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2 October 2006
Testosterone And Baldness
by Paul Aitken

"You see Homer, I too know the sting of male pattern baldness."
Montgomery Burns
I first noticed I was going bald when I was seventeen. I had suspicions for about a year before that, but at seventeen I knew. I can't remember how exactly; I guess enough hairs had fallen out so that I could detect a difference from my mental picture of how it should look. I'm sure many men reading this will have at some point in their young lives felt the same icicle of dread slide into their hearts as they inspected their hairlines. The "if" part was over, the only question that remained was; "How bad will it be?" This was in the late seventies, decades before drugs such as minoxidil and Propecia offered a possibility of salvation.

My passive-aggressive asshole barber assured me I would be bald by the age of 30. Any literature on the subject was either of the snake-oil huckster variety, or, the paternalistic medical kind which tried to convince me of two things: a) There was nothing I could do about it; and b) It was no big deal. Lots of women are attracted to bald headed men etc. I intuitively bought the first one; the second I knew to be a total lie. At the time there was no good scientific information about the causes of baldness although the scientific consensus (initially suggested by a physician named Dorothy Osborne in 1916) was that it occurred by way of a gene passed on through the mother. If you wanted to know how bad it was going to be, don't look at your father, look to the males on your mother's side. This was a pity in my case because although my father was balding, it was mostly a bald spot kind of thing; he still kept a substantial tuft up front. The guys who really looked like dorks were the ones who went bald from the forehead on back... like most of the males on my mother's side.

The mechanism by which this happened was presumably a single gene on the X chromosome. Baldness was thought to be just another sex-linked trait like hemophilia or color blindness. These are recessive traits. That is, they are expressed only in people that don't have a "normal" gene on the counterpart chromosome (all chromosomes come in pairs - one from the mother, one from the father). The X chromosome's homolog, however, is the Y chromosome, and because there are virtually no common genes between them, a recessive gene on the X chromosome will always be expressed in men. A woman, with an X chromosome from both her father and mother is more likely to have back-up. That's why rare diseases like hemophilia are almost exclusively manifested in males. But the gene for baldness is not rare. About 1-in-4 men go noticeably bald in their twenties. By their fifties, that ratio is 3-in-4. If my mother carried the baldness gene in both of her X chromosomes, why wasn't she bald? For that matter, why weren't there bald women everywhere?

The answer is that a genetic propensity for baldness is not all that's required to make your hair fall out. What are also needed are androgens. Specifically, the androgens produced in your testicles. As I mentioned in an earlier column on the Castrati, men who lose their testicles before their hair falls out will never go bald. Children and women both produce androgens but not in sufficient quantities to engender hair loss. In a nutshell, androgens + baldness gene = baldness. At least that was the equation when I was seventeen.

But a lot of scientific research has been conducted into baldness in the last thirty years and the equation has grown more complex. There are now thought to be several genes involved that are scattered throughout the genome. Some have even been identified (sort of). In retrospect, this seems obvious. If there were just one gene involved, every man affected should go bald the same way. But a glance around any crowd at a hockey game reveals an almost infinite variety in the pattern of male pattern baldness. If the bald gene was only on the X chromosome, I should have gone cue ball(ed) like my mother's uncles. Instead, I went bald almost exactly like my dad. Take an overhead shot of us 32 years apart and except for his big nose beaking out, you wouldn't know the difference.

It is now thought that the degree of baldness in any individual is dependent on two variables. The number of androgen receptors on the cell surfaces in the hair follicles of the scalp and the amount of dihydrotestosterone (DHT) available to act on those receptors. If you've never heard of DHT it's probably about time that you did. DHT is the defining hormone in male development. As its name suggests, DHT is formed from testosterone but is thought to be 30 times more powerful due to its affinity for the androgen receptor. Its production in the male fetus during the first trimester is what leads to sex differentiation. Take away the DHT in this critical period and he will be a she. It is also implicated in the masculinization of the body during adolescence. Beard growth, muscle growth, a deep voice and, yes, baldness. DHT is metabolized from testosterone by the action of an enzyme called Type II 5-alpha reductase. There is a direct relationship between the amount of 5-alpha reductase produced and the levels of DHT in the system. XY females are thought to result from a mutation in the 5p15 gene (located on the short arm of the fifth chromosome) which codes for the enzyme. Without 5 alpha reductase, DHT is not metabolized and none of its associated effects are realized. XY females never go bald.

This revelation was the inspiration behind finasteride, the anti-baldness medication marketed as Propecia. Propecia works by linking up with 5 alpha reductase and preventing it from acting on the testosterone molecule. In effect, it's a pharmaceutical version of androgen insensitivity, which is why a Propecia pill should never be handled by a pregnant woman. If the coating of the pill is damaged, sufficient quantities of the drug could be absorbed through the skin to affect the external genital development of the fetus. And get this, not only will he be born a she (or something in between), but because the androgen insensitivity effect is only temporary, he/she will go bald when he/she hits adolescence. Potentially devastating birth defects aside, Propecia has been a boon to men with male pattern baldness. And it's been a golden goose for Merck & Co. The genius of the drug is that in most men, 5 alpha reductase, is continually being produced, requiring a constant supply of the drug to block it. Once you're on Propecia, you're on it for life. If you stop taking it, you'll lose all the hair you would have lost if you had never taken the drug.

Why DHT should cause your hair to fall out is not yet understood. When DHT binds to a receptor, it initiates a complex cascade of chemical changes (signaling) within the cell that can effect any number of cytoplasmic or nuclear (ie. genetic transcription) responses. The current assumption is that a surplus of DHT induced signaling causes a disruption in the normal growth cycle of the hair follicle. Hair growth is periodic and there are growth phases and dormancy phases. Too much DHT and the hair follicle keeps repeating the dormancy phase like a broken record. This is why Propecia, if taken early enough, can result in significant regrowth. If you wait too long though, the follicle dries up and no amount of "grow" signals will induce follicular regeneration.

What is known with certainty is that the greater number of androgen receptors you have on the surface of your follicle cells, the more DHT activation is likely to be induced and the more likely it is that your hair will fall out and stay out. The distribution of androgen receptors is thought to be determined almost entirely by your genes. And guess what? According to Dr. Nothen, of the University of Bonn, one of these androgen receptor genes has been located on the X chromosome. Looks like Dorothy Osborne may have been at least partly right.

The truly big question regarding male pattern baldness is why it exists at all. Despite the assurances of some "experts," baldness is not a trait that attracts women. In fact, it's a turn-off for many, especially those in the prime of their reproductive life. How could a trait that negatively affects the reproductive success of its carrier become so widespread in the population (all populations are affected those of European descent most of all)? The logical answer is that whatever genes cause baldness must incidentally confer an advantage of some kind. What that advantage might be is anybody's guess, but it's a small consolation when you're looking in the mirror at seventeen years of age.




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