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Androgenic alopecia in women and causes

Androgenic alopecia recognizes a multigenic and multifactorial etiology; this indicates a hereditary mechanism that affects a mosaic of genes but also depends on other factors (incidences) role: weight changes, hypothyroidism, stress states, eating disorders, etc.
The term Alopecia Androgenetics was coined by Ludwig in 1962 and indicates the two major pathogenetic factors of the disease, namely androgenic hormones and heredity.
Androgenic alopecia is induced by the action of androgenic hormones on genetically predisposed subjects.
This condition is transmitted with characteristics of polygeneticity and affects both men and women.
Baldness in women can become a very important and "disabling" problem for those suffering from it, especially if you have a profession where physical appearance is important and/or you regularly interface with an audience.
In women, androgenic alopecia usually occurs between thirty and forty years of age (compared to twenty-thirty years of men). Hair problems can begin to coincide with a hormonal change such as taking or stopping a contraceptive, postpartum, perimenopausal or postmenopausal period or as a result of a significant change in weight. The frontoparietal recession occurs however at the time of sexual maturation in 80% of women (as in most men) and often in conjunction with the intake of estroprogestin oral (which may not be alien to this) and is generally much less noticeable than the male one. However, the presence of a deep frontoparietal recession is correlated with increased testosterone production rather than with the accentuated conversion of this into dihydrotestosterone. In both sexes the risk area is the entire upper part of the scalp but in women, unlike males, there is generally a widespread loss of density of the entire hair, even if more noticeable in the area of the vertex. This determines an ovary decrease in the density of hair in the central area of the scalp behind the preserved frontal bangs. This preserving frontal attachment is another typical difference between female and male androgenic alopecia.
Erich Ludwig divided female androgenic alopecia into three stages based on hair density (1977).

Women of the first group make up the large majority, and hair loss can be felt only by comparing the density on the top of the scalp with that of the occiput. The second group achieves a greater and less maskable thinning. Women in the third group are rarer and, like those who in the premenopausal period develop male pattern alopecia with deep frontal recession, require endocrinological assessment for a Potential pathological androgenic state. Even in stage III of Ludwig however, unlike the male, the area is never completely bald and persist many "normal" hair along with the miniaturized ones. Sulzberger, Witten and Kopf first reported some important clinical observations: in women with "diffuse alopecia" hair became thinner, the hair less dense and sometimes more greasy. Subjectively hair is less treatable cosmetically. Other symptoms reported by patients are: "brittleness, tingling, goose bumps, burning, itching and an unpleasant scalp hypersensitivity". The incidence of androgenic alopecia in women was estimated between 8 and 25%, but these calculations may have excluded subjects with light and easily disguised thinning. In women, a decrease in hair density often becomes visible after menopause and can be associated with further biparietal recession. It is not clear today whether this postmenopausal hair loss is due to androgenic alopecia. It would seem related to hormonal changes caused by anovulation and insufficient synthesis of estrogen and/or progesterone. The fact that the adrenal gland is experiencing changes in the androgenic production of women after the age of fifty can also play a role in this hair loss. It remains to be understood exactly how all this data is connected.

Does female androgenic alopecia really exist?

Androgenic alopecia is the result of a combined androgen-dependent process and genetic transmission.
It is now commonly accepted that male androgenic alopecia is associated with an increase in 5-alpha-reductase activity, with a local increase in dihydrotestosterone production, or increased local sensitivity to the action of DHT. This has been demonstrated mainly, if not exclusively, in men and then, we think improperly, extended to women.

Increased 5-alpha-reductase activity or local sensitivity to DHT explains the well-known efficacy of 5-alpha-reductase inhibitors.
The mechanism by which the increase in local dihydrotestosterone leads to miniaturization and then hair loss is not at all clarified. Personally, we believe that the key to understanding the process of miniaturization is in the local production of hormones during catagen.
However, if the process of baldness is considered as androgen-dependent, androgenic alopecia should be limited to androgen receptor areas only. In the scalp these receptors were detected only in the frontal and vertex area, and not in the temporal and occipital area. In fact, in men this is the case and androgenic alopecia occurs only in these areas, whereas in women hair loss is rarely localized to these areas only, even when the age progresses, there is a are large bald areas.
In addition, the hormone levels of androgens in healthy women are always much lower than those present in male. The male receiving finasteride also has DHT levels approximately 10 times higher than those of the woman with alopecia, which makes her badly defined as "androgenetics".

In essence, 5-alpha-reductase inhibitors appear ineffective in women.
Pharmaceutical doses of estrogen (pregnancy, contraception) often have a beneficial effect on many cases of alopecia probably through non-anti-androgenic mechanisms. Pharmacological doses of estrogen, usually associated with progesterone-like antiandrogenic agents, are widely used, in female alopecia, with good results which, however, have not been proven by clinical trials. It is also important to point out that the dermal papilla has an aromatase, specifically in the occipital area, whose function has not yet been well defined in the context of female alopecia.
In women, with the exception of some rare cases of abnormal adrenal or ovarian hormone production due to enzymatic defect or secreting tumor, alopecia appears very different from the male one and mechanisms appear different and, although not yet fully clarified, almost always assimilable to those of the telogen chronic effluent or to a situation of local estrone deficiency.
Cases of those girls with fine and thin hair all over the scalp (but more on the vertex and in the frontal zone) with the mother (often) in the same conditions but with normal menstruation and fertility, without excess of circulating androgens and in which it is not possible to find clear laboratory clinical elements that make us lay for an effluent telogen make us think of a family peripheral resistance of the follicle to the action of estrogen (deficiency of 17 steroid oxidoriductase, aromatase, 3 alpha reductase).


It is certainly one of the most common solutionm however, good quality ones generally have a fairly high price and many women can't wear them.
Extensions: in case of thinned areas; but it is always a temporary and questionable "solution" above all from the point of view of hygienic and sanitary.

Some women take drugs to combat hair loss; however, side effects can be numerous so it is always good to consider an alternative.
This causes a weakening of the follicle that generates increasingly thin hair until it determines the complete "death" of the follicle that at a certain stage is no longer able to produce hair.


Some researchers have attested that only 2 -5% of women can undergo a hair transplant, as only a low percentage of them have the ideal type of hair for a treatment of This guy.
Hair loss in women is manifested mainly through a fairly generalized thinning, including in the lateral and back areas of the head, areas that are used as "donor sites" in the transplants practiced on men.
In men the donor sites are defined as "stable" and this is because in these areas the follicles are not affected by dihydrotestosterone; it follows that in men it is possible to proceed without problems to the withdrawal. of follicles to be transplanted to other areas of the head.
In women, however, donor sites are unstable, as even these areas may suffer from a sharp thinning of the hair, thus making them unsuitable for withdrawal. In addition to this, women suffering from hair loss retain in most cases the natural frontal line, and therefore require a hair thickening treatment also in the back and upper head.

Why choose SMP — Tricopigmentation for women

The Scalp Micro Pigmentation, also called Permanent Tricopigmentation or Semi-Permanent is the ideal solution for women suffering from alopecia as thanks to this treatment it is possible to reduce the contrast and the transparencies produced by thinning, immediately obtaining the optical illusion of a very realistic hair thickening.
Unlike cosmetic correctors for daily use, this sophisticated treatment can have not only a permanent or semi-permanent duration, depending on the choice, but allows you to achieve a more natural result. In addition, it does not require daily applications, does not create discomfort and provides the patient with greater safety than traditional cosmetics.

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