Hair and Hormones

Sex hormones and GH heavily influence the growth of our hair. In particular, their evolution from short-haired hair with a terminal hair is regulated by the somatotropic hormone (GH), while involution depends on the activity of the androgenic hormones. In humans, the hair of the vertex and frontal areas in particular is more sensitive to the action of androgens, while in women this sensitivity is more widespread.

These hormones, typical of the mashio but present in smaller concentrations also in the females, can slowly miniaturize the hair, which becomes increasingly thin to give the impression of having "fallen". Without androgens, therefore, there can be no alopecia; however, greater androgen concentrations do not necessarily correspond to greater "hair loss". In order for this to happen, in fact, androgens must act on genetically predisposed soil; in fact, since birth, a part of our hair is genetically predisposed to undergo the negative influence of androgens. In particular, the intracellular metabolism of testosterone heavily influences the life cycle of the hair.

Testosterone is the androgen hormone par excellence, secreted by the testicles and to a lesser extent by the adrenal gland; the latter also produces other types of androgens, such as androstenedione, dehydroepiandrosterone (DHEA) and androstenediol (in women there is a very small synthesis of androgens even at the ovarian level). Once in the target organs, these hormones can be metabolized to testosterone, which in turn undergoes the action of the 5-α-reductase enzyme and turns into dihydrotestosterone. On the other hand, all androgens, including testosterone, can also be transformed into estrogens (typically female sex hormones) by intervention of the aromatase enzyme.

While estrogens have a positive effect on hair (proliferative signal), testosterone, and in particular its metabolite dihydrotestosterone, play a crucial role in thinning processes (anti-proliferative signal).

The true androgen active at the level of the piliferous and capillary matrix is ​​therefore the dihydrotestosterone. We have to use this hormone for the growth of sexual hair on the face, on the chest, on the back and on the shoulders, and hair loss in subjects and in predisposed areas. It is therefore not surprising that the 5-α-reductase activity - to which the aforementioned conversion of testosterone into dihydrotestosterone is due - is particularly marked in the frontal region of bald subjects.

Dihydrosterone binds to a specific cytoplasmic protein receptor; the complex thus formed migrates into the nucleus, where it binds to specific receptors by regulating protein synthesis. In particular, at the piliferous level, binding to nuclear receptors activates transcription processes with messenger RNA synthesis, which at ribosomal level represses (in predisposed subjects) the synthesis of structural hair and hair proteins.

For what has been said, the higher the amount of circulating androgens and the greater the possibility that - before a genetic predisposition - there is an early hair fall. At this point it is necessary to point out that androgens circulate in the blood bound to plasma proteins such as albumin and SHBG, and that only the free fraction, therefore separated from this bond, is biologically active. Consequently, in the blood testosterone dosage, from the clinical point of view it is more important to evaluate the free fraction than the total quantity.

The SHBG, to which testosterone is tenaciously bound, increase its concentration in relation to the increase (physiological, pathological or iatrogenic) of estrogen and thyroid hormones. By contrast, SHBG levels decrease in response to the increase in plasma androgens; in this case, there is an increase in the free fraction of testosterone. Consequently, the 5-α-reductase enzymes will have more substrate (free testosterone) available for the synthesis of dihydrotestorene.

IN DEFINITELY, IN ORDER TO MANIFEST ANDROGENETIC ALOPECIA (responsible for most cases of baldness) THERE MUST BE A PREPARATION ON A GENETIC BASIS, WHICH TO ACHIEVE, NEEDS A LEVEL OF ANDROGENS MORE OR LESS.

If it is true that in the absence of androgens baldness does not occur, the hormonal values ​​of the bald are generally comparable to those of the general population. Only in women with androgenetic alopecia it is not uncommon to find higher than androgenic levels than normal.

Probably, pituitary hormones such as the aforementioned GH and prolactin, can regulate the degree of activity of the enzyme 5-α-reductase; just think of the pubertal acne that afflicts boys of particularly high stature (sign of hypersecretion of GH) or of the flood (hair loss) and of the seborrhea of ​​amenorrheic or hyperprolactinemic women.

Currently, the most widely used drug in the treatment of male androgenetic alopecia is finasteride, a synthetic 5-α-reductase inhibitor.