In vitro (cell culture) studies provide evidence that vitamin B3 (niacin) coenzyme NAD content influences the cellular response to DNA damage, an important risk factor in cancer development (4, 5, 6).

 

However, little is known regarding cellular NAD levels and the prevention of DNA damage or cancer in humans (7, 8). Neither the cellular NAD content nor the dietary intake of NAD precursors (niacin and tryptophan) necessary for optimizing protective responses following DNA damage has been determined.

 

Research on biochemical and cellular aspects of DNA repair has stimulated an interest in the relationship between vitamin B3 (niacin) intake and cancer risk in human populations (9). A large case-control study found increased consumption of niacin (5.2–6.2 mg), along with antioxidant nutrients, to be associated with about a 40% decreased incidence of oral (mouth), pharyngeal (throat), and esophageal cancers (10, 11).

 

Insulin-dependent diabetes mellitus (IDDM)

Insulin-dependent diabetes mellitus in children, often called ‘type I diabetes’, is known to result from the autoimmune destruction of insulin-secreting cells in the pancreas. Evidence from in vitro and animal research indicates that high levels of vitamin B3 (nicotinamide) protect insulin-producing pancreas cells from inflammatory white blood cells and reactive oxygen species. Thus, nicotinamide might help to delay the onset of insulin dependence in individuals with type 1 diabetes.

 

An analysis of ten published trials, including five randomized placebo-controlled trials, found evidence of improved insulin-producing cell function after one year of treatment with vitamin B3 (nicotinamide), but the analysis failed to find any clinical evidence of improved blood glucose (‘glycemic’) control (12).

 

Unlike nicotinamide, nicotinic acid has not been found effective in the prevention of type 1 diabetes.