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Biotin

Biotin, also known as vitamin H or B7 and C10H16N2O3S (Biotin; Coenzyme R, Biopeiderm), is a water-soluble B-complex vitamin which is composed of an ureido (tetrahydroimidizalone) ring fused with a tetrahydrothiophene ring. A valeric acid substituent is attached to one of the carbon atoms of the tetrahydrothiophene ring. Biotin is important in the catalysis of essential metabolic reactions to synthesize fatty acids, in gluconeogenesis, and to metabolize leucine. more...

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General overview

Biotin is used in cell growth, the production of fatty acids, metabolism of fats, and amino acids. It plays a role in the Krebs Cycle, which is the process in which energy is released from food. Biotin not only assists in various metabolic chemical conversions, but also helps with the transfer of carbon dioxide. Biotin is also helpful in maintaining a steady blood sugar level. Biotin is often recommended for strengthening hair and nails. Consequently, it is found in many cosmetic and health products for the hair and skin.

Uses

Hair problems

Biotin supplements are often recommended as a natural product to counteract the problem of hair loss in both children and adults. However, there are no studies that show any benefit in any case where the subject is not actually biotin deficient. The signs and symptoms of biotin deficiency include hair loss which progresses in severity to include loss of eye lashes and eye brows in severely deficient subjects. Of note, shampoos that include biotin might be more effective if they were drunk instead of poured over the head as the absorption of biotin through the skin is limited (but drinking shampoo might cause other problems that would offset any hair growth benefit).

Cradle cap (seborrheic dermatitis)

Children with a rare inherited metabolic disorder called phenylketonuria (PKU; in which one is unable to break down the amino acid phenylalanine) often develop skin conditions such as eczema and seborrheic dermatitis in areas of the body other than the scalp. The scaly skin changes that occur in people with PKU may be related to poor ability to use biotin. Increasing dietary biotin in the diet has been known to improve seborrheic dermatitis in these cases.

Diabetes

People with type 2 diabetes often have low levels of biotin. Biotin may be involved in the synthesis and release of insulin. Preliminary studies in both animals and people suggest that biotin may help improve blood sugar control in those with diabetes, particularly type 2 diabetes.

Biotin deficiency

Biotin deficiency is a rare nutritional disorder caused by a deficiency of biotin. Biotin deficiency can have a very serious, even fatal, outcome if it is allowed to progress without treatment. Signs and symptoms of biotin deficiency can develop in persons of any age, race, or gender. Biotin deficiency rarely occurs in healthy individuals, since the daily requirements of biotin are low, many foods contain adequate amounts, intestinal bacteria synthesize small amounts, and the body effectively scavenges and recycles biotin from bodily waste. However, deficiency can be caused by excessive consumption of raw egg-whites over a long period (months to years). Egg-whites contain high levels of avidin, a protein that binds biotin stongly. Once a biotin-avidin complex forms, the bond is essentially irreversible. The biotin-avidin complex is not broken down nor liberated during digestion, and the biotin-avidin complex is lost in the feces. Once cooked, the egg-white avidin becomes denatured and entirely non-toxic.

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Biotin deficiency in pregnancy - Nutrition and Pregnancy
From Nutrition Research Newsletter, 4/1/02

It is suspected that a deficiency in biotin may be teratogenic in humans. The findings of two clinical studies suggest that a mild degree of biotin deficiency is common in normal pregnancy. Urinary excretion of 3-hydroxyisovaleric acid (3-HIA) increases as a result of the decreased activity of the biotin-dependent enzyme methylcrotonyl-CoA carboxylase. An increased urinary excretion of 3-HIA is an early and sensitive indicator of reduced biotin status. There is some speculation that the increased amount of 3-HIA observed during pregnancy may not reflect impaired biotin status, but may rather be the result of pregnancy itself.

A recent investigation evaluated the hypothesis that abnormal 3-HIA excretion reflects biotin deficiency and that biotin supplementation causes a decrease in 3-HIA excretion. Subjects included 26 healthy pregnant women with an average age of 30 years. The criteria for inclusion was: having an abnormally increased urinary excretion of 3-HIA (defined as having a 3-HIA to creatinine ratio of greater than 10.7 mmol/mol creatinine in an untimed urine sample). Five healthy, nonpregnant women were also studied to assess the effect of biotin supplementation on 3-HIA excretion in the absence of pregnancy. Subjects were randomly assigned to receive either a dose of 300 1g biotin supplement or a placebo. Women were studied either in early or late pregnancy. Complete 24-hour urine samples were collected on the day prior to initiating the intervention. The women then ingested either the placebo or the supplement for 14 days. On the last day of the supplementation, the subjects collected another 24-hour specimen.

For both the early-pregnancy and late-pregnancy groups, pretreatment urinary excretion of 3-HIA was not significantly different between the supplement and placebo subgroups. The urinary excretion of 3-HIA decreased significantly in all the subjects treated with biotin. However, 3-HIA excretion increased in the women receiving placebo. By the final day of supplementation, biotin excretion in the supplement group increased significantly and substantially.

It is concluded that increased excretion of 3-HIA seen in pregnancy does accurately reflect reduced biotin status. This poses concern regarding the potential human teratogenicity of biotin deficiency during pregnancy.

D. Mock, J. Quirk, N. Mock. Marginal biotin deficiency during normal pregnancy Am J Clin Nutr (75):295-299 (February, 2002). [Correspondence: DM Mock, Slot 516, Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, AR 72205. E-mail: mockdonaldm@uams.edu].

COPYRIGHT 2002 Frost & Sullivan
COPYRIGHT 2002 Gale Group

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