Vitamin B3 (Niacin)
Niacin is a water-soluble vitamin and is more chemically stable than thiamin or riboflavin. It exists in several forms, including nicotinic acid and niacinamide (nicotinamide). In the body, niacin functions as a coenzyme in many metabolic reactions, assisting enzymes involved in the breakdown and utilization of carbohydrates, fats, and proteins.
Niacin has historically been used to support circulation and to influence cholesterol metabolism. The amino acid tryptophan can be converted into niacin by the body, although this process is inefficient and depends on adequate intake of other nutrients. Diets high in refined sugar and starch increase metabolic demand and may contribute to depletion of niacin reserves.
At doses of approximately 100 mg or more, nicotinic acid commonly produces a flushing reaction characterized by warmth, redness, and tingling of the skin. Niacinamide does not produce this flush. Very high intakes of niacin, particularly doses of 2 grams per day or more, may cause liver toxicity. High doses can also precipitate or worsen gout by interfering with uric acid excretion. Because niacin stimulates gastric acid secretion, it is best taken with food.
Early niacin deficiency may present with muscle weakness, fatigue, loss of appetite, indigestion, skin eruptions, bad breath, small ulcers or canker sores, insomnia, irritability, nausea, vomiting, recurrent headaches, tender gums, and depression.
Severe deficiency results in pellagra, classically described by the “three Ds”: dermatitis, diarrhea, and dementia. Primary pellagra has historically occurred in populations where maize (corn) is a dietary staple. The niacin in untreated maize is bound and poorly absorbed unless the grain is processed with alkali, as in traditional tortilla preparation. Corn protein is also low in tryptophan, further contributing to deficiency. Pellagra has also been observed in populations consuming large amounts of millet, which is high in leucine and may interfere with niacin metabolism. Secondary pellagra can occur in chronic diarrhea, liver disease, and alcoholism.
Pellagra affects the skin, mucous membranes, gastrointestinal tract, and central nervous system. Cutaneous lesions are usually bilaterally symmetrical and may appear in several forms. Acute lesions begin with redness and progress to blistering, crusting, and peeling, often worsened by sun exposure. Intertriginous lesions may develop in skin folds with redness, maceration, and secondary infection. Chronic lesions may show thickened, pigmented, fissured skin over pressure points, or atrophic, dry, scaly skin that appears too large for the underlying tissue. Sun exposure may produce characteristic findings such as Casal’s necklace around the neck or butterfly-shaped facial lesions.
Mucous membrane involvement most commonly affects the mouth. Scarlet glossitis and stomatitis may begin at the tip and edges of the tongue and progress to involve the entire oral cavity, producing soreness, increased salivation, and tongue swelling. Ulcerations may develop, particularly beneath the tongue and along the lower lip.
Gastrointestinal symptoms include burning sensations in the mouth, throat, and esophagus, abdominal discomfort, bloating, nausea, vomiting, and diarrhea. In severe cases, diarrhea may become bloody due to inflammation and ulceration of the intestinal lining.
Central nervous system symptoms may include memory impairment, confusion, disorientation, and confabulation, as well as mood disturbances such as depression, excitement, mania, or delirium. Some individuals may develop paranoia. In advanced cases, an encephalopathic syndrome may occur, characterized by altered consciousness, rigidity of the limbs, and abnormal reflexes such as involuntary sucking or grasping.
