The use of androgenic-anabolic steroids (AAS) can cause baldness, which is called androgenetic. This type of alopecia (alopecia) occurs most often – it is encountered by more than half of all men at the age of about 50 years. In this case, hair loss does not occur spontaneously, but is characterized by firm signs:
1. Baldness occurs according to the male type. Here there is a clear dependence of the area of hair loss on the localization of androgen receptors located in the scalp. In men, hair falls out in the frontal and parietal areas with the formation of a bald head, in women – on both sides of the central part and on the vertex, but the bald spot is not formed.
2. The duration of the active hair growth phase (anagen) is reduced. The main is the resting phase (telogen), during which the hair does not grow, begins to die and is easily removed by washing and combing.
3. Reduces the number of hair follicles, they stop functioning normally, eventually fill with connective tissue and die.
People prone to androgenetic alopecia are under the influence of both androgenic factors, and genetic predisposition. They have more androgen receptors and more dihydrotestosterone is formed in the scalp than those who are not prone to baldness.
Dihydrotestosterone (DHT) is the main cause of alopecia. It is formed from testosterone by the action of an enzyme, which is always present in the hair follicle. Under the influence of DHT, there is a spasm of the vessels feeding the follicles. They begin to form thin, short, slightly dyed hairs in exchange for a full hair. Such gun voloski can not create a hair cover, through it becomes visible the scalp, which is perceived as visible alopecia. Due to the constant lack of nutrition, hair follicles finally cease to produce hair and gradually die off. The same principle applies to all AAS even in the absence of the required amount of testosterone.
The genetic component of baldness is not yet fully understood. Previously, it was believed that inheritance passes from the grandfather on the part of the mother, but later evidence suggests that the transmission of predisposition to baldness comes from the father. It provokes hair loss is not one gene, but a whole gene complex, responsible for both the onset of alopecia and its intensity.
For the treatment of androgenetic baldness, minoxidil and finasteride are used, which suppress the action of the enzyme that converts testosterone to dihydrotestosterone.
For the treatment of women, drugs with anti-androgenic activity and estrogens are prescribed. First of all, treatment begins with a decrease in the effect of androgens, which contributes to a marked reduction in the degree of alopecia.
That’s why athletes who use steroids to build muscle, select them in such a way as to minimize unnecessary androgenic stimulation. This is achieved by the use of optimal dosages and the correct selection of drugs, for example, oxandrolone, nandrolone, methenolone. As an alternative, injecting forms of testosterone preparations together with finasteride will be used to minimize the formation of dihydrotestosterone in the scalp.
Until now, the dependence of baldness on AAS reception has not been studied. Nevertheless, there is an increase in hair loss in people with already existing androgenetic alopecia when using AAS. If previously there were no problems with hair loss, then with the use of these drugs, alopecia can be noted only as a side effect, manifested not in everyone even after years of taking AAS.
These facts lead to the conclusion that androgens can cause baldness only in those cases when there is a genetic predisposition to this. If there is no such inclination, then it can not be said that AAS will necessarily cause baldness even in the absence of prerequisites for this.