Common Names

  • Vitamin H
  • Coenzyme R
  • D-Biotin
  • W Factor

For Patients & Caregivers

How It Works

Biotin may help strengthen brittle nails and improve peripheral neuropathy in diabetics.

Biotin is an important coenzyme involved in carbohydrate (sugar) and lipid (fat) metabolism. It is made in the intestines and is found in a variety of foods. Consuming large amounts of egg whites or taking anticonvulsant (antiepileptic) drugs may lead to biotin deficiency, although this is rare. Patients with diabetes may have a greater chance of being biotin deficient. However, supplementation may weaken the activity of interleukins and interferons, and reduce the number of white blood cells.

Purported Uses

  • To treat diabetic peripheral neuropathy
    A small clinical study supports this claim. Larger studies are needed to confirm the effects.
  • To treat brittle nails
    A small survey indicates that biotin may be effective. Further studies are needed.
  • To treat infantile seborrheic dermatitis (a skin disorder prevalent in the oily areas of the skin, resulting in itchy, scaly skin)
    A small randomized trial showed that biotin is no more effective than placebo in treating seborrheic dermatitis in infants.

Patient Warnings

  • Ingestion of large amounts of raw egg whitesand long-term anticonvulsant therapy can induce biotin deficiency.

Do Not Take If

  • You are a long term user of anticonvulsant drugs: They may accelerate biotin catabolism, which can cause biotin deficiency.

Side Effects

  • Eosinophilic pleuropericardial effusion (inflammation and filling of the lining around the heart and lungs with fluid) was reported in a woman who took biotin along with Vitamin B5.
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For Healthcare Professionals

Scientific Name

Cis-hexahydro-2-oxo-1H-thieno[3,4-d]-imidazole-4-valeric acid

Clinical Summary

An important coenzyme in carbohydrate and lipid metabolism, biotin has been claimed to treat brittle finger nails, acne, seborrhoeic dermatitis, hair fragility, and alopecia. Infants who died from sudden infant death syndrome (SIDS) were found to have significantly lower levels of biotin in their livers; however, evidence that biotin deficiency contributes to SIDS is lacking (1). Deficiency of biotinidase, an enzyme that converts biotin into its active form, has been implicated in myelopathy (13), epileptic encephalopathy (14), and spastic tetraparesis (15) in children.

A small randomized controlled trial showed that biotin was no more effective than placebo in the treatment of seborrheic dermatitis in infants (2).

Biotin supplementation may be effective in strengthening brittle nails (3). Preliminary data also suggest that biotin may have beneficial effects in patients with severe diabetic peripheral neuropathy (4), and when combined with chromium, it may be effective as an adjunct therapy to improve glycemic control in patients with type 2 diabetes (5).

Food Sources

Liver, kidney, eggs, soy beans, peanuts, wholegrain cereals, and dairy products.

Purported Uses

  • Acne
  • Alopecia
  • Brittle nails
  • Diabetic neuropathy
  • Infantile seborrheic dermatitis
  • Thyroid disorder

Mechanism of Action

Biotin is an essential part of carbohydrate and lipid metabolism via transporting carboxyl units and fixing carbon dioxide. It is commonly found in a wide variety of foods. Biotin is converted into the active form by an enzyme, biotinidase. It is also synthesized in the intestine by bacteria. Patients who are deficient in biotinidase or those with malabsorption syndromes may develop biotin deficiency. Although biotin deficiency is rare, symptoms include anorexia, nausea, vomiting, dermatitis, somnolence, seizures, ataxia, and increase in serum cholesterol levels and bile pigments (1).

Biotin may also be deficient, inactive, or unavailable in patients with diabetes. Therefore, it is suggested that biotin supplementation may be effective against diabetic peripheral neuropathy (4); biotin induces microtubule formation in neurons (7), and biotin deficiency slows myelination (8).

However, biotin supplementation may reduce the activity of interleukins and interferons, and reduce the number of leukocytes (9).


  • Ingestion of large amounts of raw egg whites (1) and long-term anticonvulsant therapy (11) can induce biotin deficiency.

Adverse Reactions

  • Eosinophilic pleuropericardial effusion was reported in a woman following concomitant use of biotin and pantothenic acid (vitamin B5(6).

Herb-Drug Interactions

Long term use of certain anticonvulsant drugs may accelerate biotin catabolism, which can theoretically cause biotin deficiency (11).

Herb Lab Interactions

  • Free Thyroxine (FT4): There is a report of a false high FT4 in an assay by the Boehringer Mannheim ES 700 analyzer attributed to high serum biotin levels in a neonate (12).
  • Thyroid Stimulating Hormone (TSH): There is also a report of a false low TSH in an assay by the Boehringer Mannheim ES 700 analyzer attributed to high serum biotin levels in a neonate (12).

Dosage (OneMSK Only)


  1. Mason P. Dietary Supplements. London: Pharmaceutical Press; 2001.

  2. Hochman LG, Scher RK, Meyerson MS. Brittle nails: response to daily biotin supplementation. Cutis 1993;51:303-5.

  3. Koutsikos D, Agroyannis B, Tzanatos-Exarchou H. Biotin for diabetic peripheral neuropathy. Biomed.Pharmacother. 1990;44:511-4.

  4. Debourdeau PM, et al. Life-threatening eosinophilic pleuropericardial effusion related to vitamins B5 and H. Ann.Pharmacother. 2001;35:424-6.

  5. Braguer D, Gallice P, Yatzidis H, et al. Restoration by biotin of the in vitro microtubule formation inhibited by uremic toxins. Nephron. 1991;57(2):192-196.

  6. Said HM, Redha R, Nylander W. Biotin transport in the human intestine: inhibition by anticonvulsant drugs. Am J Clin Nutr 1989;49:127-31.

  7. Mock DM, et al. Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. J Pediatr.Gastroenterol.Nutr 1998;26:245-50.

  8. Singhi P, Ray M. Ohtahara syndrome with biotinidase deficiency. J Child Neurol. 2011 Apr;26(4):507-9.

  9. Komur M, Okuyaz C, Ezgu F, Atici A. A girl with spastic tetraparesis associated with biotinidase deficiency. Eur J Paediatr Neurol. 2011;5(6):551-3.

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