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Ingredient Type: Vitamin

Also Known As: Vitamin H, Vitamin B7, Coenzyme R, Cis-hexahydro-2-oxo-1H-thieno[3,4-d]-imidazole-4-valeric Acid, D- biotin, Bios II, Factor S, Bioepiderm, Biodermatin, Medebiotin, Meribin, Injacom H, Lutavit H2, Vitamin Bw, 3H-Biotin, Biotin forte, Rovimix H2 (1)

Biotin is a water-soluble B vitamin that is usually bound to proteins in almost every living cell (2).  B complex vitamins are essential nutrients because they help our body convert food into energy. In this process, the carbohydrates that we eat are converted into glucose, which is then used by our body to produce energy. Biotin not only helps metabolize carbohydrates but also helps the body metabolize fats and proteins.  This makes biotin essential to maintain healthy hair, skin, and nails.  Biotin can be found in small amounts in many foods we eat every day, such as eggs, milk, banana, nuts and whole grains (2). The bacteria that live in our large intestines also can produce biotin naturally (3).

Biotin’s structure and function were discovered over many years. To understand the unearthing of biotin, we must look at everyone who contributed to its discovery. The discovery began in 1901 when E. Wildiers, a Belgian microbiologist, was conducting an experiment on the culture of yeast cells. He noticed that the yeast cells were not growing properly until he added extracts of dead yeast cells. He named this extract Bios. In 1916, W.G. Bateman became one of the first notable contributors to the discovery of biotin after finding toxic levels of biotin within an organism following the addition of excess raw egg white to a nutritionally adequate diet. It was not until 1935, however, that scientists Fritz Kogl and Paul Gyory suggested the name “biotin” for the pure vitamin concentrations that they derived (4).


There is not any known use of biotin before its discovery in the 1900s.


Biotin Possibly Strengthens Hair:

Three studies present consistent results supporting the use of biotin for the strengthening of hair and the treatment of hair loss.  Biotin levels under 200 ng/l are considered as biotin deficiency.

A study performed on 541 women who experienced hair loss found that 38% of the women had a biotin deficiency.  In this study, 5mg of oral biotin was prescribed to one participant with biotin deficiency resulting in a positive outcome in hair growth in 3 months.  The causes of hair loss in the other women could not be treated with biotin and were addressed by the medical professional (2).

Another study was conducted on three children with uncombable hair syndrome.  They described their hair to be slow-growing, straw-colored scalp hair that could not be combed flat.  The hairs appeared normal on light microscopy but on scanning electron microscopy were triangular in cross-section with canal-like longitudinal depressions.  The children were prescribed 0.3mg of oral biotin three times a day.  The results produced significant improvement after 4 months in one patient.  The patients experienced increased growth rate, strength, and combability of the hair.  The other two patients had different results, possibly due to their associated ectodermal dysplasia.  Their hair slowly improved in appearance and combability over 5 years without biotin therapy (5).  Both studies indicate that biotin had positive effects on hair growth and strength.

In a third study, biotin was investigated along with zinc aspartate and clobetasol propionate as a treatment for childhood alopecia areata.  An oral dose of 20mg biotin, 100mg zinc aspartate and 0.025% topical clobetasol propionate was administered daily for one year.  The treatment promoted the regrowth of hair in the young subjects (6).

Biotin Might Strengthen Nails:

Three studies of varying strengths of scientific evidence provide consistent support for the positive effect of biotin on human nails.

In an early study on onychoschizia (a medical condition with symptoms including thinness, splitting, brittleness, and softness of nails) (7), a significant (25%) increase in nail thickness was observed in 32 subjects with normal or brittle nails examined pre- and post-treatment. This group also experienced increased regularity in the cellular arrangement of the nails’ dorsal surfaces and a decline in nail-splitting. A 7% increase in nail thickness and an increased regularity in the cellular arrangement of the nails’ dorsal surfaces was also observed in participants whose initial and final nail-clipping did not coincide with the administration of the biotin treatment. These results indicate that biotin may be effective in improving nail brittleness and other symptoms of onychoschizia (8).

