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Anabolic Steroids and Hair Loss

While some men voluntarily shave their heads these days and the stigma of baldness isn’t as great as in the past, many men still dread the loss of hair on their heads.

In a recent letter to a major medical journal, a physician who's treated many athletes suggested that other doctors look for three initial signs of anabolic steroid use in athletes: acne, gynecomastia (male breast development) and male-pattern baldness (MPD). Those three signs must be accompanied with extensive muscular size, since they also manifest in men who've never taken any type of anabolic steroid.

Two of the overall signs of steroid use are related to a by-product of testosterone metabolism, an androgen steroid called dihydrotestosterone. DHT plays key roles in the onset of both acne and male-pattern baldness. The third sign, gynecomastia, is related to increased estrogen production in men, which happens when the enzyme aromatase meets testosterone in the body.

While some men voluntarily shave their heads these days and the stigma of baldness isn't as great as in the past, many men still dread the loss of hair on their heads. An abundant head of hair is associated with youth and vitality, while loss of hair conjures images of old and sick men'though I wouldn't tell that to Mr. Olympia Ronnie Coleman.

Some studies even link male-pattern baldness to cardiovascular disease, particularly if the hair loss is most extensive in the vertex, or crown (back), of the head. One study that examined that hypothesis, however, found no clear-cut connection to any established cardiac risk factor, such as high blood pressure or elevated blood cholesterol.1

Another apparent truth about MPB in athletes who use anabolic steroids is that not everyone who uses them loses hair. MPB requires two conditions: 1) a genetic predisposition to baldness and 2) an exposure of hair follicles to increased levels of DHT. So even when DHT is present, if you don't have the genes that code for baldness, you won't lose your hair'at least not because you're using steroids.

Hair is produced and lost during three phases, termed anagen, catagen and telogen. Anagen is the growth phase, which lasts from two to six years. The longer the anagen phase, the longer your hair can grow. Catagen, lasting two to three weeks, is considered an 'involutional' phase, in which the hair follicle, or the portion of the scalp that sprouts hair, undergoes cellular change. That's followed by the telogen, or resting, phase, which lasts for two to three months. That's when the hair falls out, at the rate of about 100 hairs a day. Most of the time 90 to 95 percent of hair follicles are in the anagen phase, with 5 to 10 percent in telogen and 1 percent in the catagen phase.

The good news is that when the hair is lost during telogen, the anagen phase begins, resulting in new hair. That all changes, of course, with MPB, wherein a combination of genes and DHT extends the telogen phase indefinitely, preventing the return of the growth phase. Physically, an apparent, or terminal, hair is converted into a nearly invisible vellus hair. That's because DHT promotes a shrinkage of hair follicles, which can then only produce miniature and comparatively weaker hairs that tend to fall out.

Anabolic steroids promote MPB because they're based on testosterone. Interestingly, testosterone itself doesn't cause MPB. (In fact, drugs that treat MPB, such as Propecia, increase scalp levels of testosterone an average of 41 percent.) For some mysterious reason, however, test does cause baldness in women, who, conversely, aren't affected by DHT when they lose scalp hair. What happens is that testosterone converts in the scalp to DHT by way of an enzyme called 5 alpha-reductase (5AR). Other steroids, such as Primobolan, are directly based on the DHT structure, which offers the advantage of not converting into estrogen but the notable disadvantage of promoting MPB in men genetically predisposed to it.

DHT Has Its Uses

Why does the body produce DHT? Male sex organs don't develop without it. In fact, one way that scientists figured out that DHT was involved in MPB was by observing that men born without genes that coded for 5AR never went bald. They could produce normal levels of testosterone in their bodies, but without the presence of 5AR, their DHT production was zero. Another problem they had was ambiguous genitalia, since DHT is needed for full development of male sex organs'a high price to pay for not losing your hair. Eunuchs never go bald because they don't produce enough testosterone. Castration prior to puberty is one painful 'cure' for male-pattern baldness.

