Written By Dr. Shalaka Samant, PhD
Biotin, also called vitamin H or vitamin B7 is a water-soluble vitamin. It is a member of the B-complex family of vitamins. Biotin is vital to many body functions. It is used by the body to metabolize carbohydrates, fats and amino acids for the formation of fatty acids and glucose, which are used as energy in our body. It is found in small amounts in many foods such as cauliflower, salmon, carrots, bananas, soy flour, yeast, wheat germ, whole-grain cereals, whole wheat bread, and eggs. Not only in higher organisms like humans, biotin is also a crucial vitamin playing an essential role in various metabolic pathways in many microbes (1).
While humans and animals require several hundred micrograms of biotin per day, most microbes, plants and fungi are able to synthesize this factor themselves. Yeasts like Saccharomyces cerevisiae (Baker’s yeast) and the opportunistic fungal pathogen, Candida albicans are an exception. C. albicans is a biotin auxotroph (2,6). Like many other yeasts, it cannot synthesize its own biotin, and only has the ability to accumulate biotin for periods of growth when biotin is scarce (13). Therefore, biotin is an important vitamin requirement for C. albicans (3).
C. albicans is an important fungal pathogen of humans. C. albicans infections represent a significant public health problem and is a common complication in immunodeficient individuals such as AIDS patients, cancer patients undergoing chemotherapy and organ transplant recipients (4).
While some treatments are available, their efficacy can be compromised by the emergence of drug-resistant strains. Therefore, there has been intense interest in the virulence factors which make C. albicans such a versatile pathogen. Of its various virulence factors the one which has received most attention is the ability of C. albicans to interconvert between the yeast and hyphal growth forms which are the long, branching filamentous structures or mycelia of a fungus (dimorphism).
The role of this morphological transition between the two forms of the fungus in C. albicans infections has been a topic of hot debate for a long time (7). It is generally accepted that hyphal cells are more invasive (8) and indeed, most histological pictures of invading C. albicans cells show hyphae, while there are rare reports of invading yeast cells. Based on these observations, a popular view is that, yeast are the non-invasive, commensal morphology, and some authors go even further, suggesting that hyphae are the pathogenic form while yeasts are the non-pathogenic form. This is an oversimplified view. Rather, it would appear that both morphological forms are of relevance during infection: yeast and hyphal cells are both found in infected organs (2) and, depending on the organ, one or the other morphology predominates.
For example, filamentation is regularly observed in the kidney, but not in the spleen or liver during invasive candidiasis. Both forms appear to be important during different stages of disease development (5). In contrast, it is generally accepted that C. albicans dimorphism is required for full virulence. C. albicans mutants trapped in either form show markedly reduced virulence (10, 11, 12). Understanding the environmental cues that trigger the yeast to switch between these two forms is therefore important for arriving at novel therapeutic strategies for targeting Candida infections.
An early study that implicated biotin to play a major role in the C. albicans dimorphic switch was the 1974 study by Yamaguchi at the University of Tokyo. This study showed that media containing very low levels (0.1 ng/ml) of biotin caused C. albicans to convert to the hyphal form i.e. growth conditions with limiting biotin promote hyphae formation (14,15).
This study is primarily cited as the scientific basis for the supposed health benefits of taking biotin pills to prevent/cure C. albicans infections as advertised by many health and wellness websites. The rationale behind this therapy being, in the presence of biotin, C. albicans would be incapable of converting into its pathogenic mycelial form, which is the form in which it invades tissues. These supposed therapeutic biotin preparations recommend a dosage of 1000-2000 micrograms for Candida infection treatment and if the infestation is severe, they recommend increasing the dose to 5000-6000 micrograms daily.
However, apart from the Yamaguchi study there appears to be no other study supporting the hypothesis that biotin limiting conditions promote C. albicans to switch to the invasive hyphal form. In fact, there are two studies that fail to substantiate this claim. A 1988 study by Vidotto et al, shows that biotin is not an important factor for the dimorphic switch (9). While, a 2016 study reports no evidence supporting prior claims by Yamaguchi that C. albicans forms hyphae at very low biotin growth conditions (7). Moreover, the 2016 study shows that higher amounts of biotin in the growth media support Candida hyphae formation in a dose-dependent manner and does not inhibit the switch from yeast to hyphae.
There could be several reasons for the seemingly opposite results obtained in the two studies. The growth conditions employed by Yamaguchi were unusual in terms of the temperature used for cell culture. Also, the Candida strain used in the Yamaguchi study would now be reclassified as a closely related species, C. dubliniensis, which is notorious for producing fewer hyphae independent of the growth conditions being tested.
A perfect example of the conflicts in studies, is a study that was performed in 2018 and published in The Journal of Contemporary Dental Practice using xylitol on C. albicans infections in the mouth. The study concluded that xylitol has considerable antimicrobial effects against C. albicans. However, a different study by Gutierrez et. al that was published in FEMS Microbiology Ecology in 2020 concluded that xylitol increased the growth of C. albicans by 200%!
Therefore, given that biotin is a growth requirement for this auxotrophic pathogen and in view of poor experimental evidence substantiating the claim that biotin limiting conditions promote hyphae formation in C. albicans, the use of biotin for treating candida infections is not warranted. Moreover, infections in organs such as the spleen or liver where filamentation is not observed would remain unaffected by biotin therapy.
