That receding hairline – what treatment is best?

Androgenetic Alopecia

13th August 2023, Dr Chee L Khoo

Many of the male doctors are slowly losing the battle against male pattern alopecia. It’s either thinning or receding. For those who are not there yet, it’s coming. We are also seeing women joining the club. Androgenetic alopecia (AGA) is the most common form of hair loss in humans affecting 80% of Caucasian men and 50% of Caucasian women.[1]. There are many options out there, not including hair transplants, scalp laser or wigs. We have various pharmaceutical agents that claim to do better than the rest. What are the options and which is the better agent?

Hair loss typically begins with bitemporal recession of the frontal hairline, followed by diffuse hair thinning at the vertex, and eventual complete loss of hair at the center of the vertex. The bald patch at the vertex subsequently joins the frontal receding hairline, leaving an island of hair on the frontal scalp. This island finally disappears leaving hair only in the parietal and occipital zones. Other less common patterns include more rapid hair loss over the vertex than the frontal area, frontal hairline loss before the vertex bald patch develops and also, a Ludwig-type pattern with preservation of the frontal hair line.[2]

Let’s look at how hair comes out – the hair cycle. Each hair originates in a hair follicle. The hair growth cycle has four phases:

(1) The anagen or growth phase, which is the longest and lasts 2 to 7 years

(2) The catagen or transition phase, which lasts approximately 2 weeks and includes hair follicle involution due to apoptosis

(3) The telogen or resting phase, which lasts 12 weeks when old hair is removed and

(4) The exogen phase, which is the release phase of the telogen hair.

Miniaturisation of the hair follicle is the hallmark of androgenetic alopecia [3]. This occurs usually in the late catagen phase but occasionally, in the early anagen phase. The dermal papilla and sheath is affected which leads to a shrinking follicle and a shorten anagen phase. This miniaturisation is generally irreversible although sometimes, there is a partial regrowth or partial reversal.

There are a number of processes leading to miniaturisation:

  • Abnormal sensitivity of follicles to circulating androgen – there is close interaction between the mesenchyme cells and epithelial cells. There is evidence that androgens affect that interaction but the molecular mechanism is still unclear.
  • Disregularities of arrector pili muscles with dysfunction of follicle stem cells leading to replacement by adipose tissue. It appears that the arrector pili muscles is a source of hair follicle stem cells. It is unclear why and how the arrector pili cells undergo degeneration and are replaced by adipose tissues.
  • Micro-inflammation of the follicles leading to progressive fibrosis.

The enzyme, 5-alpha reductasecatalyse the conversion of testosterone to 5-alpha–dihydrotestosterone. There are two isoforms of the enzyme, I and II. There are more 5-alpha reductase type 1 in hair follicles suggesting a key role of androgens in hair growth. In androgenic alopecia, there is an increase in androgen receptors in the scalp especially in the frontal scalp area.

Finasteride and dutasteride are 5-α reductase inhibitors (5-ARIs).4 Minoxidil is another drug for AGA; but surprisingly, its mechanism of action is not fully understood.  Numerous studies have investigated the efficacy of minoxidil and the 5-ARIs for the treatment of male AGA (4,5). However, evidence on their relative efficacy is scant.

The relative efficacy of oral and topical minoxidil was recently examined using network meta-analyses (6). How do the oral and topical agents compare?

23 studies were eligible for quantitative analyses. Mean (SD) age of patients ranged from 22.8 (3.3) years to 41.8 (12.3) years. 15 regimens were identified:

(1) 0.02 mg/d of oral dutasteride,

(2) 0.1 mg/d of oral dutasteride,

(3) 0.5 mg/d of oral dutasteride,

(4) 0.2 mg/d of oral finasteride,

(5) 1 mg/d of oral finasteride,

(6) 5 mg/d or oral finasteride,

(7) 1% topical finasteride,

(8) 0.25 mg/d of oral minoxidil,

(9) 5 mg/d or oral minoxidil,

(10) 0.1% topical minoxidil,

(11) 1% topical minoxidil,

(12) 2% topical minoxidil,

(13) 3% topical minoxidil,

(14) 5% topical minoxidil, and

(15) placebo or vehicle.

Oral minoxidil has never been approved as a hair loss treatment in any country.

The greatest increase in total hair count at 24 weeks (ie, first end point) was with 0.5 mg/d of dutasteride, which was significantly more efficacious than 1 mg/d of finasteride and minoxidil oral followed by minoxidil topical. The higher potency can be ascribed to the fact that dutasteride, compared with finasteride, is 100 times more potent in inhibiting the type I isoenzyme of 5-α reductase and 3 times more potent in inhibiting the type II isoenzyme. Furthermore, finasteride inhibits only the type II isoenzyme.

The greatest increase in terminal hair count at 24 weeks was with 5 mg/d of minoxidil, which was significantly more efficacious than the 0.25-mg/d dose and its topical forms 2% and 5% 5mg/d of minoxidil was significantly more efficacious than 1 mg/d of finasteride.

There were insufficient data available on dutasteride after 48 weeks of therapy. Thus, the greatest increase in total hair count at 48 weeks was with 5 mg/d of finasteride, which was significantly more efficacious than 2% topical minoxidil. The greatest increase in terminal hair count at 48 weeks was with 1 mg/d of finasteride, which was significantly more effective than topical minoxidil 2% and 5%.

It would seem from this network meta-analysis that a possible ranking of efficacies—in decreasing order is 0.5 mg/d of oral dutasteride, 5 mg/d of oral finasteride, 5 mg/d of oral minoxidil, 1 mg/d of oral finasteride, 5% topical minoxidil, 2% topical minoxidil, and 0.25 mg/d of oral minoxidil.


  1. Heilmann S, Brockschmidt FF, Hillmer AM, Hanneken S, Eigelshoven S, Ludwig KU, et al. Evidence for a polygenic contribution to androgenetic alopecia. Br J Dermatol 2013;169:927-30
  2. Sinclair R. Male pattern androgenetic alopecia. BMJ 1998;317:865-9.
  3. Jahoda CA. Cellular and developmental aspects of androgenetic alopecia. Exp Dermatol 1998;7:235-48.
  4. Blumeyer  A, Tosti  A, Messenger  A,  et al; European Dermatology Forum (EDF).  Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men.   J Dtsch Dermatol Ges. 2011;9(suppl 6):S1-S57. doi:10.1111/j.1610-0379.2011.07802.x
  5. Kanti  V, Messenger  A, Dobos  G,  et al.  Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men – short version.   J Eur Acad Dermatol Venereol. 2018;32(1):11-22. doi:10.1111/jdv.14624
  6. Gupta AK, Venkataraman M, Talukder M, Bamimore MA. Relative Efficacy of Minoxidil and the 5-α Reductase Inhibitors in Androgenetic Alopecia Treatment of Male Patients: A Network Meta-analysis. JAMA Dermatol. 2022;158(3):266–274. doi:10.1001/jamadermatol.2021.5743