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Nicotinamide adenine dinucleotide (NAD) is defined as a coenzyme that plays a central role in energy-producing pathways within cells. It exists in reduced form as NADH, which is naturally fluorescent and can be used to investigate the redox state in living tissues.
AI generated definition based on: Free Radical Biology and Medicine, 2016
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2020, Textbook of Natural Medicine (Fifth Edition) John Nowicki ND, ... Mark Dreher PhD
Nicotinamide adenine dinucleotide (NADH), the active coenzyme form of vitamin B 3, has been shown to be effective in countering the negative effects of jet lag on cognition and wakefulness.51 It is also known to encourage energy production through increased ATP generation. One small trial of NADH found a beneficial effect and improvement in quality of life in patients with CFS. This study supplemented the stabilized oral absorbable form in a 26-subject randomized, double-blind, placebo-controlled crossover study. Subjects were randomly assigned to receive either 10 mg of NADH or placebo for 1 month. After a 1-month washout period without supplement, subjects were then crossed to the alternate regimen for a final 1-month period. Within this cohort of 26 patients, 8 of 26 (31%) responded favorably to NADH, in contrast to 2 of 26 (8%) to placebo. No severe adverse effects were observed related to NADH,52 nor have studies in animals shown any toxicity, even at megadoses.53 More clinical research is necessary to fully elucidate the possible beneficial effects of NADH in patients with CFS.
2022, International Review of Cell and Molecular Biology Sebastian J. Hofer, ... Oliver Kepp
Nicotinamide-adenine dinucleotide (NAD+/NADH) is a universal coenzyme central to cellular metabolism. Via its donor and acceptor function of electrons, it is critically involved in redox reactions throughout all eukaryotic cells, acting on various enzymes, including sirtuins and poly ADP-ribose polymerase 1 (Covarrubias et al., 2021). Parallel to de novo synthesis, several precursors of NAD+, including nicotinic acid (niacin), nicotinamide riboside (NR), nicotinamide mononucleotide (NMN) and niacinamide, best known as nicotinamide (NAM), are vital for human NAD+ metabolism and an indispensable part of the human diet (Hofer et al., 2021a). These precursors are collectively known as vitamin B 3 and can be converted to NAD+ in the body (Canto, 2022). Numerous recent studies reported lifespan-prolonging and broad health-promoting effects of NAD+ precursors supplementation in pre-clinical models of metabolic and age-associated diseases (Abdellatif et al., 2021; Chi and Sauve, 2013; Covarrubias et al., 2021; Katsyuba et al., 2020; Zapata-Perez et al., 2021).
Dietary intake of NAD+ precursors is estimated at ∼20–40 mg niacin equivalents (NE) per day (NE includes NAD+ precursors and tryptophan, which can be converted to niacin), obtained from both animal- and plant-based foods (Hofer et al., 2021a). All precursors are absorbed in the intestinal tract and feed into the NAD metabolism (Bogan and Brenner, 2008). Recent pre-clinical and clinical trials have shown that precursor supplementation is sufficient to increase NAD levels (Blanco-Vaca et al., 2021; Conze et al., 2019; Trammell et al., 2016) and that niacin, NR and NAM are generally safe for application in humans at relatively high doses (Knip et al., 2000; MacKay et al., 2012). Interestingly, higher dietary intake of NAD+ precursors is linked to improved cardiovascular function and reduced mortality risk (Abdellatif et al., 2021), lower hepatocellular carcinoma risk (Antwi et al., 2020) and a statistical trend toward lower liver cancer (Zhang et al., 2012). A deficiency of dietary niacin intake causes the pellagra disease (Carpenter, 1983), which nowadays is rare in Westernized regions. However, sub-clinical deficiency of dietary NE intake might be oncologically relevant. Some epidemiological studies associate diets low in tryptophan or nicotinamide with increased occurrence of esophageal, oral, or intestinal cancers (Surjana et al., 2010). Likewise, it has been suggested that many cancer patients are at risk for niacin deficiencies (Dreizen et al., 1990; Inculet et al., 1987).
Along these premises, supplementations of NAD+ precursors have been extensively studied in rodents, showing low toxicity and favorable tolerability, prompting numerous clinical trials against various ailments (Katsyuba et al., 2020). NAM does not induce carcinogenesis in mice, even at high doses and when administered lifelong (Toth, 1983). Instead, supplementation with nicotinic acid or NAM caused growth inhibition and reduced metastasis in different mouse cancer models (Santidrian et al., 2013). Several studies suggest a broad pre-clinical anticancer potential of NAM via different application routes and against various tumor models in mice and rats (Buque et al., 2021; Surjana et al., 2010). Moreover, NAD+ precursors might be viable options to support chemotherapeutic treatments. NAM synergized the anticancer effects of gemcitabine against mouse pancreatic cancer models via increased T cell