Symptoms of nutritional biotin deficiency include dry skin, seborrheic dermatitis, fungal infections, skin rashes, brittle hair, alopecia, and hyperglycemia. Nutritional deficiency of biotin is rare. However, some individuals lack the enzyme biotinidase, which plays an important role in recycling biotin. Individuals with this rare metabolic disorder can display clinical symptoms similar to those of biotin deficiency, such as alopecia and scaly dermatitis (18). C. albicans can often be cultured from the skin lesions in these patients (16).
Also, some of the women who experience recurrent or persistent episodes of vaginal candidiasis might be carriers of this inborn error of biotinidase deficiency (17). In a 1998 study where such a chronic vaginal candidiasis patient with a biotinidase deficiency, who was unresponsive to other therapies, was administered 10 mg biotin daily for 3 months, her symptoms of the fungal infection resolved completely (17).
There is also a more severe biotin responsive disease, holocarboxylase deficiency, that also results in biotin deficiency and candida infections (21). Biotin deficiency, whether nutritional or the one resulting from enzyme deficiency, is thought to lead to significant immune dysfunction (19, 20).
It could be postulated that in patients with metabolic disorders where biotin is not efficiently recycled or transported, secondary to a weakened immune system, recurrent candida yeast infections might arise. In such patients, it is possible that biotin therapy could help resolve the symptoms of the metabolic disorder including candidiasis by providing the biotin that the body needs to support a healthy immune system which in turn targets the Candida to eliminate it. The therapeutic dose of biotin is much higher (10 mg daily) in such cases as compared to that reported on various wellness websites (maximum of 5000 micrograms).
To conclude, based on the available studies and scientific literature, one successful study in 1998 does not make a trend, biotin therapy at doses commonly suggested on most wellness websites cannot be deemed sufficient to treat Candida albicans infections. However, in patients with rare metabolic disorders such as a biotinidase deficiency, significantly high doses of biotin daily might help resolve symptoms of Candidiasis, potentially by strengthening the host’s immunity. But because biotin is required for Candida growth, it is best to be tested for biotin and biotinidase deficiency before pursuing this line of treatment.
Dr. Shalaka Samant PhD earned her B. Pharm degree from Mumbai University where she was a gold-medalist. Later, she received her PhD in Pharmaceutical Biotechnology from the University of Illinois – Chicago, followed by, postdoctoral training from Yale University and University of Texas-Health Science Center. For her pre-doctoral work, she was the recipient of the prestigious American Heart Association pre-doctoral fellowship award.
She has over a decade of experience in the areas of molecular biology, microbial strain manipulation, and synthetic biology amongst other areas. She was a postdoctoral research associate in the lab of Dr. Jorge Galan, a renowned gastrointestinal infectious disease researcher.
Dr. Samant has functioned as the principal investigator on several biotechnology research projects funded by the Department of Biotechnology (DBT), Govt. of India. She has mentored several graduate students towards their dissertation research in diverse areas such as therapeutic protein expression and development of cell-based assay platforms for drug discovery.
She is now the founder and chief consultant at Biombrella, a life science consulting firm that provides deep-dive research, scientific writing and content generation services to various pharmaceutical, nutraceutical and biotech start-ups. She was recently interviewed for the Summer 2019 issue of ‘The Pharmacist’ – University of Illinois-Chicago.
Do you have any questions about biotin for yeast infections or yeast infections in general? Ask your question here or contact us using the contact page of this website. It is also always a good idea to talk to your doctor as well.
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This supplement contains 2000 mcg of biotin per serving, along with other ingredients (magnesium 45mcg, caprylic acid 500 mg, Pau D’Arco 300mg, black walnut …
Dr. Samant's References
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2. Odds F.C. Candida and candidosis: A review and bibliography. J. Basic Microb. 1988;30:382–383
3. Firestone BY et al, Growth promoting effects of some biotin analogues for Candida albicans. J Bacteriol. 1960 May; 79(5): 674–676
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9. Vidotto V et al, Importance of some factors on the dimorphism of Candida albicans. Mycopathologia. 1988 Dec;104(3):129-35.
10. Lo HJ, et al Nonfilamentous C. albicans mutants are avirulent. Cell90(5), 939–949 (1997).
11. Zheng X, Wang Y. Hgc1, a novel hypha-specific G1 cyclin-related protein regulates Candida albicans hyphal morphogenesis. EMBO J.23(8), 1845–1856 (2004).
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14. Yamaguchi, H. Mycelial development and chemical alteration of Candida albicans from biotin insufficiency. Sabouraudia 1974, 12, 320–328.
15. Yamaguchi, H. Effect of biotin insufficiency on composition and structure of cell wall of Candida albicans in relation to its mycelial morphogenesis. J. Gen. Appl. Microbiol. 1974, 20, 271–228.
16. Mock DM, Skin manifestations of biotin deficiency. Semin Dermatol, 1991 Dec;10(4):296-302.
17. Strom CM et al, Chronic vaginal candidiasis responsive to biotin therapy in a carrier of biotinidase deficiency. Obstetrics and Gynaecology, 1998, 92(4-2): 644-646.
18. J. Zempleni, D.M. Mock, Biotin, Physiology, in Encyclopedia of Food Sciences and Nutrition (Second Edition), 2003.
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20. Agrawal S, et al. Biotin deficiency enhances the inflammatory response of human dendritic cells. Am J Physiol Cell Physiol. 2016;311(3):C386–C391.
21. Wolf B, Heard GS. Disorder of biotin metabolism. In: Scriver CR, Beaudet A, Sly W, Valle D, eds. The metabolic basis of inherited disease. 6th ed. New York: McGraw Hill, 1989:2083–103.
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