In a Swiss retrospective study, 35 patients consumed an undisclosed dosage of biotin for 6 months. While 37% of subjects experienced no change, 63% experienced a 25% increase in the thickness of their nail plates (9).  In a German study, 71 subjects with dystrophic fingernails were treated with 2.5mg/day biotin, resulting in harder and firmer fingernails for 91% of subjects following a mean intervention period of 5.5 +/- 2.3 months. All the subjects agreed that the treatment was effective in some way (10).

Biotin Possibly Helps Alleviate Muscle Cramps:

In one supporting study, 1mg/day biotin was orally administered to 14 patients for muscle cramps induced by hemodialysis. 12/14 patients rapidly experienced declines in the onset and severity of cramps. Other measures indicated that biotin supplementation may be effective in relieving cramps despite already elevated plasma levels of biotin (11).

Biotin Possibly Helps Support Healthy Skin:

While one study of good scientific robustness reported that biotin has no effect on seborrhoeic dermatitis, another study of poor scientific robustness reported that biotin had positive effects on skin rashes.

In a prospective study, an undisclosed dosage of biotin was administered to treat skin rash in patients being treated with gefitinib or erlotinib for non-small cell lung cancer. Biotin reduced erythema in all patients and enabled long-term gefitinib or erlotinib treatment in 2 patients (12).

However, in a double-blind, placebo-controlled trial, an undisclosed dosage of orally ingested biotin resulted in no significant effect on the seborrhoeic dermatitis of infants as compared to placebo (13).

It should be noted that both these studies did not disclose the dosages of biotin administered, that the patients were adults in one study and infants in the other and that the skin conditions treated were notably different.

Biotin Possibly Supports Blood Health:

Insufficient but positive evidence exists on the effect of biotin on the proliferation of peripheral blood mononuclear cells. In a 14-day dietary intervention, 5 healthy subjects consumed 3.1micromol/day biotin. A decline in the proliferation of peripheral blood mononuclear cells was observed, as well as a decrease in interleukin-1beta and interleukin-2 synthesis (14).

Biotin Might Help Support a Healthy Central Nervous System:

Three studies support the alleviating effect of biotin on the symptoms of multiple sclerosis. In an uncontrolled, open-label proof of concept study, 23 participants with primary and secondary progressive multiple sclerosis consumed 100-300mg/day biotin for 2 to 36 months. A significant increase in visual acuity was experienced by 4 participants with prominent visual impairment. One participant with vision loss in the left eye experienced improvements 2-16 months after the commencement of biotin administration. 89% of participants with spinal cord involvement experienced improvements from 2-8 months after the onset of biotin treatment (15).

In an open-label pilot study, 154 subjects with progressive multiple sclerosis that had become worse within the last 24 months of the study and with baseline Expanded Disability Status Scale (EDSS) scores of 4.5-7 were administered either a placebo or 100mg biotin thrice daily for 12 months, followed by a 12-month period in which all subjects received the stated mega-dose of biotin. 12.6% of subjects in the biotin group achieved disability reversal at 9 months, compared to no subjects in the placebo group (p=0.005). The biotin mega-dose also decreased the progression of baseline EDSS scores (16).

In a randomized, double-blind placebo-controlled trial, 74 patients with non-active progressive multiple sclerosis were administered either a placebo or high-dose biotin for 12 months. After 12 months, there was a significant difference in whole brain volume and grey matter volume between the treatment group and the placebo group. At 24 months, with continued treatment, volumes of the brain, grey matter, and white matter were relatively stable as compared to their levels at 12 months. The placebo group experienced similar volumetric measures at month 24 after starting high-dose biotin treatment at month 12. No inter-group differences were observed at month 24 (17).

Insufficient yet positive scientific evidence exists on the alleviating effects of biotin on diabetic peripheral neuropathy.  Three diabetic patients being treated with insulin and experiencing neuropathy (nerve dysfunction) in both upper and lower limbs were daily administered 10mg biotin intramuscularly for 6 weeks, then administered this intramuscular dosage thrice weekly for a further 6 weeks, then orally administered 5mg daily for 52 to 112 weeks. Restless leg syndrome was eradicated after 4 to 8 weeks, and improvements were experienced in paresthesias, muscle cramps, and the capacity to stand, walk, and climb staircases. All patients were able to walk over 300 meters without assistance and were paresthesias-free after 1 year of biotin treatment.  This suggests that biotin treatment may be effective in alleviating symptoms of diabetic peripheral neuropathy (18).

