Alternative Medicine Review 2007 (Mar); 12 (1): 73–78 ~ FULL TEXT
Biotin is a water-soluble B vitamin that is an essential cofactor for four carboxylase enzymes, each of which catalyzes an essential step in intermediary metabolism. Because humans and other mammals cannot synthesize biotin, it must be derived from dietary sources and de novo synthesis by intestinal bacteria. Biotin was originally recognized when rats fed protein derived from egg whites developed severe dermatitis, hair loss, and neuromuscular dysfunction. A growth factor found in liver, then called “Protective Factor X,” cured the condition; this growth factor is now known as biotin. It was later discovered that uncooked egg whites contain a glycoprotein, avidin, that binds to biotin and prevents its absorption, whether biotin is from the diet or from intestinal bacterial synthesis.  Besides genetic inborn errors of metabolism, biotin deficiency can occur during extended parenteral nutrition, pregnancy, or long-term anticonvulsant therapy. Conditions that may benefit from biotin supplementation include dyslipidemia, brittle nails, diabetes, dermatitis, and candidiasis.
Biotin deficiency in humans is rare and generally associated with extended parenteral nutrition, consumption of large quantities of raw egg whites, severe malnutrition, or inborn errors of metabolism (e.g., biotinidase deficiency, multiple carboxylase deficiency).
Studies of biotin status during pregnancy suggest marginal biotin deficiency, occurring in a significant number of otherwise normal pregnancies, may be teratogenic.  One study found 50 percent of pregnant women had increased urinary excretion of 3-hydroxyisovaleric acid
(a reflection of biotin deficiency) that was reversed by supplementation of 300 mcg biotin for 14 days.  Individuals on long-term anticonvulsant therapy are also at high risk for a biotin deficiency (see Drug-Nutrient Interactions below). Signs and symptoms of severe biotin deficiency include erythematous skin lesions, vomiting, seizures, developmental delay, hypotonia, and ataxia.  One study found 3-hydroxyisovaleric acid to be the most reliable urinary indicator of biotin deficiency; urinary 3-hydroxypropionic acid and methylcitric acid
were not as reliable.  The most sensitive indicator of a biotin deficiency, reliably detecting even a marginal deficiency, appears to be measurement of lymphocyte propionyl-CoA carboxylase activity.