest Orthomolecular product was formulated to make a major improvement in your Cardiovascular health.” 

Gene Silencing and Anti­Aging:

Genes and gene therapy are proving to be a powerful tool in the latest frontier in the fight against aging. Genes are actually a small part of the DNA structure and cellular differentiation depends on not only gene expression but also on gene silencing. In other words, which genes are ‘expressed’ determines the cell purpose and activity. Recent research has identified genes that influence longevity. In particular, a gene labeled, Sir2, for silent information regulator 2, has been shown to produce a protein, Sir2p, that extends cell life. Recent research has shown that Sir2p is a NAD‐dependent histone deacetylase that connects metabolism, gene silencing, and cellular life extension (Imai, et.al. 2000). Niacinamide, by increasing NAD, enhances Sir2p activity. 

Caloric restricted diets have long been known for their ability to extend the lifespan by slowing metabolism. NAD is essential in cellular metabolism. It was proposed by MIT researchers that by slowing metabolism NAD is spared, thereby enhancing Sir2p activity. Increasing intracellular NAD not only mimics the metabolic benefits of calorie restricted diets, but also helps maintain a balance of silent and active genes. 

Better for Arthritis than NSAIDS:

Niacinamide has been known for over fifty years for its benefit in the treatment of arthritis. Niacinam