Evidence for Supplemental Treatments in Androgenetic Alopecia

July 2014 | Volume 13 | Issue 7 | Original Article | 809 | Copyright © July 2014

Shannon Famenini MD and Carolyn Goh MD

Department of Medicine, Division of Dermatology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA

Currently, topical minoxidil and finasteride are the only treatments that have been FDA approved for the treatment of female pattern hair loss and androgenetic alopecia. Given the incomplete efficacy and sife effect profile of these medications, some patients utilize alternative treatments to help improve this condition. In this review, we illustrate the scientific evidence underlying the efficacy of these alternative approaches, including biotin, caffeine, melatonin, a marine extract, and zinc.

J Drugs Dermatol. 2014;13(7):809-812.


Female pattern hair loss (FPHL) and androgenetic alopecia are estimated to affect at least 40% of women and 50% of men by the age of 50.1,2 Without intervention, FPHL may be expected to progress at a rate of 10% per year and can cause significant psychological distress for patients.1 Androgens and genetic factors are both involved in male pattern hair loss, but their role has yet to be elucidated in women. In men, testosterone is converted to dihydrotestosterone by 5-alpha reductase, which then binds to the androgen receptors of the hair follicle dermal papillae and activates the genes responsible for follicular miniaturization.3 In women, FPHL is the term that has been used to describe this type of hair loss, since the role of androgens is unclear.4 Although recent evidence has shown that females and males share similar genetic polymorphisms,5 in this paper, we will use AGA to refer to both male and female pattern hair loss, but use FPHL when specifically referring to studies in women.
Topical minoxidil and oral finasteride are the mainstay of therapy for men. Placebo-controlled randomized trials have revealed both therapies to be efficacious and well-tolerated. A meta-analysis of randomized trials demonstrated treatment with finasteride results in a 24% increase in hair count after 48 months when compared to placebo administration.6 Finasteride acts as a competitive inhibitor of 5-alpha reductase, and minoxidil increases the length of the anagen phase and decreases the telogen phase. For women, topical minoxidil is currently the only FDA approved treatment for FPHL but primarily halts progression of hair loss.7 Anti-androgen therapy such as spironolactone has also been suggested as effective therapy for FPHL. In a small study, 88% of 80 women showed either no progression or improvement of their FPHL with anti-androgen therapy.8
Given the partial results obtained from these medications and potential adverse effects, both men and women often seek alternative treatments for AGA and FPHL. While a wide array of alternative therapies exists, here we present a review of biotin, caffeine, melatonin, marine protein extract, and zinc solution and their potential role in androgenetic alopecia treatment.


Biotin is an essential water-soluble vitamin that acts as a cofactor in carbon dioxide transfer in some carboxylase enzymes which are involved in fatty acid synthesis, amino acid catabolism, and gluconeogenesis.9 Biotin is also a coenzyme for mitochondrial carboxylases in hair roots.10 Biotinidase is a critical enzyme in releasing biotin from foods and biotin-containing peptides so that the body can absorb biotin.10 Genetic causes of biotin deficiency, such as both partial and profound biotinidase deficiency, result in a variety of symptoms including seizures, hypotonia, ataxia, dermatitis, hair loss, mental retardation, ketolactic acidosis and organic aciduria.11 Interestingly, alopecia resulting from valproic acid administration in rats, likely due to biotin deficiency, was shown to reverse with biotin supplementation.12 Biotin administration in children who had experienced alopecia after valproic acid treatment also produced a beneficial effect. Interestingly, no significant differences in biotin or biotinidase levels were found in 20 children treated with valproic acid and 10 children treated with carbamazepine when compared to 75 controls. Despite this, the alopecia was reversed in 3 patients treated with oral biotin administration for 3 months.13 In 32 pediatric patients treated with valproic acid, the mean biotinidase activity was found to be reduced in the first three months of treatment but returned to normal in the sixth month of treatment, although the difference was not statistically significant.14 In another study of 75 pediatric patients treated with valproic acid, the biotinidase activity was significantly reduced as compared with controls (P<0.001) and again alopecia was improved with biotin (10 mg/day) administration.15 These results suggest that valproic acid therapy may cause alopecia through an initial reduction in biotinidase activity, which may account for the utility of biotin therapy in reversing this type of alopecia.
Isotretinoin - associated telogen effluvium may also be attributed to an effect on biotinidase activity as evidenced by a study of 42 patients under isotretinoin (Roaccutane 0.5 mg/kg/24 h) who showed significantly reduced biotinidase levels (P<0.001) when compared to 52 controls.16