Biotin Possibly Helps Support Brain Health:

Two studies with small sample sizes are presented on the effect of biotin on a novel basal ganglial disease. Both studies support biotin’s positive effect, albeit to different strengths.

In a 1998 study, 5-10mg/kg/day of biotin was effective in treating the symptoms of 10 patients with a novel basal ganglial disease. The disease presents as a subacute encephalopathy with other neurological symptoms, progressing to dystonia, limb weakness, and cogwheel rigidity. Symptoms disappeared within a few days of biotin administration and reappeared within a month of treatment cessation. It is noteworthy that the cause of the disease is unknown as well as the mechanism of the biotin treatment (19).

In a far more recent study, less positive results were observed. In a non-blinded prospective comparative study, 20 children with a biotin-responsive basal ganglial disease were randomly assigned to receive either 40mg/kg/day thiamine or the thiamine dosage along with 5 mg/kg/day biotin for at least 30 months. Following 2 years of post-treatment care, the symptoms of only 6/20 subjects were completely eradicated. 4 patients with delayed diagnosis and symptom management experienced severe neurologic sequelae, and 10 other patients had minimal sequelae presenting as mild dystonia and dysarthria. In the biotin-thiamine group, a significant difference in the length of crisis recovery period was observed as compared to the thiamine only group (2 days vs 3 days) (p=0.005). However, no other significant differences were observed (20).

Biotin Might Decrease Levels of Plasma Lipids:

Six studies provide varying levels of support for the lipid-decreasing effect of biotin. Three of these six studies investigated biotin as an isolated treatment, while the other three investigated a biotin/chromium picolinate treatment option. The first three studies described below present the results of blended treatment, while the latter three consider biotin as a stand-alone treatment.

In a randomized, double-blind, placebo-controlled trial, 348 subjects with type 2 diabetes were administered either a placebo or 600 mcg chromium as chromium picolinate and 2mg biotin daily for 90 days. The members of the treatment group who had both type 2 diabetes and hypercholesterolemia experienced significant declines in low-density lipoprotein cholesterol (LDL-C), total cholesterol, and atherogenic index (p<.05). The members of the treatment group who were also being treated with statins experienced declines in total cholesterol, LDL-C, and very low-density lipoprotein levels (p<.05). These lipid-lowering effects are correlated to improvements in coronary risk factors (21).

In a double-blind, placebo-controlled trial, 36 obese participants with impaired glucose control and Type 2 diabetes mellitus were administered either a placebo or 600 mcg chromium and 2mg biotin per day for a 4-week period.  The ratio of triglycerides to high-density lipoprotein cholesterol (HDL-C) concentration in blood plasma may be represented as the logarithm ‘atherogenic index of plasma’ (AIP). At the end of the trial, the treatment group was observed to have a significantly lower AIP than the placebo (p<0.05). Significant inter-group differences were also observed for levels of triglycerides (p<0.02) and for the ratio of LDL-C to HDL-C (22).

In a placebo-controlled pilot study, the effect of biotin and chromium picolinate supplementation was observed in type 2 diabetes patients who experienced impaired glycaemic control despite treatment with oral antihyperglycemic agents. For 4 weeks, the subjects were administered 2 mg biotin with chromium picolinate (600 mcg Cr (+3)) per day. In the treatment group, a significant decline was observed in triglyceride levels (p<0.02) and in the ratio of triglycerides to HDL-C (p<0.05) (23).

The following three studies investigated the effect of biotin only on plasma lipid levels. In a double-blind, placebo-controlled study, 15 non-diabetic and 18 diabetic participants were administered a placebo or 61.4 micromol/day biotin for 28 days. Biotin produced a significant reduction in plasma triglycerol levels from the start to the end of the trial (-0.92+/-0.36 in the nondiabetic group, triacylglycerol -0.55+/-0.2 in the diabetic group; p=0.005). A significant reduction in very low-density lipoprotein (VLDL) was also observed (-0.18+/-0.07 in the nondiabetic group, -0.11+/-0.04 in the diabetic group, p=0.005). These results indicate that biotin supplementation may be effective in treating hypertriglyceridemia (24).

