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Biotin

Biotin, also known as vitamin B7, is a water-soluble vitamin from the vitamin B complex that is essential for the growth and development of all organisms (1). As a coenzyme of carboxylase enzymes, biotin is involved in the metabolism of fatty acids, amino acids and carbohydrates (2). Biotin has also been shown to be important for many health factors, including neurological function, maintenance of stable blood sugar levels, DNA stability and the health of hair, skin and nails (3, 4). The body cannot produce biotin itself, which is why it must be supplied through food or produced by intestinal bacteria (5).

Biotin is found in a variety of foods including liver, egg yolk, cow's milk and some fruits and vegetables (6). Although biotin deficiency is rare, it can be dangerous if left untreated. Suboptimal biotin levels or minor deficiencies, which are more common, have been linked to a number of negative health effects such as delayed growth, neurological disorders, hair loss, skin rashes, muscle pain and anemia (1). Groups of people at increased risk of biotin deficiency include smokers, alcoholics, pregnant women and people suffering from irritable bowel syndrome (7, 8, 9, 10).

Pharmacokinetics

Oral biotin supplements are completely absorbed even at high pharmacological doses (81.9 mcg taken orally or 18.4 mcg administered intravenously) (11). Biotin is absorbed via a sodium-dependent multivitamin transporter (SVMT) in the small and large intestine (5). After being transported from the intestine into the systemic circulation, biotin is taken up by the liver and finally reaches the central nervous system via the blood-brain barrier (12). Soon after oral consumption by humans, high single doses of biotin (600 mcg and 900 mcg) are eliminated from the circulation, leading to increased excretion via the urine. For this reason, lower doses (300 mcg) every day for one week are recommended for longer-term maintenance of blood biotin levels (13). About half of the absorbed biotin undergoes metabolism to bisnorbiotin and biotin sulfoxide before excretion. Biotin, bisnorbiotin and biotin sulfoxide are present in human blood and urine in molar ratios of approximately 3:2:1 (14). The elimination half-life of biotin is about 1 hour, 50 minutes (13).

Tasks of biotin

In human metabolism, the tasks of biotin are limited to a few reactions:

  • Degradation of the amino acids leucine, isoleucine and valine,
  • biosynthesis and utilization of fatty acids and
  • gluconeogenesis.

Biotin as a prosthetic group

Biotin is the cofactor (prosthetic group) of carboxylases (more precisely: carboxy-transferases). Through their action, carbon dioxide can also be fixed in the animal organism. Examples are

  • pyruvate carboxylase, a key enzyme in gluconeogenesis, which converts pyruvate into a metabolite of the citrate cycle;
  • Acetyl-CoA carboxylase, which provides malonyl-CoA for the starting step of fatty acid synthesis.

Health benefits of biotin

Biotin is effective when used to prevent and treat biotin deficiency. Symptoms of biotin deficiency include thinning hair (often accompanied by a loss of hair color) and a red, scaly rash around the eyes, nose and mouth. Other symptoms include depression, lethargy, hallucinations and a tingling sensation in the arms and legs. There is evidence that smoking may cause a mild biotin deficiency.

Biotin is important for energy metabolism

Biotin is a coenzyme for carboxylases, the enzymes that support the metabolism of fat, proteins and carbohydrates for energy production (15).

These enzymes are essential for the following processes:

  • Gluconeogenesis, the metabolic pathway that produces glucose from sources other than carbohydrates such as amino acids (16).
  • Cellular energy production (17).
  • The use of branched-chain amino acids (leucine, valine and isoleucine) to produce neurotransmitters and energy (18).
  • Synthesis and breakdown of fatty acids for the purpose of energy supply (19).
  • The secretion of insulin (17).

Inadequate biotin levels in the body can slow down the metabolism, which can lead to fatigue, digestive problems and weight gain (1).

