As men grow older, many of them will develop hair loss in a characteristic pattern. It can start at the frontal scalp, moving upwards on the sides (‘bitemporal’), or at the back/top of the head at an area called the crown (also ‘vertex’). This hair loss progressively continues up to the mid scalp. Hair on the sides of the head and below the crown at the back are spared (the ‘occipital region’). This pattern of hair loss is known as male-pattern hair loss or androgenetic alopecia.
Androgenetic alopecia has the word ‘androgen’ in it, and with good reason. A phenomenal paper published in 1942 dubbed “Male hormone stimulation is prerequisite and an incitant in common baldness” [1] eloquently addresses the link between androgens and androgenetic alopecia. As you’ve probably derived from the name of the paper, the condition was then still dubbed “common baldness”. The author made some keen observations. First, the author observed that eunuchs and prepubertally castrated men didn’t develop alopecia. He writes: “Even the recession of the line of hair on the temples and foreheads which is observed in the majority of normal men failed to appear.” Second, when given testosterone, some of the men developed hair loss. Interestingly, when two of these men discontinued testosterone therapy for a year, baldness stopped to progress. However, when they were put back on testosterone again, the progression of hair loss resumed. Third, he also observed that the men who developed alopecia upon androgenic treatment belonged to families in which normal adult male members tend to be bald. Similarly, those who didn’t develop alopecia belonged to families without pronounced tendencies to baldness among the normal men. As such, a genetic predisposition to alopecia is suspected.
A paper published in the journal Science in 1974 demonstrated the pivotal role of dihydrotestosterone (DHT) in mediating testosterone’s effect on this condition [2]. DHT is a metabolite of testosterone that is formed by the 5α-reductase family of enzymes. DHT is a more potent androgen than testosterone, and thus testosterone’s effect is amplified in tissues expressing these enzymes. It was found that subjects with a 5α-reductase deficiency didn’t develop recession of their hairline. Indeed, a later review paper mentions that androgenetic alopecia has never been observed in people with this condition [3].
The important role of genetics in developing androgenetic alopecia is underscored in a twin study examining physical aging and longevity [4]. 76 identical twin pairs (monozygotic twins) participated, of which 65 (42 male, 23 female) also were included in the analysis of hair loss. A smaller sample of 21 nonidentical twin pairs (dizygotic twins) also participated, of which 16 were included in the analysis of hair loss (14 male, 2 female).