In a randomized, double-blind placebo-controlled trial, 70 subjects with poorly-controlled type 1 diabetes were administered either a placebo or 40 mcg/kg/day biotin for 3 months, both with a standardized insulin regimen. While a decrease in plasma lipids was observed in the biotin group, a significant reduction was observed only for low-density lipoproteins (p=0.016). Statistically significant inter-group differences were observed for triglycerides, total cholesterol, and low-density lipoprotein cholesterol (25).

In a double-blind, placebo-controlled study, 40 subjects were treated with biotin for 71 days. Within the first 2 weeks of the trial, significant reductions were observed in alpha and beta-lipoprotein cholesterol, total lipid, and total phospholipid levels. However, by day 71, there were no significant results (26).  These results indicate that biotin may only be effective for short-term decreases in lipid levels.

Biotin Might Improve Control of Blood Sugar Levels:

Ten studies on the effect of biotin on blood sugar control are presented below.  Eight of these ten studies support the positive effect of biotin while two present no significant results (22,23,27,28).  Both the studies presenting no significant results investigated biotin as a stand-alone treatment, while only 2/8 of the supporting studies share this quality.  The other 6/8 supporting studies investigated a treatment of biotin paired with chromium in the form of chromium picolinate.

In a placebo-controlled study, 43 participants with non-insulin dependent diabetes mellitus were administered 9mg/day biotin as compared to 64 healthy controls who were administered a placebo instead. It was observed pre-treatment that serum biotin levels were lower for the treatment group and were inversely related to fasting blood glucose levels. This hyperglycemia of the treatment group was corrected with the biotin treatment, accompanied by increased sensitivity to glibenclamide in patients who were previously non-responsive (29).

In a randomized, double-blind, placebo-controlled trial, 348 subjects with type 2 diabetes were administered either a placebo or 600 mcg chromium as chromium picolinate and 2mg biotin daily for 90 days. The treatment group experienced a significant decline in levels of glucose and glycated hemoglobin as compared to the placebo group (p<.02). A significant decline in glycated hemoglobin levels was also observed in those members of the control group receiving statins (21).

The lead researcher of the previous study continued his research a year later with a randomized, double-blind, placebo-controlled study. 447 participants with mildly controlled type 2 diabetes mellitus were administered 2mg biotin with chromium picolinate (600 mcg Cr (+3)) or a placebo along with stable oral anti-diabetic agents. Participants in the treatment group experienced a significant (0.54%) decrease in glycated hemoglobin (p=0.03). Treated participants with baseline glycated hemoglobin levels less than or equal to 10% experienced a significant decline as compared to the placebo group (-1.76% vs – 0.68%; p = 0.005). This group also experienced highly significant reductions in fasting blood glucose as compared to the control group (-35.8 mg/dL vs. 16.2 mg/dL; p = 0.01). Significant reductions in fasting blood glucose levels were also seen in the overall treatment group (-9.8 mg/dL vs 0.7 mg/dL; p = 0.02) as compared to the placebo group (30).

In a randomized, double-blind placebo-controlled trial, 70 subjects with poorly-controlled type 1 diabetes were administered either a placebo or 40 mcg/kg/day biotin for 3 months, both with a standardized insulin regimen. Post-treatment, a significant difference was observed between the means of the biotin and the placebo group (p<0.001). There was a significant decline in levels of glycated hemoglobin in the treatment group from a baseline measurement of 9.84±1.80 to 8.88±1.73 post-treatment (p<0.001). The control group experienced a significant increase in glycated hemoglobin. Fasting blood glucose levels were reduced in the treatment group from 275±65.76 mg/dl at baseline, down to 226± 41.31 post-treatment (p<0.001) (25).

In contrast to all these supporting studies are 2 studies in which biotin produced no significant effect on glycogen control. Both these studies investigated biotin in isolation.