DHT is also a more potent androgen than testosterone in most tissues, including the prostate gland. Scientists think that DHT amplifies the cellular signals of testosterone, thus making test more of a pro-hormone in many tissues besides muscle. DHT has a roughly fivefold greater affinity for binding to the androgen receptor than testosterone. In muscle, however, testosterone is the primary androgen; DHT is largely inactivated by certain enzymes in muscle.

You need DHT to grow body hair, except for eyelashes and eyebrows, which grow independently of androgens. DHT is also involved in the production of neurosteroids in the brain, which may influence feelings such as aggression and depression.2 In the skin DHT promotes secretion of a natural moisturizer called sebum. Too much sebum, however, fuels acne bacteria. That's why DHT is linked to acne. MPB and Drug Research

Studies show that most men with MPB genetics begin to lose hair at age 30. By age 50 half of all men are bald. If you do nothing to offset the natural progression of MPB, you'll lose about 5 percent of your hair each year, commencing in your early 30s. If you use anabolic steroids, however, and have MPB genes, you can lose hair at any age. In years past the only options for treating MPB involved surgery to replace hair follicles, transplanting hair from the side of the head to the balding area. Occipital hair doesn't readily fall out for two reasons: It's less sensitive to the effects of DHT, and it contains a high level of aromatase, the enzyme that converts testosterone into estrogen. Women lose hair less readily than men because their scalps contain higher estrogen levels than men have there. Among other things, estrogen opposes the activity of DHT in hair.

ALLSeveral pharmacological approaches to treating MPB have emerged. The first medication approved for sale was Rogaine lotion in a 1 percent concentration. Its generic name is minoxidil, and in oral form it was most often used to treat high blood pressure. But a frequently noted side effect was excessive hair growth. That led to its development in topical form for treating MPB. It was approved for sale in 1988, and since then, 5 percent and 7 percent topical forms have also been approved.

Exactly how minoxidil leads to hair growth isn't known. Some suggest that it affects calcium entry into hair follicles in a way that favors hair growth. Another theory is that it promotes increased blood flow into follicles, which makes sense, since DHT restricts blood flow. Still another is that it increases local growth factors in the hair follicles. In any case, minoxidil is hardly a miracle cure; it has a success rate of about 20 percent for sprouting new hair on bald pates.

Minoxidil doesn't significantly affect DHT. That breakthrough arrived with the drug finasteride, approved in December 1997. Finasteride was initially marketed to treat benign prostatic hypertrophy, or enlarged prostate glands, at a dose of five milligrams a day. Later studies showed that a dose of only one milligram proved most effective for MPB, with higher doses showing only slight improvement, though far more costly. The form of finasteride marketed to treat prostate problems was called Proscar and the form for MPB treatment Propecia.

Finasteride works by inhibiting 5 alpha-reductase, which has two forms: types 1 and 2. Type 1 works in the sebum system of the skin, and type 2 is most active in the scalp and prostate gland. Type 1 is responsible for one-third of circulating DHT, and the other two-thirds come from the activity of type 2. Finasteride inhibits mainly type 2, weakly affecting type 1. The one-milligram dose in Propecia lowers scalp DHT by 64 percent and serum DHT by 68 percent. The main side effects are impotence and loss of sex drive, which affect about 2 percent of users. A recent study showed that finasteride also appears to help prevent prostate cancer.3 Propecia must be used continually and begins to show effects after about three months of steady use. Cessation of use causes hair to again fall out after 12 months. The good news is that a recent five-year study of men using finasteride for MPB showed that it continued to work effectively.

Last year a drug similar to finasteride was approved for treating prostate disease. Dutasteride, marketed as Avodart in the U.S. and Avolve in Europe, differs from finasteride in that it inhibits the activity of both types of 5AR. Like finasteride, Avodart increases serum testosterone an average of 20 percent, although total sperm count drops by 25 percent. The usual dose is a half milligram, which lowers DHT by 90 percent after four weeks and 94 percent after 24 weeks, thus making it more potent than finasteride. At a dose of 2.5 milligrams, Avodart blocked DHT synthesis by 100 percent. Although not yet approved for use in treating MPB, preliminary studies show that Avodart is about 30 percent more effective than finasteride in promoting hair regrowth.