Biotin is needed for brain function

Biotin is needed for the formation of the myelin sheath - a fatty substance that surrounds the nerves and supports the transmission of stimuli through the nerves. A biotin deficiency can therefore slow down myelination (20). Biotin deficiency can also lead to a range of other neurological symptoms including seizures, poor muscle coordination, learning difficulties, hallucinations, depression and lethargy. Most of these problems can be reversed with biotin supplementation (21, 22, 20).

High-dose biotin supplementation (5 to 10 mg per kilogram per day) was also effective in the treatment of biotin-responsive basal ganglia - a rare metabolic disorder of the brain characterized by seizures, confusion and abnormal coordination - in a review of 18 cases (23). Multiple sclerosis is an autoimmune disease characterized by myelin damage and loss. Considering biotin's role in fatty acid synthesis and energy production (both required for myelin repair and axon survival), scientists hypothesize that biotin may be effective in limiting or reversing impairments associated with multiple sclerosis (24).

In fact, two clinical trials with a total of 177 participants found that high-dose biotin treatment in patients with progressive multiple sclerosis was able to prevent disease progression and reduce symptoms. However, in another study, such treatment was only minimally effective or completely ineffective in improving visual acuity in 93 patients with multiple sclerosis (25, 26, 27).

Biotin is important for the function of the immune system

Biotin is required for the development of white blood cells and biotin deficiency is associated with impaired immune function and increased risk of infection (28, 29). Biotin also increases the production of Th1 cytokines such as IL-1-Betz and IFN-y which are essential for triggering immune function to fight bacterial and viral infections (30). Inadequate biotin levels have been associated with reduced antibody synthesis, T cell decline and lower levels of splenocytes and T cells (31, 28, 32). Reduced rates of cellular proliferation during biotin deficiency may be responsible for some of the negative effects of such deficiency on the immune system (33). A deficiency of biotinidase - an enzyme that helps recycle biotin - is associated with chronic vaginal candidiasis and can be treated with biotin supplementation. Since it is believed that one in 123 people suffer from biotinidase deficiency, women with chronic vaginal candidiasis may respond to biotin treatment (34).

Biotin could be helpful in type 2 diabetes

Biotin may help lower blood glucose levels by increasing insulin production, increasing glucose uptake into muscle cells and stimulating the glucokinase enzyme, which stimulates glycogen synthesis in the liver (35, 36, 37). Daily supplementation with biotin reduced fasting blood glucose levels by an average of 45% in a clinical study of 43 subjects with type 2 diabetes (38). Biotin also increased the activity of 3 enzymes (pyruvate carboxylase, acetyl-CoA carboxylase and propionyl-CoA carboxylase) involved in glucose degradation in a clinical study of 30 subjects (39).

In addition, a combination of biotin with chromium picolinate improved glycemic control in 2 clinical trials involving nearly 500 uncontrolled diabetics (40, 41). Furthermore, high doses of biotin improved the symptoms of nerve damage frequently observed in diabetic patients (diabetic neuropathy) (42). All in all, the study results suggest that supplementation with biotin - especially in combination with chromium in the form of chromium picolinate - could help to control blood glucose levels and reduce the risk of diabetic neuropathy. Biotin could be used as an adjunctive approach to controlling blood glucose levels in consultation with the treating physician. Under no circumstances should biotin be used in place of diabetes medications without consultation with the treating physician.

Biotin could reduce the risk of heart disease

Biotin is needed for normal lipid metabolism, which is essential for maintaining heart and blood vessel health (43, 44, 45). In combination with chromium in the form of chromium picolinate, biotin helped reduce risk factors for heart disease by increasing HDL cholesterol levels and lowering LDL cholesterol levels in 2 clinical trials involving nearly 400 diabetic patients with heart disease (46, 47). Pharmacologic doses of biotin (15,000 mcg per day) were also effective in reducing blood triglyceride levels in a study of 33 patients with elevated triglyceride levels (48). Although studies are limited, research suggests that biotin may help reduce the risk of heart disease.

