Brewer’s yeast, broccoli, cauliflower, cheese, corn, egg yolks, dairy products, fish, meat, peanuts, peas, soybeans, whole-grain cereal and other foods. Herbs rich in biotin include soybeans, garlic, American ginseng, oats, barley, Asian ginseng, avocado, cottonseed, alfalfa, sesame, corn, fava beans and elderberry.
Standardized supplements containing biotin including liquid multi-vitamin and mineral products, capsules and tablets and fortified foods.
– Aging Disorders
– Antibiotic Use
– Birth Defect Prevention
– Brain Functioning
– Fetal Development
– Hair Health Maintenance
– Hair Loss
– Heart Health Maintenance
– Hormone Balance
– Muscular Coordination
– Nervous Disorders
– Neurological Disorders
– Parkinson’s Disease
– Pregnancy-related Disorders
– Skin Disorders
– Vascular System Disorders
– Vitamin H Deficiency (RDA = 30 mcg/day)
Biotin, which is water soluble, is a member of the vitamin B family. It has also been called vitamin H. Biotin is a very important vitamin for good health. Biotin is a coenzyme involved in the synthesis and utilization of fats, glycogen and amino acids. It is particularly important for fetal and infant growth. Biotin deficiency is teratogenic (i.e. causes birth defects) in several mammalian species. Recent studies in humans have shown that marginal biotin deficiency occurs frequently in the first trimester of pregnancies and this finding raises concern about potential human teratogenicity from inadequate biotin intake. Biotin maintains nervous tissue, skin, hair, blood cells and sex organs. Fortunately, biotin deficiency is very rare in the average population since it is found readily in both plant and animal foods. Biotin is also manufactured by beneficial intestinal microflora within the human digestive tract, with enhanced synthesis and absorption in the presence of a vegetarian diet. Studies reveal a definite benefit with biotin for promoting strong nails and healthy hair, and for treating seborrheic dermatitis, diabetes and diabetic neuropathy. Its benefit in promoting healthy hair and treating seborrheic dermatitis (an inflammation (dermatitis) of the scalp) may relate to its important role in fatty acid metabolism, in turn connected to scalp oils and seborrhea. It enhances insulin sensitivity and increases the activity of glucokinase, an enzyme necessary for liver utilization of glucose. These effects relate to its benefit in diabetes and diabetic neuropathy. Dr. James Duke in the book, The Green Pharmacy recommends using biotin for treating dandruff. Dandruff is a common scalp condition that causes unsightly white flakes of dead scalp skin to appear on the scalp, hair and shoulders and is most often caused by seborrhea. Dr. Duke notes that Naturopaths recommend getting 6 milligrams daily of biotin for preventing and treating both dandruff and seborrhea.
Biotin, also known as vitamin H, is an acidic water soluble 10 carbon B vitamin with 2 adjacent rings, one containing sulfur, the other two nitrogen. It is involved in the activation of carboxylase enzymes responsible for gluconeogenesis, energy production and fatty acid synthesis.
The current RDA for biotin is only 30 micrograms daily for adults including for pregnant women. The RDA is only 35 micrograms for lactating women. In view of recent findings it may be concluded that these RDAs may be too low – particularly for pregnant women. In diabetes and diabetic neuropathy, 8 mg daily has been used. For treating dandruff and seborrhea it is recommended to get 6 milligrams daily. Dr. Duke’s database of plant constituents reveals that soybeans are very rich in biotin (750 parts per million). Only a handful of soybeans provide the 6 milligrams required for treating dandruff and seborrhea. Biotin is also concentrated in garlic and other herbs.
There are no side effects known for taking biotin at recommended dosages. The National Academy of Sciences notes that there are no reported adverse effects of biotin that have been found in humans or in animals. However, because studies on the higher dosages have not been done they do recommend caution. It is important to note that studies have documented many health benefits of foods with high biotin content (i.e. soy and garlic). Conversely, decreased biotin absorption and utilization has been shown to result from the consumption of raw eggs and results in a serious biotin deficiency. This is due to the presence of a protein in uncooked egg whites called avidin that strongly binds to biotin and prevents its bioavailability. Biotin absorption is also decreased in the presence of alcohol and certain anticonvulsants. Persons suffering with an alcohol addiction often develop a biotin deficiency. Antibiotics also decrease levels of biotin within the body due to the destruction of biotin-producing gut bacteria.
