I flipped on the TV the other day and was greeted with a view of the top of a middle-aged man’s head. In high definition. I think I was supposed to be paying attention to the guy’s bald spot, because an authoritative voice posed this question:
If you had a choice between baldness and a full head of hair, which would you choose?
Uh, is this a trick question?
Of course, this was a commercial for some sort of hair restoration method, but where I’m headed (no pun intended) is that I often see questions on the lists from guys who want to know how to stem the tide of male-pattern baldness that they experience after going on testosterone.
I also have heard trans guys question themselves about their concerns over losing their hair while on testosterone. Does that make them shallow? Does them make them vain? Don’t they have more important things to worry about than baldness? Does worrying about it make them less of a man?
Although hair loss doesn’t happen to all trans guys, it happens to some, just like it happens to some non-trans guys. The spot I saw on TV was just one of a gajillion commercials and ads for products that are designed to combat hair loss — obviously there are lots of men who are concerned about hair loss, or these products wouldn’t be out there. In other words, if some trans men are wanting to do something about male-pattern baldness, then aren’t they’re just being… men?
So you might be wondering, what causes male-pattern baldness and how can it be stopped? Well, okay, you might not really be wondering, but I’ll tell you anyway, because it’s interesting. (No, honest, it is.)
Explaining hair loss is easier when starting from the point of hair growth.
Hair shafts are manufactured in the hair follicles, which are considered “skin appendages” (as are bird feathers and fish scales). Hair follicles cycle through phases of growth (anagen), transition (catagen) and rest (telogen). In humans, hair follicles are asynchronous in their cycles, with about 85% of the follicles in anagen and 10-15% in telogen at any given time. (Some animals, like mice and rabbits, have waves of hair growth during which the hair follicle cycles are synchronized.)
The longer the duration of the follicular cycle, the longer the hair shaft; follicles in the scalp have a cycle that lasts two-to-five years and so have longer hair shafts than the vellus follicles which are located on the body and have much shorter cycles.
[On a side note, each human hair follicle sports a single shaft, whereas the hair follicle of the chinchilla manufactures 50 to 100 shafts, which explains the incredibly dense nature of, and the market for, chinchilla fur coats.]
In natal men and in trans men who undergo testosterone hormone replacement therapy (I will leave women out of the discussion – they can experience hair loss too but with a slightly different scalp pattern) , the testosterone (T) is converted in the skin to dihydrotestosterone (DHT) by the action of an enzyme called 5-alpha-reductase.
Actually, there are two forms of 5α-reductase, Type 1 and Type 2. Type 1 is mainly found in skin whereas Type 2 is predominant in the prostate and external genitalia – more on that later.
DHT is a more powerful androgen than T because it binds to the androgen receptor with higher affinity than T and thereby causes more significant effects. And although T can be converted to estrogen by an enzyme called aromatase (a chemical reaction called aromatization), DHT cannot.
In the case of male-pattern baldness, the hair follicles in the top and front center part of the scalp have a genetically-based sensitivity to DHT, which is why male-pattern baldness is also called “androgenetic alopecia” or “androgenic alopecia.”
Current dogma says that the genes that underlie male-pattern baldness are linked to the X-chromosome and are inherited from a person’s mother. In fact, the genetics behind androgenic alopecia are more complex than that, involving multiple genes that can be inherited from both or either parent.
So how does this hair loss business come about? Over time, the DHT causes a reduction the duration of the hair growth cycle, and as the cycle of the hair follicle becomes shorter and shorter, the hair shaft has less and less time to grow, so it becomes shorter and shorter, and thinner and thinner, and wee and tiny (called “miniaturization”), until the follicle finally burns out — more with a whimper than with a bang — as a “terminal follicle.”
And then what are you left with? Pure, unadulterated scalp.
There is hope, though, for the guy who is on T and wants to stem the migration of hair from his scalp to the shower drain. Finasteride, a drug that is available in tablet form, inhibits the Type 2 form of the 5α-reductase enzyme and is a treatment for androgenic alopecia. Now I know that I said that Type 1 is the predominant 5α-reductase in skin, but the Type 2 isoenzyme is present in skin as well and appears to be the form that is mainly responsible for male-pattern baldness, presumably because of its specific location within the hair follicle.
