Our need for biotin, a member of the vitamin B complex, was first demonstrated in 1942 in a rather unpalatable way. A deficiency was induced in a group of adult volunteers by feeding them generous amounts of a common substance containing avidin, a carbohydrate complex that ties up biotin and prevents the body from absorbing it. The substance? Raw egg whites, served in quantity.
Within three to four weeks the volunteers developed symptoms similar to ones that had been observed in animals 15 years earlier. The so-called "egg white injury" produced a scaly dermatitis and a striking grayish pallor, followed by changes in mental state, loss of appetite and nausea. Remarkably, therapeutic doses of biotin totally reversed all symptoms within three to five days.
Before this experiment, there were two reasons why biotin deficiency had been so difficult to identify. First, the vitamin occurs in many foods, especially liver, kidney, legumes, nuts, egg yolk (cooking eggs alters the avidin so that it cannot bind up biotin), and some vegetables.
Second, the bacteria in our bodies synthesize significant amounts of biotin, which we then absorb and use. Both because the amounts in body fluids are so small, and because its importance is similarly difficult to quantify, it is only in the most recent edition of the Recommended Dietary Allowance (RDA) that a "safe and adequate" range of intake -- a minuscule 100 to 200 micrograms a day -- was established.
Biotin is an essential component, or "cofactor," in certain enzymes the body uses in carbohydrate and fat metabolism. It acts to lengthen carbon chains, serving as a kind of shuttle to carry carbon-containing fragments from one site to another. And biotin is important in the metabolism of certain amino acids. Given these many roles, it is not surprising that severe symptoms develop when ample amounts are unavailable for basic body reactions.
Until fairly recently, reports of spontaneous biotin deficiency had been limited to rare cases involving excessive consumption of raw egg whites. In these situations, some 30 percent of the individual's total calories came from egg white.
In the 1960s, however, a new technique of intravenous feeding was introduced making it possible to nourish patients completely by vein. Total parenteral nutrition is used for individuals who cannot absorb adequate nutrients through the gastrointestinal tract because of surgery or illness. (Examples include severe gastrointestinal diseases, serious burns or tissue damage from radiation.)
The ability to sustain patients in this way for extended periods has highlighted the need for supplemental biotin in certain unusual circumstances. The vitamin is thought to be absorbed in the upper part of the small bowel. Patients who undergo small bowel resection, or surgical removal of diseased bowel, lose some of the intestinal area necessary for the nutrient to be absorbed. If they then receive antibiotics, which significantly reduce the bacterial population of the intestine, they may be at risk of a biotin deficiency.
In fact, such a deficiency has been documented in several patients maintained on long-term total parenteral nutrition (TPN). Since microbial sources generally provide adequate amounts of this nutrient, biotin has not been routinely added to these specialized solutions, which aim to satisfy all nutritional needs.
These patients lost excessive amounts of body hair after receiving TPN for anywhere from 5 to 19 months. When biotin was added to the solution, healthy hair growth was restored.
The vast majority of Americans who eat normally and possess intact gastrointestinal tracts have no need to focus nutritional concern on biotin. And contrary to the message perennially put forth by certain late-night television commercials and newspaper advertisements, biotin does not offer the ultimate antidote to baldness. Nothing could be further from the truth. Hair loss in mice made experimentally deficient in biotin is unrelated to the gradual falling out of human hair that is part of the normal aging process.