Hochman LG, et al. 1993. Brittle nails: Response to daily biotin supplementation. Cutis 51: 303-307.
Koutsikos D, Agroyannis B and Tzanatos-Exarchou H. 1990. Biotin for diabetic peripheral neuropathy. Biomed Pharmacother 44: 511-514.
Maibashi M, Makino Y, Furukawa Y, et al. 1993. Therapeutic evaluation of the effect of biotin on hyperglycemia in patients with non-insulin dependent diabetes mellitus. J Clin Biochem Nutr 14: 211-218.
Nisenson A, 1972. Treatment of seborrheic dermatitis with biotin and vitamin B complex. J Ped 81: 630-631.
Said HM. 2002. Biotin: the forgotten vitamin. Am J Clin Nutr 2002 Feb; 75(2): 179-80
Mock DM, Quirk JG, Mock NI. 2002. Marginal biotin deficiency during normal pregnancy. Am J Clin Nutr 2002 Feb; 75(2): 295-9.
Biotin Deficiency Symptoms:
Biotin deficiency results in both neurologic and cutaneous (skin) symptoms including severe dermatitis, loss of hair, and lack of muscular coordination and can be easily diagnosed with urine tests that screen for organic aciduria. Other biotin deficiency problems include deafness, dystonia, encephalitis and Parkinson’s disease-like symptoms. Biotin deficiency is rare in healthy individuals who consume a regular diet unless they are being treated either with certain anticonvulsants or with broad-spectrum antibiotics. Biotin deficiency in adult life can develop equally in men and in women.
Important Findings on Biotin Deficiency during Pregnancy:
Marginal biotin deficiency during normal pregnancy.
Mock DM, Quirk JG, Mock NI. Am J Clin Nutr 2002 Feb; 75(2): 295-9.
Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, 72205, USA. firstname.lastname@example.org
Abstract from Medline: BACKGROUND: Biotin deficiency is teratogenic in several mammalian species. Approximately 50% of pregnant women have an abnormally increased urinary excretion of 3-hydroxyisovaleric acid (3-HIA), which probably reflects decreased activity of the biotin-dependent enzyme methylcrotonyl-CoA carboxylase. However, increased 3-HIA excretion could result from pregnancy per se (eg, from an effect of pregnancy on renal handling of organic acids).
OBJECTIVE: We tested the hypothesis that biotin supplementation significantly decreases 3-HIA excretion in pregnant women with abnormally increased 3-HIA excretion.
DESIGN: Twenty-six pregnant women with increased 3-HIA excretion were studied in a randomized, placebo-controlled trial; 10 women were studied during early pregnancy (6-17 wk gestation) and 16 women during late pregnancy (21-37 wk gestation). Urine samples were collected before and after 14 d of supplementation with 300 microg (1.2 micromol) biotin/d or placebo. RESULTS: In the early-pregnancy group, 3-HIA excretion decreased (P < 0.006) by 11.7 +/- 3.6 mmol/mol creatinine (mean +/- SEM) in the 5 women who received biotin supplements, whereas 3-HIA excretion increased by 1.6 +/- 0.6 mmol/mol creatinine in the 5 women who received placebo. In the late-pregnancy group, 3-HIA excretion decreased (P < 0.002) by 7.1 +/- 1.2 mmol/mol creatinine in the 8 women who received biotin supplements, whereas 3-HIA excretion increased by 0.9 +/- 1.8 mmol/mol creatinine in the 8 women who received placebo. CONCLUSIONS: This study provides evidence that the increased excretion of 3-HIA seen frequently in normal pregnancy reflects reduced biotin status. The conclusion that marginal biotin deficiency occurs frequently in the first trimester further raises concern about potential human teratogenicity. Complete biotinidase deficiency presenting as reversible progressive ataxia and sensorineural deafness. Tsao CY, Kien CL. J Child Neurol 2002 Feb; 17(2): 146. Department of Pediatrics, The Ohio State University, Columbus, USA. email@example.com Abstract from Medline: Most symptomatic patients with biotinidase deficiency have both neurologic and cutaneous symptoms and typical organic aciduria. We encountered a previously healthy girl with complete biotinidase deficiency presenting initially at age 17 months with episodic ataxia that became severe progressive ataxia in 2 months, but without skin rash or typical organic aciduria, which resolved completely with biotin treatment. Additionally, moderate sensorineural deafness also improved to the normal range. Even without typical cutaneous findings or organic aciduria, biotinidase deficiency should be considered among the differential diagnosis in any child presenting with either episodic or progressive ataxia or sensorineural deafness as prompt diagnosis and treatment