Biotin could promote skin, hair and nail health

Biotin deficiency has been associated with a number of skin conditions including seborrheic dermatitis and eczema (49, 50). This may be related to biotin's role in fatty acid synthesis and metabolism, which are critical to skin health (50).Skin cells are particularly dependent on lipid production as they need extra protection from damage and water loss due to direct exposure to the outside world (51).

Inadequate biotin levels can also lead to hair loss, which is reversible when biotin is supplemented. However, although there are studies that have found that biotin can promote hair growth in women with thinning hair, there is minimal evidence that biotin can promote hair growth in otherwise healthy individuals (17, 52, 53, 54). Biotin could improve the quality of brittle nails. In affected patients, the development of more resistant, harder and thicker nails has been observed after treatment with biotin (55, 56, 57). Although the evidence is limited, it suggests that biotin could improve the health of skin, hair and nails.

Biotin could prevent birth defects

Marginal biotin deficiency is common during pregnancy due to the increased biotin requirements of the growing fetus (58). In animals, even subclinical biotin deficiencies can lead to cleft palate and limb abnormalities (59). It is hypothesized that low biotin status during pregnancy increases the risk of birth defects in humans by altering lipid metabolism and increasing genome instability, both of which can lead to the development of chromosomal abnormalities and fetal malformations (60, 61).

In human embryonic palatal stem cells, biotin deficiency has been shown to suppress carboxylase production and cellular proliferation, suggesting that low levels of biotin may delay or arrest growth of the embryonic palate, which may result in the development of cleft palate (61). However, there is currently a lack of definitive evidence linking biotin deficiency to birth defects in humans, so further research is needed (62).

Biotin could prevent DNA damage

Biotin forms a covalent bond with histones - DNA-forming proteins that help to fold and package DNA into chromatin. The addition of biotin to histones plays a significant role in cellular proliferation, gene silencing and DNA repair and stability (63, 17, 1). Low biotin levels can lead to inadequate hoston biotinylation, which can result in genome instability and abnormal gene expression (cell production) and thus increase the risk of cancer.

These effects have been shown to increase cancer risk in fruit flies and in cell-based studies (64, 65, 66). However, it has been shown in a human study that higher biotin levels (up to 600 mcg) can increase genome instability and damage. This suggests that the DNA stabilizing effects of biotin may be dose-dependent (67). Thus, further studies are needed to better understand the link between histone biotinylation and risk of DNA damage (68).

Biotin could alleviate inflammation and allergic disorders

Studies in mice and human white blood cells suggest that biotin deficiency can increase the production of pro-inflammatory cytokines and exacerbate inflammatory diseases (69, 70). In mice suffering from nickel allergy and deficient in biotin, biotin supplementation reduced the production of pro-inflammatory cytokines and reduced allergic inflammation, suggesting a potential therapeutic effect of biotin in inflammatory and allergic diseases (69). These effects may be the result of reduced NF-kB activity, which is activated during biotin deficiency (71, 72).

Safety and side effects

Biotin is probably safe and harmless for most people when taken orally in amounts up to 300 mg per day (25, 14). Biotin is potentially safe and safe for intramuscular injections of up to 20 mg per day. As biotin is a water-soluble vitamin, biotin overdose is unlikely as excess amounts are excreted in the urine (1).

Precautions and warnings

Pregnancy and lactation: Biotin may be safe and harmless when used in the recommended amounts during pregnancy and lactation.

Kidney dialysis: People undergoing kidney dialysis may require additional biotin.

Interactions

Lipoic acid competes with biotin in the intestine for binding to the sodium-dependent multivitamin transporter (SMVT), which means that long-term use of lipoic acid could result in a reduction in biotin levels (73). High doses of vitamin B5 (pantothenic acid) also have the potential to compete with biotin for absorption by the SMVT (74, 75). Prolonged use of antibiotics such as tetracycline antibiotics and sulfonamides can lower biotin levels as these antibiotics kill biotin-producing bacteria in the gut (1). In addition, some anticonvulsant drugs such as primidone and carbamazepine can inhibit biotin absorption. Chronic use of anticonvulsant drugs can therefore increase biotin depletion (76).