The drawback with Avodart is that 55 percent of an oral dose is unaccounted for in the body. The half-life, or time it takes the body to eliminate half the initial dose, is five weeks, compared to five to eight hours for finasteride. Drugs with longer elimination times could pose problems, especially since no one knows the long-term effects of Avodart. It costs about twice as much as finasteride, which itself averages $2 per pill. 

Creative Treatment Options

One approach to maximizing the effects of either drug is to supplement with Nizoral shampoo.4 Nizoral, which has the generic name ketoconazole, is normally used to treat scalp fungal infections, or systemically as a potent anti-androgen. The latter use is what makes it good for MPB. Nizoral as a 2 percent shampoo works locally in the scalp to not only inhibit 5AR and thus lower DHT levels in hair follicles but also block androgen receptors in the scalp. Nizoral shampoo, which does require a prescription, may extend the benefits of either finasteride or Avodart.5

One study found that, over a six-month period, a cell-culture medium made into a topical form and smeared on the scalps of balding men resulted in their losing 7 percent of their hair, compared to a 40 percent loss in a group not using the treatment.6 The treatment also involved supplementing the culture treatment with insulin, thyroxine and growth hormone, which are all popular with athletes. While the study subjects reported that hair loss stopped after only two weeks, they had to keep the stuff on their heads for three hours a day. After four months hair count increased by 50 percent. Although the researchers reported no side effects, you'd have to be highly motivated to sit around for three hours a day with a gel smeared on your scalp.

A new topical drug, currently available only in the Czech and Slovak republics under the trade name Eucapil (generic name fluridil) may represent the next generation of MPB drug therapy. The lotion differs from the other drugs in that it is a direct androgen blocker in the scalp, which means that no matter how much DHT your body produces, the lotion will prevent its promotion of MPB. Because it doesn't inhibit the production of DHT, you won't experience any side effects linked to DHT loss, such as erectile or sex-drive dysfunction. Because none of the drug gets absorbed by the body, it won't adversely affect normal androgen activity.

Last year a Japanese company claimed to have found two of the genes linked to MPB. It also claimed to have found a natural substance, 6-benzyl aminopurine, that makes the genes turn on. When the genes fail to work, likely by being influenced by the presence of DHT, MPB is produced. The claims await further testing.

French scientists recently reported that 83 percent of 93 healthy study subjects with hair loss showed a decrease in hair loss after undergoing therapy that involved placing a combination of essential oils on their scalps and subjecting their scalps to electromagnetic pulse energy.7 How that technique may work to promote hair growth remains obscure.

Another offbeat technique features the use of a device called a LaserComb. One six-month study of 28 men and seven women with hair loss found a significant increase in hair growth and hair tensile strength with the LaserComb.8 The device seems to promote hair growth by decreasing scalp inflammation, which is emerging as a theory of a secondary cause of adult hair loss.9

The natural forms of 5AR inhibitors include gamma-linoleic acid found in borage or primrose oil, and alpha-linoleic acid from flaxseed oil and green tea.10 The isoflavones in soy inhibit 5AR,11 and omega-3 fatty acids exert weak but definite 5AR-inhibiting effects.12 A flavone derived from apples, Procyanidin B-2, was credited with hair growth in one human study.13 A substance derived from a Chinese herb, called impatienol, showed significant 5AR inhibition,14 as did a type of parsley commonly found in Japan.15 Arbor vitae appears to work like finasteride in inhibiting type 2 5AR.16

Another study showed that a 7.5 percent extract of various herbs, including fennel, polygonum, mentha, chamomile, thuja and hibiscus, in an aqueous cream base resulted in significant improvement when applied to the scalps of 24 balding men each day for 40 weeks.17 Men using the herbal formula increased their terminal-hair count by 169 percent compared to only 33 percent for a placebo group.