Finasteride comes in two doses — the more-expensive 1 mg Propecia tablet for treatment of hair loss and the less-expensive 5 mg Proscar tablet prescribed for benign prostatic hyperplasia (BPH), a.k.a. enlarged prostate. [DHT in prostate, converted from T by Type 2 5α-reductase, is one culprit behind BPH.]
To stop hair loss, I know some guys who get a script for Proscar, because it’s the cheaper of the two finasteride drugs, and then they use a pill-cutter to break it into quarters to arrive at a dose similar to the single tablets of Propecia. [I’m not giving advice that anyone should or should not do that – I’m just saying that I know guys who do. That’s something to discuss when asking a doctor for the prescription. Although many people take finasteride without any issues, there are side effects associated with the drug that, as with any drug, should be considered before taking it.]
Problem solved, right? Take a little pill and stop hair loss. Well, hold off on that trip to the pharmacy, because there is a paradox about this whole DHT/finasteride/hair growth business.
The trouble is, while DHT is pushing scalp hair follicles to their doom, it is also stimulating facial hair follicles in the beard area to produce heavier, longer shafts. So if a trans guy takes finasteride to arrest the loss of scalp hair, he might also be stopping or slowing new facial hair growth. I have a friend who experienced this.
If that is an issue, a guy might have to hold off on the finasteride and take a hit on the male-pattern hair loss until his beard grows in completely. In the meantime, he could use Rogaine (minoxidil) to try to stop the hair loss. Other than finasteride, minoxidil is the only other drug that has been approved by the FDA for the treatment of androgenic alopecia.
Originally developed as a drug to treat high blood pressure, one of minoxidil’s side effects was hair growth! But no one knows how it works. An increase in blood flow to the hair follicles is presumed to be part of the mechanism of action. Results from minoxidil vary from person to person, but some people can slow or stop hair loss with this product. The down side — it ain’t cheap.
What about saw palmetto? A member of the traditional medicine arsenal, saw palmetto is an extract of the Serenoa reppens plant and is used to treat enlarged prostate and androgenic alopecia. In case you’re thinking of using it, here’s a word about saw palmetto:
Finasteride (sort of).
Okay, so that was more than one word, but my point is that one of the ways that saw palmetto works to (supposedly) stop or slow male-pattern baldness (and treat enlarged prostate) is the same way that finasteride works — by inhibiting 5α-reductase. So if a guy is avoiding finasteride so that it doesn’t interfere with his whisker development, he should avoid saw palmetto as well for the same reason.
What’s in Your Pants
Lastly, and certainly not leastly, we come to the genitals, so to speak. Believe it or not, hair growth, male-pattern baldness and genital growth all have something in common: 5α-reductase and DHT. While testosterone is responsible for development of the internal male reproductive organs (including the testicles because they develop inside the body), DHT directs development of the male external genitalia.
This role of DHT becomes evident in cases of the intersex condition 5α-reductase deficiency which is due to mutation of the gene for the Type 2 form of the enzyme. These individuals are genetically male (XY chromosomes), usually with female or ambiguous genitalia, although some can have male genitalia with a micropenis. At puberty, the internal testes in these individuals produce testosterone and often descend, and some virilization of the body occurs.
Why does the external genitalia of genetic males with this condition fail to develop completely? No 5α-reductase –> no DHT. No DHT –> no “traditional” external male genitalia. What does that mean for a trans guy on T? Well, with DHT’s importance in growth and development of external genitalia in natal men, it stands to reason that it is involved in growth of the genitalia of trans men who are on testosterone.
Bottom line? If you’re in your first couple of years of testosterone hormone therapy and you want to do something about your thinning scalp hair, but you also want your beard to come in better and your penis to grow, it might be a good idea to stay off the finasteride and saw palmetto and go with Rogaine. Or nothing at all.
If all goes well, you’ll be doubly endowed (if that’s what you want) with facial hair and what’s growing on your head. I will post another time about potential ways to improve endowment of what’s in your pants, but in the meantime, here is some informative reading material regarding DHT for transgender men that was written by another trans guy.
Reference: Controls of hair follicle cycling, K.S. Stenn & R. Paus, Physiological Reviews 81:449-494, 2001
The Straight Dope: Is Male Pattern Baldness Inherited? Who’s to Blame? (August 19, 2005)
USNLM Genetics Home Reference: Androgenetic Alopecia