Niacin: No flush, No good.

More on niacin: No flush, no good

Several readers wrote in wanting to know more about why we don’t recommend no-flush niacin products. A little bit of background will help us explain.

The term niacin comes from nicotinic acid vitamin, but it’s used to refer to both nicotinic acid and a closely related molecule, nicotinamide. Both nicotinic acid and nicotinamide are necessary to prevent pellagra, a disease that causes skin inflammation, diarrhea, and dementia. After they were first discovered in the 1930s, nicotinic acid and nicotinamide were known for a time as the pellagra-preventing vitamins.

In the mid-1950s, researchers discovered that nicotinic acid — but not nicotinamide — was remarkably effective at lowering cholesterol and triglyceride levels. We talk about niacin having these good effects, partly because niacin appears on ingredient and nutrition labels, but strictly speaking, it’s just nicotinic acid that does.

Nicotinic acid — but again, not nicotinamide — also triggers the release of prostaglandins that cause flushing, a more severe and sometimes uncomfortable form of the blushing that occurs when we’re embarrassed. So researchers have looked for ways to chemically package nicotinic acid so it retains its cholesterol- and triglyceride-lowering effects but doesn’t turn people red-faced.

Inositol hexaniacinate looked like it might be the answer. It’s a combination of six molecules of nicotinic acid (thus hexaniacinate) and one molecule of inositol. The hope was that it would break down slowly so the nicotinic acid would hit the bloodstream gradually and not cause flushing.

Results in rabbits were promising. But in a number of trials conducted in people in the late 1970s, the compound had little, if any, effect on cholesterol. Other research has shown peak levels of nicotinic acid in the blood from inositol hexaniacinate were a tiny fraction of those seen after a person took crystalline or sustained-release forms of niacin.

The niacin in every no-flush product we’ve seen comes as inositol hexaniacinate. The no-flush claim is true enough, but the credible evidence we know of suggests that you aren’t likely to see the cholesterol or triglyceride benefits, either. For a niacin product to have an effect on cholesterol and triglyceride levels, the niacin must be in the form of nicotinic acid — not inositol hexaniacinate or nicotinamide.

Vitamin B-3, Popcorn and Recovery

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.

Vitamin B-3 Therapy Reports

The Vitamin B-3 Therapy-2nd Communication

The Vitamin B-3 Therapy-3rd Communication

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.

Nicotine, Niacin and Double Vision

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.