Methyltestosterone and Hair: The Risk of Androgenic Balding

"Steroids make you go bald" is one of the most widespread claims in the sports world. It is only partly true: androgens do not create balding from scratch, but they can substantially accelerate it in people with a genetic predisposition. The editorial team examined how methyltestosterone is connected to androgenic alopecia and what research says about it.

What androgenic alopecia is

Androgenic alopecia is the most common type of hair loss in men. It manifests as a gradual recession of the hairline at the temples and thinning at the crown. The degree of balding in men is traditionally assessed on the Hamilton-Norwood scale, and in women on the Ludwig scale, where diffuse thinning along the part predominates.

The key word in the name is "androgenic." As early as 1942, the American anatomist James Hamilton showed that men castrated before puberty do not go bald. When such men were given testosterone, some of them - those with balding in the family - began to lose hair. The conclusion was formulated clearly: androgens are a necessary condition, and genetics determines whether balding is realized.

This scheme still remains the basis for understanding the disease. Androgenic alopecia is polygenic; the best-known candidate gene is the androgen receptor gene on the X chromosome. That is why the predisposition is often associated with the mother's line, although it is inherited from both parents.

Balding is not a one-time process. The follicle does not "fall out" but gradually miniaturizes: the growth phase (anagen) shortens, the hair becomes thinner, lighter, and shorter, until it turns into barely noticeable down. In the later stages some follicles lose the ability to recover.

The role of testosterone and DHT in the follicle

The main "executor" in the hair follicle is considered to be not testosterone itself but dihydrotestosterone (DHT). It is formed from testosterone by the action of the enzyme 5α-reductase, primarily type 2, and binds to the androgen receptor more strongly than the parent hormone.

The most convincing evidence of DHT's role is men with a congenital deficiency of 5α-reductase type 2, who do not develop androgenic alopecia. The second piece of evidence is pharmacological: finasteride, which blocks this enzyme, slowed balding in randomized studies and, in some men, caused hair regrowth.

An interesting paradox is that androgens act on the follicles of different zones in opposite ways. On the face, chest, and armpits they stimulate the growth of terminal hair, while at the crown and temples in predisposed people they, on the contrary, suppress it. That is why the simultaneous strengthening of beard growth and thinning of scalp hair is a typical picture.

The mechanism of suppression is associated with a change in signals from the dermal papilla - a group of cells at the base of the follicle. Under the action of androgens it produces factors that shorten anagen and speed up the follicle's transition to the resting phase.

Methyltestosterone: what is known about the risk

There are practically no direct controlled studies that separately measure the effect of methyltestosterone on hair. However, in the medical prescribing information for methyltestosterone products, male-pattern balding is mentioned among the androgenic side effects. This is consistent with the fact that the drug is a full agonist of the androgen receptor.

Does methyltestosterone form a metabolite analogous to DHT? According to metabolic studies, part of methyltestosterone undergoes 5α-reduction, so theoretically it can create an additional burden on follicles through this pathway. However, the exact proportion of such conversion in the human scalp has not been established, and the editorial team will not cite invented figures.

In observational studies of people who use anabolic steroids without medical supervision, hair loss consistently appears among the frequently mentioned side effects. These data have limitations: most respondents used several drugs at once, so the contribution of each substance separately cannot be assessed.

The practical conclusion is this: the main risk factor is genetic predisposition. A person without it may not notice any changes, while a person with a family history of early balding risks accelerating the process by years. Part of the lost hair may recover after the androgen excess is removed, but far-advanced miniaturization is often irreversible.

Women, body hair, and other effects

In women, androgen excess manifests in two ways: thinning of scalp hair and increased hair growth on the face and body (hirsutism). Methyltestosterone was used in women in the past, in particular in combination with estrogens for menopausal symptoms, and hirsutism, acne, and voice deepening were well-known side effects.

Some of these changes in women, especially the change in voice timbre, may be irreversible. We examined this topic in more detail in the material on the risks of virilization.

In men, increased body hair growth is usually perceived neutrally, but it is precisely this that clearly shows how one and the same hormone acts differently on different follicles. The beard thickens while the hair at the crown thins - this is not a contradiction but a feature of biology.

Hair loss can have other causes not related to androgens: iron deficiency, thyroid dysfunction, telogen effluvium after stress or illness. So one should not attribute any thinning to hormones alone.

Diagnosis and treatment of balding

A diagnosis of androgenic alopecia is made by a dermatologist or trichologist based on examination and trichoscopy. If needed, the doctor orders tests to rule out other causes of hair loss.

• Complete blood count and ferritin - to rule out iron deficiency.
• TSH - to assess thyroid function.
• Sex hormones - as clinically indicated, especially in women.
• Trichoscopy - to assess follicle miniaturization.

Among treatment methods with proven effectiveness are topical minoxidil and oral finasteride in men. Both have their limitations and side effects, so the decision is made by a doctor. Hair transplantation is possible only with a stable process and a sufficient donor zone.

Self-directed combination of androgens with 5α-reductase inhibitors "to protect the hair" is a practice from forums that has no evidence base and is associated with additional risks. The editorial team does not recommend such experiments.

Editorial conclusions

Androgens, including methyltestosterone, do not cause balding in people without a genetic predisposition, but they can noticeably accelerate it in those who have such a predisposition.

The main role in follicle miniaturization is played by DHT, and alopecia itself is a gradual and partly irreversible process. Seeing a dermatologist early gives a better chance of keeping the hair.

If there is early balding in the family, any experiments with androgens should be evaluated primarily from the standpoint of risks rather than expected benefits.

We also recommend reading our articles on the effect of methyltestosterone on the skin, on its side effects in general, and on the risks of virilization in women.

References

1. Hamilton JB. Male hormone stimulation is prerequisite and an incitant in common baldness. Am J Anat. 1942;71(3):451–480.
2. Kaufman KD, Olsen EA, Whiting D, et al. Finasteride in the treatment of men with androgenetic alopecia. J Am Acad Dermatol. 1998;39(4 Pt 1):578–589.
3. Kelly Y, Blanco A, Tosti A. Androgenetic alopecia: an update of treatment options. Drugs. 2016;76(14):1349–1364.
4. Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
5. U.S. Food and Drug Administration. Methyltestosterone tablets/capsules: prescribing information (labeling).
6. Nieschlag E, Behre HM, Nieschlag S (eds). Testosterone: Action, Deficiency, Substitution. 4th ed. Cambridge University Press; 2012.