Nicotinamide is an amide of vitamin B3. Enrichment of diet with nicotinamide in the West was introduced in the 1940s to prevent the dietary deficiency disorder Pellagra. Pellagra was caused by a particular form of poor vegetarian diet leading to Nicotinamide and Tryptophan deficiency. Nicotinamide is available in two supplements, MultiVit-Rx, a potent daily multivitamin, and Vitamin-B-Coenzyme. You may consider subscribing to a FREE supplement NEWSLETTER.

Nicotinamide and Aging
Since the beginning of the last century, seminal discoveries have identified pyridine nucleotides as the major redox carriers in all organisms. Recent research has unravelled an unexpectedly wide array of signalling pathways that involve nicotinamide adenine dinucleotide (NAD) and its phosphorylated form, NADP. NAD serves as substrate for protein modification including protein deacetylation, and mono- and poly-ADP-ribosylation. Both NAD and NADP represent precursors of intracellular calcium-mobilizing molecules. It is now beyond doubt that NAD(P)-mediated signal transduction does not merely regulate metabolic pathways, but might hold a key position in the control of fundamental cellular processes.

Nicotinamide and Alcohol
Nicotinamide protects the developing mouse brain from some of the deleterious effects of ethanol. Researchers investigated whether the nutrient nicotinamide could prevent the neurotoxic effects of ethanol exposure in the postnatal brain of mice and analyzed whether inhibition of ethanol-induced apoptotic neuronal death could prevent behavioral impairment in adult mice. The brain-growth spurt that occurs in the 7-day postnatal period in mice correlates with neural development that takes place in the third trimester in humans. Seven-day-old mice injected with ethanol showed a 15- to 20-fold increase of cleaved caspase-3 and widespread apoptotic neural cell death in the forebrain. However, administration of nicotinamide significantly reduced caspase-3 activation. Nicotinamide treatment 0, 2, 4, or 8 hours after ethanol administration prevented activation of caspase-3, with the strongest effect observed when nicotinamide was administered between 0 and 2 hours after ethanol exposure. Sourcer: PLoS Medicine, 2006.

Nicotinamide and Multiple Sclerosis
Boosting concentrations in the nervous system of a vital compound called NAD, by giving its chemical precursor, nicotinamide has shown considerable therapeutic potential in a mouse model of multiple sclerosis (MS). In mice with the MS-like disease EAE, nicotinamide treatment profoundly prevents the degeneration of axons already showing signs of degeneration. Daily under-the-skin injections of nicotinamide in the EAE mouse also prevents inflammation of the axons and loss of myelin -- the underlying problem in MS -- and delays the onset and severity of disability.
Nicotinamide had beneficial effects even when treatment was delayed until 10 days after the induction MS-like disease, when most of the animals had clear signs of neurologic disability, hinting that it may have an impact at later stages of MS. The Journal of Neuroscience, September 20, 2006.

nicotinamide adenine dinucleotide

Nicotinamide adenine dinucleotide phosphate
The increased expression and activity of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex has emerged as a major common factor in the cause of many forms of cardiovascular diseases since the upregulation of intravascular NADPH oxidase results in the formation of superoxide (O(2)(-)), which in turn promotes vascular damage. An ever-increasing number of drugs commonly used in cardiovascular medicine have been shown to influence NADPH oxidase expression and activity. These include nitric oxide donors, nitroaspirin, eicosanoids, phosphodiesterase inhibitors, corticosteroids, antioxidants, and specific inhibitors.