Stanozolol and hair: the risk of androgenic baldness

Among the reasons men fear anabolic steroids, baldness is one of the most common. Stanozolol is often called a drug «dangerous for the hair» because it is a derivative of dihydrotestosterone. The editors explain how androgens affect hair follicles, why genetics matters more than any drug's name, what baldness medications change and what cannot be expected of them when stanozolol is used.

How androgenic baldness arises

Androgenic alopecia is the most common cause of hair loss in men. It manifests as a gradual recession of the hairline at the temples and thinning at the crown. The basis of the process is miniaturization of follicles: under the action of androgens the active growth phase of hair (anagen) shortens, and the follicles themselves shrink and with each cycle produce thinner, shorter and lighter hair, until it becomes a barely noticeable down.

A key role in this is played by dihydrotestosterone (DHT). It is formed from testosterone under the action of the enzyme 5α-reductase, particularly its type 2, which is active in the skin of the scalp. DHT binds to the androgen receptors of the dermal papilla cells — the follicle's «command center» — and triggers changes in the signals that regulate hair growth.

At the same time, blood androgen levels in people with baldness are mostly normal. What matters decisively is the sensitivity of the follicles, which is determined by genetics. Variants of the androgen receptor gene on the X chromosome and a number of other genetic loci explain why in some men hair is preserved into old age while in others it disappears already in their twenties.

An interesting paradox: androgens stimulate hair growth on the face and body but suppress it on the crown and temples of genetically predisposed people. That is, the same hormone acts on different follicles in opposite ways, depending on their location and «program».

Stanozolol and the follicle: what is known

Stanozolol is a synthetic androgen, a derivative of DHT, with a pyrazole ring attached to ring A. It no longer requires 5α-reductase and does not aromatize. Thus it can bind directly to the androgen receptors of follicles and act on them similarly to DHT.

The editors are not aware of any direct clinical studies measuring the rate of baldness specifically on stanozolol. The available data are observations by dermatologists and reviews describing alopecia as one of the common androgenic side effects of anabolic steroids in general (Pope et al., 2014). So claims like «stanozolol leads to baldness fastest» have no quantitative confirmation, but neither is the notion of its «safety for the hair» justified.

The follicles' response depends primarily on genetic predisposition. A person without a hereditary predisposition to androgenic alopecia may notice no changes, whereas in a predisposed person a process that would have started anyway can be accelerated. An androgen does not «create» baldness out of nothing, but it can substantially speed its development.

It is also important that stanozolol lowers the level of sex hormone-binding globulin. Because of this the proportion of free androgens rises, including one's own testosterone while it is not yet suppressed. This is another route to strengthening the androgenic action on the follicles.

In women the use of stanozolol can cause male-pattern androgenic alopecia along with other signs of virilization. For women the risks are much higher, and some of the changes are irreversible.

Why finasteride will not help here

Finasteride and dutasteride are drugs that inhibit 5α-reductase and thereby reduce the formation of DHT from testosterone. Finasteride is registered for treating androgenic alopecia in men; in randomized studies (Kaufman et al., 1998) it slowed the progression of baldness and in some patients promoted hair regrowth.

However, finasteride's mechanism has a fundamental limitation: it works only where DHT is formed from testosterone. Stanozolol is already a DHT derivative and does not require 5α-reductase. Thus blocking this enzyme does not reduce stanozolol's direct action on the follicles. Pharmacologically there are no grounds to count on finasteride to «protect» the hair when using stanozolol.

Moreover, 5α-reductase inhibitors themselves have side effects, particularly regarding sexual function, and their prescription requires a doctor's assessment. Independently combining several hormonally active drugs makes it harder to understand what exactly caused a particular reaction of the body.

Thus the myth «with finasteride you need not fear for your hair» has, in the case of stanozolol, no pharmacological basis.

Diagnosis: how to tell baldness from other causes

Not every case of hair loss is androgenic alopecia. In people who train intensely, follow strict diets and use various drugs, telogen effluvium often occurs — a massive loss of hair 2–3 months after a stress to the body: sharp weight loss, illness, surgery, nutrient deficiency.

• Androgenic alopecia:gradual thinning at the temples and crown, hair becomes thinner, with a characteristic pattern.
• Telogen effluvium:diffuse, even across the whole head, hair falls out with a white bulb, often resolves on its own.
• Alopecia areata:clearly outlined patches of baldness, with an autoimmune nature.
• Other causes:thyroid disease, iron deficiency, skin diseases of the scalp.

The diagnosis is made by a dermatologist or trichologist on the basis of examination, trichoscopy (examination of hair and skin under magnification) and, if needed, blood tests. Trichoscopy allows follicle miniaturization to be seen before thinning becomes noticeable to the naked eye.

To assess the dynamics it is useful to take photos under identical lighting conditions once every few months. The subjective feeling that «there is less hair» is often inaccurate in both directions.

Whether hair loss is reversible and what a doctor can do

Follicle miniaturization in the early stages is partly reversible: if androgenic stimulation decreases, some follicles may restore a normal cycle. However, follicles that have been miniaturized for a long time are eventually replaced by connective tissue and stop producing hair. So hair lost at late stages, as a rule, does not return.

After stanozolol is discontinued, the direct androgenic stimulation of the follicles disappears. However, if a person has a genetic predisposition, baldness will continue at its natural pace — the drug could only have accelerated it. It is not always possible to regain hair lost during the period of use.

Modern methods of treating androgenic alopecia include topical minoxidil, 5α-reductase inhibitors (in the absence of contraindications and after discontinuing external androgens), in-clinic procedures and hair transplantation. Guidelines and reviews (including Lolli et al., 2017) stress that the best results are achieved with an early start of treatment.

It is important that the dermatologist knows about the use of anabolic steroids: this changes the tactics and prognosis of treatment. A hair transplant against a backdrop of prolonged androgen use may give a worse long-term result, because the surrounding «native» follicles will continue to miniaturize.

Editorial conclusions

Stanozolol, as a DHT derivative, acts on the androgen receptors of hair follicles directly and in genetically predisposed people can accelerate androgenic alopecia. There are few direct quantitative studies, but the mechanism is well understood.

5α-reductase inhibitors, in particular finasteride, do not reduce stanozolol's direct action on the follicles, so they should not be counted on for «protection» from baldness.

Not every case of hair loss is androgenic: telogen effluvium after diets and stress occurs often. An accurate diagnosis is made by a dermatologist, and the earlier treatment is started, the better the prognosis.

We also recommend reading our articles on the effect of stanozolol on the skin, on its action on the prostate and on male fertility.

References

1. 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.
2. Lolli F, Pallotti F, Rossi A, et al. Androgenetic alopecia: a review. Endocrine. 2017;57(1):9–17.
3. 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.
4. Schänzer W. Metabolism of anabolic androgenic steroids. Clin Chem. 1996;42(7):1001–1020.
5. Bolognia JL, Schaffer JV, Cerroni L (eds). Dermatology. 4th ed. Elsevier; 2018.