Minoxidil was considered a powerful option for treating hypertension. It was a potent vasodilator, albeit a variety of side effects made it out of the choice. Yet, one of the unintended consequences opened up a new pathway: hypertrichosis. This phenomenon made Minoxidil a new medication for androgenetic alopecia in 1986 [1]. This essay will briefly review a chronological sequence of Minoxidil’s applications to its current resurgence in the oral form.
As a vasodilator, Minoxidil, which is more potent than hydralazine, with 10-40 mg dosages, was an option to harness severe and recalcitrant hypertension back 50 years ago. Its exact mechanism of action is not yet established, but it appears to be via affecting potassium channels of vascular smooth muscles and hair follicles [2]. Significant side effects of taking Minoxidil, such as fluid retention, pulmonary hypertension, and heart failure, led to crossing it out of the hypertension medications of choice. However, hypertrichosis became a new rise for further investigations and applications [3]. Subsequently, in 1986 and 1993, 2% and 5% topical solutions of Minoxidil were developed as a treatment for androgenetic alopecia (AGA) and female pattern hair loss (FHL), respectively. Topical forms could avoid systemic side effects and cure AGA and FHL. In 2006, FDA approved topical Minoxidil as a medication for hair loss in men and women [4].
Even though topical Minoxidil has remarkable success in hair regrowth, some inconvenience comes from wetting the hair or applying it twice daily, or in some regions, a higher price of this form. Thus, some studies intended to increase the efficacy of the treatment turned the oral formulation of Minoxidil with a non-effective dose for hypertension back to the table [5].
Some studies have investigated oral Minoxidil with a dosage lower than 5mg (mostly lower than 2.5 mg) to evaluate its efficacy for treating alopecia. Most of the results were positive and promising. M. Vastarella et al. assessed oral minoxidil for androgenic alopecia in female patients. The starting dose was 0.5 mg daily, then gradually increased to 2 mg in 24 weeks. The quantitative assessment showed an overall 38% and 23% improvement in hair density in the frontal and vertex area, respectively [6].
J. Jimenez-Cauhe et al. also recruited 41 men with androgenic alopecia in a study to evaluate the efficacy of taking 2.5—5 mg of oral minoxidil daily for more than six months. Overall clinical improvement was obtained in 90% of the cases, and marked alteration was seen in about 26% of the patients. Not any serious side effect was reported [7].
Some studies suggest that Minoxidil bolsters hair regrowth by affecting hair follicles and dermal papilla cells. Since topical minoxidil has relatively poor availability to the hair follicles and dermal papilla cells, a low dose of oral Minoxidil seems to be a reasonable and worthwhile option for treating alopecia [8]. Although most of the studies could support using oral minoxidil in androgenic alopecia cases, their structures were not designed to evaluate the superiority of each form of minoxidil over the other [9]. Potential cardiovascular effects of prescribing oral minoxidil may lead to prudence in dermatologists. Albeit, reported consequences related to the cardiovascular system were not remarkable [7, 10].
The positive outcomes in hair regrowth have made a vouge for the oral form of Minoxidil. Yet, there’s still a lack of a systematic comparison of the present studies on the dosage efficacy of Minoxidil and robust clinical trials on patients with different underlying medical conditions and potential risk factors. Accordingly, we suggest designing robust large-scale studies to evaluate the safety of using oral minoxidil in treating androgenic alopecia.