The widespread bad habit of consuming raw eggs in bodybuilding can also lead to a biotin deficiency, as raw egg white contains the protein avidin, which binds biotin and inhibits its absorption by the body (77). Smoking - especially in women - accelerates biotin depletion, which can result in a marginal biotin deficiency (7). Chronic alcohol consumption can inhibit the absorption of biotin in the digestive tract (8). High-dose biotin supplementation could falsify the results of a thyroid test and mimic the laboratory pattern of Basedow's disease (78).

Occurrence of biotin in food

Biotin is found (in combination with sulfur) in dairy products, as well as in grain cereals, grain rice, vegetables, fish, egg yolk, nuts, liver, soybeans, mushrooms, brewer's yeast.

Dosage

There is no defined daily requirement for biotin. An adequate intake is 7 mcg for children up to 12 months, 8 mcg for children from 1 to 3 years, 12 mcg for children from 4 to 8 years, 20 mcg for children from 9 to 13 years, 25 mcg for adolescents from 14 to 18 years, 30 mcg for adults over 18 years and pregnant women and 35 mcg for breastfeeding women.

Requirements for sport

100-1000 mcg per day, taken several times a day with meals.

How can you recognize a biotin deficiency?

There is no really good laboratory test to detect a biotin deficiency, so it is usually identified by its symptoms. These symptoms include thinning hair, often accompanied by a loss of hair color, and a red, scaly rash around the eyes, nose and mouth. Other symptoms affecting the nervous system include depression, fatigue, hallucinations and a tingling sensation in the arms and legs. There is evidence that diabetes could lead to a biotin deficiency. Furthermore, the regular consumption of raw eggs can lead to a biotin deficiency, as the avidin contained in the egg white blocks the absorption of biotin in the intestine.

Biotin deficiency is generally not observed in adults, regardless of diet. In infants up to 12 months of age, the biotin requirement is relatively high. Infants who are fully breastfed may experience deficiency symptoms, as the required amount of biotin is not present in breast milk. This is significant due to the fact that a biotin deficiency in infancy is associated with "sudden infant death syndrome".

Consequences of an overdose (hypervitaminosis)

Delayed or reduced insulin secretion, increased need for vitamin C and vitamin B6, increased blood sugar levels.

