INTRODUCTION
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
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