with biotin may induce an excellent recovery. Biotin dependency due to a defect in biotin transport. March R, Zeppelin J, Wolf B, Cannon MJ, Jennings ML, Cress S, Boylan J, Roth S, Cederbaum S, Mock DM. J Clin Invest 2002 Jun; 109(12): 1617-23. Regional Metabolic Service, Kaiser Permanente, Los Angeles, California, USA. Abstract from Medline: We describe a 3-year-old boy with biotin dependency not caused by biotinidase, holocarboxylase synthetase, or nutritional biotin deficiency. We sought to define the mechanism of his biotin dependency. The child became acutely encephalopathic at age 18 months. Urinary organic acids indicated deficiency of several biotin-dependent carboxylases. Symptoms improved rapidly following biotin supplementation. Serum biotinidase activity and Biotinidase gene sequence were normal. Activities of biotin-dependent carboxylases in PBMCs and cultured skin fibroblasts were normal, excluding biotin holocarboxylase synthetase deficiency. Despite extracellular biotin sufficiency, biotin withdrawal caused recurrent abnormal organic aciduria, indicating intracellular biotin deficiency. Biotin uptake rates into fresh PBMCs from the child and into his PBMCs transformed with Epstein Barr virus were about 10% of normal fresh and transformed control cells, respectively. For fresh and transformed PBMCs from his parents, biotin uptake rates were consistent with heterozygosity for an autosomal recessive genetic defect. Increased biotin breakdown was ruled out, as were artifacts of biotin supplementation and generalized defects in membrane permeability for biotin. These results provide evidence for a novel genetic defect in biotin transport. This child is the first known with this defect, which should now be included in the identified causes of biotin dependency. [The varied etiologies of childhood-onset dystonia] [Article in French] Roubertie A, Rivier F, Humbertclaude V, Tuffery S, Cavalier L, Cheminal R, Coubes P, Echenne B. Rev Neurol (Paris) 2002 Apr;158(4):413-24. Service de Neuropediatrie, Hopital Saint Eloi, CHU de Montpellier, France. Abstract from Medline: Dystonia is not uncommon in childhood, and identification of its etiology is an ultimate aim in the clinical evaluation of dystonia. Advances in neuroimaging, recent identification of gene or loci implicated in dystonic syndromes, and characterisation of new pathological entities (creatine deficiency, biotin-responsive basal ganglia disease) enlarge our understanding of childhood dystonia, and expend its diagnosis spectrum. Awareness of the diverse etiologic categories of childhood-onset dystonia is necessary to accurate diagnosis approach. Clinical examination and cerebral magnetic resonance imaging are the keys of this diagnosis approach. Primary dystonia is defined as syndromes in which dystonia is the sole phenotypic manifestation (especially no cognitive deterioration is observed, and brain MRI is normal); DYT1 dystonia, in which the abnormal gene is located on chromosome 9, is the most frequent childhood-onset primary dystonia; progressive generalisation of the abnormal movements occur in 70p.cent of the patients. Dopa - Responsive Dystonia are characterized by marked diurnal fluctuations of the dystonic symptoms and by their marked and sustained response to dopaminergic therapy; associated parkinsonian signs are usually observed later in the course of the disease. Clinical presentation of DRD might be atypical (mimicking cerebral palsy or isolated limb pain without diurnal fluctuation). DRD is rare, but a trial of L-dopa should be performed on all patients with childhood-onset dystonia, lasting at least one month. Secondary dystonias or heredodegenerative diseases are the most frequent etiology of childhood-onset dystonic syndromes. Among a huge range of heredodegenerative disease, those that are amenable to a specific treatment, such as Wilson's disease or creatine deficiency, should be particularly investigated. The main objective of investigation of dystonia is to identify secondary dystonias or heredodegenerative diseases. Further investigations will be performed according to the clinical characteristics of the dystonia, to the presence of associated neurological or extraneurological symptoms, and according to brain imaging; this approach must be discussed for each single patient. The aim of the diagnosis strategy is the rapid identification of the etiology of dystonia which will lead to accurate treatment and pertinent genetic counselling.