Those who still worry about hair loss from anabolic steroids may choose to stick with nandrolone drugs, such as Deca-Durabolin, which induce MPB little or not at all, though Deca is the worst drug for drug-testing procedures. In addition, if you use higher-than-usual doses of finasteride or Avodart, your estrogen levels may rise as a result of less testosterone conversion into DHT, leaving the hormone open to the effects of aromatase and calling for use of an aromatase-inhibiting drug like Arimidex. To further confuse you: One of the most effective drugs for treating incipient gynecomastia stemming from excess estrogen in men is a topical drug called Andractim (not available in the U.S.), which contains 2.5 percent of'DHT. As suggested above, DHT opposes the activity of estrogen and vice versa.


1 Ellis, J.A., et al. (2001). Male pattern baldness is not associated with established cardiovascular risk factors in the general population. Clin Sci. 100:401-44.
2 Stoffel-Wagner, B. (2001). Neurosteroid metabolism in the human brain. Eur J Endcrinol. 145:669-79.
3 Thompson, I., et al. (2003). The influence of finasteride on the development of prostate cancer. New Eng J Med. 349:213-22.
4 Khandpur, S., et al. (2002). Comparative efficacy of various treatment regimens for androgenetic alopecia in men. J Dermatol. 29:489-98.
5 Perez, H. (2004). Ketoconazole as an adjunct to finasteride in the treatment of androgenetic alopecia in men. Med Hypotheses. 62:112-15.
6 Lindenbaum, E.S., et al. (2003). Pilot study of a novel treatment for androgenetic alopecia using enriched cell culture medium: clinical trials. Dermato Online J. 9:4.
7 Bureau, J.P., et al. (2003). Essential oils and low-intensity electromagnetic pulses in the treatment of androgen-dependent alopecia. Advances in Therapy. 20:220-29.
8 Satino, J.E., et al. (2003). Hair regrowth and increased hair tensile strength using the HairMax LaserComb for low-level laser therapy. Int J Cosmet Surg and Aest Dermatol. 2:113-117.
9 Mahe, Y., et al. (2000). Androgenetic alopecia and microinflammation. Int J Dermatol. 39:576-84.
10 Hiipakka, R.A., et al. (2002). Structure-activity relationships for inhibition of human 5 alpha-reductases by polyphenols. Biochem Pharmacol. 63:1165-76.
11 Yi M, et al. (2002). Regulation of male sex hormone levels by soy isoflavones in rats. Nutr Cancer. 42:206-10. 12 Pham, H., et al. (2002). 5 alpha-reductase-catalyzed conversion of testosterone to dihydrotestosterone is increased in prostatic adenocarcinoma cells: suppression by 15-lipoxygenase metabolites of gamma-linoleic acid and eicosapentaenoic acids. J Steroid Biochem Mole Biol. 82:393-400.
13 Takahashi, T., et al. (2001). The first clinical trial of topical application of Procyanidin B-2 to investigate its potential as a hair-growing agent. Phytotherapy Res. 15:331-36.
14 Ishiguro, K., et al. (2000). Testosterone 5 a-reductase inhibitor bisnaphthoquinone derivative from Impatiens balsamina. Phytotherapy Res. 14:54-56.
15 Park, W.S., et al. (2003). Torilin from Torilis japonica, as a new inhibitor of testosterone 5-alpha-reductase. Planta Med. 69:459-61.
16 Park, W.S., et al. (2003). The extract of Thujae occidentalis semen inhibited 5 alpha-reductase and androgenetic alopecia of B6CBAF1/J hybrid mouse. J Dermato Sci. 31:91-8.
17 Greenberg, J.H., et al. (1996). Treatment of androgenic alopecia with a 7.5% herbal preparation. J Dermat Treat. 7:159-62. IM

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