Hair Today, Gone Tomorrow. What's Testosterone Got To Do With It?
For women in menopause, hair loss threatens one’s self-image and social confidence. Termed androgenic alopecia (AGA), or “female pattern hair loss,” it is misinterpreted as “going bald.” Even if a woman is reassured that this is not the case, or that it affects men as well, the phenomenon evokes fear and even depression.
Under the influence of our androgens, formation of a hair begins in a follicle consisting of epidermal cells that grow down into the dermis. At the base of the follicle is the papilla, a living organ surrounded by capillaries, where the hair is created and which responds to circulating hormones. As the hair forms, it grows toward the surface in a shaft of two layers, the inner layer ending below a sebaceous gland and an outer layer that attaches to the gland. The sebrum, produced by the gland, offers conditioning to the hair, which is composed of dead proteinaceous material. The growth phase of normal hair (anagen phase) lasts up to three years, followed by the catagen phase (a brief intermediate period), and then a short (100 days) resting (telogen) period before the hair is discarded.
The androgen, testosterone, when converted to its active form, 5-alpha dihydrotestosterone by the enzyme 5-alpha reductase, is essential for hair on our face and body, and less for our axilla and pubic area. But age, gender, and genetics also influence this process. In early puberty, androgens initially elicit the development of tiny vellus hairs that later become pigmented, followed by larger hairs that appear differently in different parts of the body.
The formation of 5-alpha dihydrotestosterone is key to normal hair growth. Yet excessive activity by the enzyme 5-alpha reductase produces the thinning or miniaturization of hair characteristic of AGA. In this process, over several hair cycles, there is a shortened growth or anagen phase, (a reduction from three years to 1.5 to 3 months) leading to thin, colorless hairs instead of long, firm-colored hairs. No change in number of follicles, however, occurs. If the normal growth cycle of anagen to telogen ratio is 9:1, miniaturization reduces this ratio to 2:1.
That the process is selective to certain areas of the scalp reflects the differences in embryologic origin of these scalp areas. In men and women, there is more 5-alpha reductase in frontal follicles than in occipital follicles. Additionally, women have more of the enzyme, aromatase, in the frontal and occipital scalp, which metabolizes testosterone to estrogen. Most women with AGA have normal menses. Measuring blood levels of hormones, therefore, offers little value in the evaluation. Moreover, there is no relationship of AGA to other testosterone effects on muscle, bone, or sebrum secretion.
Treatment of AGA addresses the unique aspects of this biologic event. Biotin, a water soluble B7 vitamin, improves keratin, a structural protein in hair and nails. Oral finasteride, a 5-alpha reductase type 2 inhibitor, may slow the AGA process in premenopausal but not menopausal women. Spironolactone, an aldosterone antagonist, offers mild anti-androgenic effects. Minoxidil, initially used as an antihypertensive agent, stimulates the vellus follicles. Finally, non-androgenic hair follicles transplanted from the occipital scalp to the androgen-dependent frontal areas provide a permanent solution.
Hair loss is a major insult to our sense of self-worth. Understanding the biology provides opportunities for new and innovative therapies.
By James Woods, M.D. and Elizabeth Warner, M.D.
Dr. Woods treats patients for menopause at the Hess/Woods Gynecology Practice.
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James Woods |