References

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726758/
  2. https://www.ncbi.nlm.nih.gov/pubmed/22869039
  3. https://www.ncbi.nlm.nih.gov/pubmed/15992685
  4. https://www.sciencedirect.com/science/article/pii/S095528630300130X
  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646215/
  6. https://www.ncbi.nlm.nih.gov/pubmed/16648879
  7. https://www.ncbi.nlm.nih.gov/pubmed/15447901
  8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3064116/
  9. https://www.ncbi.nlm.nih.gov/pubmed/25122647
  10. https://www.ncbi.nlm.nih.gov/pubmed/2500847
  11. https://www.ncbi.nlm.nih.gov/pubmed/10075337
  12. https://www.ncbi.nlm.nih.gov/pubmed/3098919
  13. https://www.ncbi.nlm.nih.gov/pubmed/2722429
  14. https://www.ncbi.nlm.nih.gov/books/NBK114297/
  15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3508090/
  16. https://www.ncbi.nlm.nih.gov/pubmed/18613815/
  17. https://www.ncbi.nlm.nih.gov/pubmed/19727438
  18. https://www.ncbi.nlm.nih.gov/pubmed/15930469
  19. https://www.ncbi.nlm.nih.gov/pubmed/1596846
  20. https://www.ncbi.nlm.nih.gov/pubmed/18545994
  21. https://www.ncbi.nlm.nih.gov/pubmed/21696988
  22. http://journals.sagepub.com/doi/abs/10.1177/0883073807300307
  23. https://ojrd.biomedcentral.com/articles/10.1186/1750-1172-8-83
  24. https://www.ncbi.nlm.nih.gov/pubmed/2632767
  25. https://www.ncbi.nlm.nih.gov/pubmed/25787192
  26. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098693/
  27. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6061426/
  28. http://jn.nutrition.org/content/130/2/335S.full
  29. https://www.ncbi.nlm.nih.gov/pubmed/9497186
  30. http://jn.nutrition.org/content/133/3/716.full
  31. https://www.ncbi.nlm.nih.gov/pubmed/88554
  32. https://www.ncbi.nlm.nih.gov/pubmed/6195318
  33. https://www.ncbi.nlm.nih.gov/pubmed/14991266
  34. https://www.ncbi.nlm.nih.gov/pubmed/9764646
  35. https://www.ncbi.nlm.nih.gov/pubmed/22841397
  36. https://www.ncbi.nlm.nih.gov/pubmed/10540872
  37. https://www.sciencedirect.com/science/article/pii/0003986168901951
  38. https://www.jstage.jst.go.jp/article/jcbn1986/14/3/14_3_211/_pdf
  39. https://www.ncbi.nlm.nih.gov/pubmed/14749229
  40. https://www.ncbi.nlm.nih.gov/pubmed/17109595
  41. https://www.ncbi.nlm.nih.gov/pubmed/17506119
  42. https://www.ncbi.nlm.nih.gov/pubmed/2085665
  43. http://www.nrjournal.com/article/S0271-5317(00)00201-3/abstract
  44. https://www.ncbi.nlm.nih.gov/pubmed/7011260
  45. https://www.ncbi.nlm.nih.gov/pubmed/15992683
  46. https://www.ncbi.nlm.nih.gov/pubmed/17496732
  47. https://www.ncbi.nlm.nih.gov/pubmed/17684468
  48. https://www.ncbi.nlm.nih.gov/pubmed/16677798
  49. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1545716/
  50. https://www.ncbi.nlm.nih.gov/pubmed/1764357
  51. http://ajcn.nutrition.org/content/73/5/853
  52. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509882/
  53. https://www.ncbi.nlm.nih.gov/pubmed/26705444
  54. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989391/
  55. https://www.ncbi.nlm.nih.gov/pubmed/2648686
  56. https://www.ncbi.nlm.nih.gov/pubmed/2273113
  57. https://www.ncbi.nlm.nih.gov/pubmed/8477615
  58. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1426254/
  59. https://www.ncbi.nlm.nih.gov/pubmed/10632957/
  60. https://www.ncbi.nlm.nih.gov/pubmed/19056637
  61. https://www.ncbi.nlm.nih.gov/pubmed/18356320
  62. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646213/
  63. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1226983/
  64. https://www.ncbi.nlm.nih.gov/pubmed/17056793
  65. https://www.ncbi.nlm.nih.gov/pubmed/16177192
  66. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1832083/
  67. https://academic.oup.com/carcin/article/26/5/991/2390856/Low-intake-of-calcium-folate-nicotinic-aci
  68. https://www.ncbi.nlm.nih.gov/pubmed/19022951
  69. http://jn.nutrition.org/content/139/5/1031.full
  70. https://www.ncbi.nlm.nih.gov/pubmed/26168302
  71. https://www.ncbi.nlm.nih.gov/pubmed/15296080
  72. https://www.ncbi.nlm.nih.gov/pubmed/15681168
  73. https://www.ncbi.nlm.nih.gov/pubmed/9516450
  74. https://www.ncbi.nlm.nih.gov/pubmed/23578027
  75. https://www.ncbi.nlm.nih.gov/pubmed/9814986
  76. https://www.ncbi.nlm.nih.gov/pubmed/15539280/
  77. https://www.ncbi.nlm.nih.gov/pubmed/14747666/
  78. http://www.nejm.org/doi/full/10.1056/NEJMc1602096#t=article