In a double-blind, placebo-controlled study, 17 non-diabetic subjects or subjects with type 2 diabetes were administered 5mg biotin or a placebo thrice daily for 28 days. Increases in Lymphocyte propionyl-CoA carboxylase and pyruvate carboxylase activity were observed after 28 days (p<0.05). A significant increase of approximately 90% was observed for acetyl-CoA carboxylase activity (p<0.05). However, no significant effects were observed for fasting glucose, insulin, triacylglycerol, cholesterol, and lactate concentrations (31).

Two years prior to this study, in a double-blind, placebo-controlled trial, 15 non-diabetic and 18 diabetic participants were administered a placebo or 61.4 micromol/day biotin for 28 days. No significant effect was observed on glucose or insulin concentration (24).


Biotin is considered safe as a human supplement when orally ingested at the recommended dosage (32,33).  Biotin is also considered safe when taken intramuscularly at the recommended dose (18). Studies in which biotin has been administered to infants present no adverse effects due to biotin intake (34,35).  Biotin has also presented no adverse effects when consumed by pregnant women (36).  Nevertheless, it is important to consult a medical provider before taking biotin while being treated with other medication. The adequate daily intakes (AI) for biotin are 7mcg for infants 0-12 months, 8mcg for children 1-3 years, 12 mcg for children 4-8 years, 20mcg for children 9-13 years, 25mcg for adolescents 14-18 years, 30mcg for adults over 18 years and pregnant women, and 35mcg for breastfeeding women (37).

Several studies implicated biotin in decreasing levels of plasma lipids and plasma glucose. As such, patients already on medication for hyperlipidemia (21,25) or hyperglycemia (22,23,28) should consult a medical professional when taking biotin supplements to avoid dangerously low levels of plasma lipids or glucose.



  • Biotin may decrease liver function in metabolizing some medications, which can increase the side effects of those medications. Some medications that have been affected by biotin are clozapine (Clozaril), cyclobenzaprine (Flexeril), fluvoxamine (Luvox), haloperidol (Haldol), imipramine (Tofranil), mexiletine (Mexitil), olanzapine (Zyprexa), pentazocine (Talwin), propranolol (Inderal), tacrine (Cognex), theophylline, zileuton (Zyflo), zolmitriptan (Zomig). Evidence suggests that some supplements should be taken with caution when consuming biotin. Vitamin B5 and Alpha lipoic acid are two such supplements that have shown decreased absorption when taken with biotin (37).
  • Biotin may lead to false laboratory results due to immunoassay interference. Such erroneous results can lead to the misdiagnosis and imprudent treatment of patients (38,39,40,41,42,43,44,45,46,47).
  • Patients with biotinidase deficiency may be required to consume larger doses due to the nature of biotin’s role in the etiology of the disease (48).
  • Patients receiving peritoneal or renal dialysis may also require higher doses of biotin due to the absorption mechanism of biotin in the medical conditions warranting such dialysis (48).


  • While taking biotin one should not consume more than two raw eggs a day. Raw egg whites contain a substance that binds to biotin and causes a decline in biotin absorption (37,49)
  • Doses of 300 mg/day biotin may present false hormone, vitamin and other chemical levels on immunoassays utilizing sandwich biotin-streptavidin capture (46,50).
  • This dosage has factitiously presented elevated levels of vitamin B12, 25-hydroxyvitamin D (leading to false vitamin D toxicity reports), DHEA sulfate, folate, estradiol, progesterone, and testosterone immunoassays.
  • The dose has also presented erroneously low levels of sex-hormone-binding globulin, prostate-specific antigen, prolactin, parathyroid hormone, insulin, growth hormone, luteinizing hormone, and follicle-stimulating hormone. A 72-hour biotin-free period should be observed before laboratory measurements.
  • Patients being treated with primidone (Mysoline), phenytoin (Dilantin), phenobarbital or the anticonvulsant drug carbamazepine (Carbatrol, Tegretol) may result in low plasma biotin levels (51,52,53).


Biotin has presented no adverse side-effects dissimilar to those presented by a placebo in a number of studies with varying levels of scientific robustness (22,23,27,30).


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See the entry for biotin, the MedlinePlus entry for biotin, or the Michigan Medicine Health Library entry for biotin for more information.