How Dihydrotestosterone (DHT) Affects Male Baldness?
How Dihydrotestosterone (DHT) Affects Male Baldness?
Men are often troubled with onset of premature baldness particularly peculiar male-pattern baldness. Men who are in their 30’s have 30% chance, men who are in their 50’s have 50% risk whereas men who are in their 60’s have 57% chance of developing male- pattern baldness. The root cause is still unknown but various research studies suggests that dihydrotestosterone (DHT) has something to do with it. DHT is one of the key molecules involved in the pattern baldness. DHT is androgenic in nature and is responsible for the development of male traits.
Testosterone is converted into DHT, its potent form, by an active enzyme called 5-alpha-reductase (5-AR). Men born with the deficiency of this enzyme suffers from the poor development of external genitalia and prostate gland. Penis of such men seems more like an enlarged clitoris or at times it may be completely absent. Such men are usually infertile but at the time of puberty, they may show mail traits like deep voice or hair on the chest.
What Should You Know About Male Pattern Baldness?
Also referred to as androgenic alopecia, male pattern baldness is characterized by gradual thinning and subsequent loss of hair on the crown and the temples. Hair growth may be divided into 3 phases:
- Anagen: The phase usually lasts for 2-6 years and almost 85% of total hairs present on head remain in this phase.
- Catagen: The phase lasts for a period of 2 weeks. In this phase, the follicles are renewed.
- Telogen: This phase lasts for 1-4 months as the follicles become dormant. Usually 10-15% of hairs are present during this phase. The cycle goes on repetition as the new growth pushes out the existing hair out of the follicles, which then naturally shed.
Male pattern baldness is characterized by miniaturization of follicles and the duration of anagen phase being short. As a result of this, hair stops growing to its maximal length and the duration of telogen phase begins to increase. With time the duration of anagen phase becomes extremely shortened, preventing the sprouting hair to even get past the surface. The existing hairs become thinner and eventually reduced to villus hairs, the soft ones present on the baby skin.
Armpit and pubic hair along with beard grow in response to DHT unlike hair present on the head. DHT binds to an androgenic receptor and triggers miniaturization of follicles. To support this theory, it has been studied that the DHT levels are greater in the skin and follicles plucked from a balding scalp as compared to the ones from non-balding scalp.
The DHT mechanism in male pattern baldness is not fully understood but it may be due to:
- Presence of greater number of DHT receptors at the follicle
- Amplified local production of DHT
- Pronounced sensitivity of androgen receptor
- Elevated levels of testosterone that functions as DHT precursor.
Increased levels of 5-AR will result in increased conversion of testosterone into DHT resulting in pronounced hair loss. Therefore, individuals who are 5-AR deficient never suffer from male pattern baldness. The enzyme has two types, type 1 and type 2. Type 2 plays a more defined role in pattern baldness than type 1.
Since male pattern baldness is very undesirable, it can be reversed to some extent. For instance, DHT induced baldness can be minimized by Finasteride, a selective inhibitor of type-2 5-AR. However, to have a clear understanding regarding the role of DHT in male pattern baldness, further research work is required.
References
- Heilmann-Heimbach, S., Herold, C., Hochfeld, L. M., Hillmer, A. M., Nyholt, D. R., Hecker, J., … & Heng, X. T. (2017). Meta-analysis identifies novel risk loci and yields systematic insights into the biology of male-pattern baldness. Nature Communications, 8, 14694.
- Caserini, M., Radicioni, M., Leuratti, C., Terragni, E., Iorizzo, M., & Palmieri, R. (2016). Effects of a novel finasteride 0.25% topical solution on scalp and serum dihydrotestosterone in healthy men with androgenetic alopecia. Int J Clin Pharmacol Ther, 54(1), 19-27.
