William Griffith Wilson, or Bill W., is regarded as the father of addiction treatment due to his leadership in establishing Alcoholics Anonymous. While Bill W. pioneered a movement that has helped millions achieve sobriety, in the final years of his life, he explored how alternative treatment methods, such as Niacin (a precursor to NAD Therapy), could improve the recovery process.
Why does it work? What is it working on?
Skin flushing is one major side effect of the therapeutic use of nicotinic acid and the primary reason for non-adherence to treatment. Flushing is caused by the activation of phospholipase A2, an enzyme that stimulates the production of a specific lipid from the prostanoid family called prostaglandin D2. Prostaglandin D2, synthesized by antigen-presenting cells of the skin and mucosa (i.e., the Langerhans cells), can induce the dilation of blood vessels and trigger a flushing response. ~LINK
ANTIGEN: a toxin or other foreign substance which induces an immune response in the body, especially the production of antibodies.
Linus Pauling Institute – NIACIN Deficiency – Got [pop]Corn?
The late stage of severe niacin deficiency is known as pellagra. Early records of pellagra followed the widespread cultivation of corn in Europe in the 1700s. The disease is generally associated with poorer social classes whose chief dietary staple consisted of cereal like corn or sorghum. Pellagra was also common in the southern United States during the early 1900s where income was low and corn products were a major dietary staple. Interestingly, pellagra was not known in Mexico, where corn was also an important dietary staple and much of the population was also poor. In fact, if corn contains appreciable amounts of niacin, it is present in a bound form that is not nutritionally available to humans. The traditional preparation of corn tortillas in Mexico involves soaking the corn in a lime (calcium oxide) solution, prior to cooking. Heating the corn in an alkaline solution results in the release of bound niacin, increasing its bioavailability. Pellagra epidemics were also unknown to Native Americans who consumed immature corn that contains predominantly unbound (bioavailable) niacin.
Niacin deficiency or pellagra may result from inadequate dietary intake of NAD precursors, including tryptophan. Niacin deficiency — often associated with malnutrition — is observed in the homeless population, in individuals suffering from anorexia nervosa or obesity, and in consumers of diets high in maize and poor in animal protein. Deficiencies of other B vitamins and some trace minerals may aggravate niacin deficiency. Malabsorptive disorders that can lead to pellagra include Crohn’s disease and megaduodenum. Patients with Hartnup’s disease, a hereditary disorder resulting in defective tryptophan absorption, have developed pellagra. Carcinoid syndrome, a condition of increased secretion of serotonin and other catecholamines by carcinoid tumors, may also result in pellagra due to increased utilization of dietary tryptophan for serotonin rather than niacin synthesis. Further, prolonged treatment with the anti-tuberculosis drug isoniazid has resulted in niacin deficiency. Other pharmaceutical agents, including the immunosuppressive drugs azathioprine(Imuran) and 6-mercaptopurine, the anti-cancer drug 5-fluorouracil (5-FU, Adrucil), and levodopa/carbidopa (Sinemet; two drugs given to people with Parkinson’s disease), are known to increase the reliance on dietary niacin by interfering with the tryptophan-kynurenine-niacin pathway. Finally, other populations at risk for niacin deficiency include dialysis patients, cancer patients, individuals suffering from chronic alcoholism, and people with HIV (see HIV/AIDS below). Further, chronic alcohol intake can lead to severe niacin deficiency through reducing dietary niacin intake and interfering with the tryptophan-to-NAD conversion.