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The usual belief associated with androgens and pattern baldness is that excessive androgen production usually leads to balding in males, such as that of frontal recession and cephalic balding. However, unlike males who exhibit balding not always related with androgen excess, women with excessive androgenic production show a pattern of hair loss.

The precise function of hyperandrogenism, its activity and receptors in pattern baldness in females remain vague. Although testosterone activity proves to be essential in balding among males, there appears to be no scientific study to prove the same of women. However, clinical studies imply that balding in females occur with hyperandrogenism, particularly if it is comes with other signs of androgen excess such as menstrual irregularities, infertility, hirsutism or excessive hair production, acne formation and oily skin.

The form and section of different androgens produced, both centrally and peripherally differ in male and females. On the average, about 30 percent of a female’s testosterone is formed in the ovaries. The other 70 percent is developed from transformation of adrenal androgen precursors such as dehydro epiandrosterone (DHEA) and androstenedione, both of which are greatly reduced by aging.

In totality, testosterone production of ovaries is far lesser than that of the testes’, resulting in an extremely lower testosterone plasma level in women, as compared to men. However, the frail androgens prove to be sources of precursors for potent androgens, which provide the physiologic or pathyphysiologic androgen activity. Only a small portion of androgens survive as free steroids in the circulation, with balance between free hormones and protein-bound androgens.

Therefore, in some females, there may be hyperandrogenism like androstenediol or testosterone, produced by the adrenal gland or ovary. The skin is produces active androgens from its whole precursor DHEA sulfate. Convergence of these hormones at follicular hair level directs to more tissue levels of the dynamic androgenic hair follicle, dihydrotestosterone (DHT). DHT triggers hair loss in the scalp.

A significant protein for androgen binding is the sex-hormone binding globulin (SHBG). This globulin is a glycoprotein metabolized by the liver. Studies reveal that SHBG levels co-relate with the degree of baldness. The more potent androgens and estradial attach to the plasma to SHBG, although the binding resemblances vary. In DHT, the resemblance is three times as much that of testosterone and nine times as much that of estradiol. Increased levels of testosterone becomes the basis for SHBG synthesis to be reduced which adds to the excessive activity of 5-Reductase, the enzyme liable for the synthesis of testosterone to DHT.

Much androgen production has been linked to hirsutism. The ovary is the major source of androgen production in females with practical hyperandrogenism. Gonadotropin-releasing hormone or GnRH comes from the hypothalamuns and causes the pituitary gland to produce luteinizing hormone (LH) and follicle stimulating hormone (FSH), both of which are engaged in reproduction. In most females with ovarian hyperandrogenism, the pituitary becomes more responsive to GnRH. Pituitary secretion of LH therefore increases and FSH decreases, which stimulates excessive androgen formation and anovulation or the malfunction of ovaries to manufacture and discharge mature eggs.

Research reveals a connection between polycystic ovarian syndrome and pattern baldness. The shortage of two main enzymes for biosynthesis of estrogen may be seen in polycystic ovarian syndrome. This leads to an overproduction of androgen and the reduced creation of estrogen by the ovaries. In addition, polycystic ovarian syndrome includes more insulin levels, which involves hormonal production and SHBG

Hyperprolactinemia is a state in which there is an increased serum levels of the hormone prolactin in pre-pregnancy condition. It has been linked to be the likely basis for adrenal overproduction of androgens. It could have been related to excessive pattern hair loss in females. Women with hyperprolactinema may have an excess in free testosterone, a reduction in SHGB, and a slight raise in DHEAs. Prolactin transforms ovulation by hindering the reaction of gonads to LH and stopping the positive feedback of estrogen in encouraging the ovulatory LH flow. As a result, lesser estradiol and increased androstenedione are developed.

Research Outcomes

Clinicians have studied the flow of androgen levels in females with alopecia and have linked it to the androgen-dependent nature of pattern hair loss in some women with noticeable androgen increase, either exogenous or endogenous. Research reveal the females most likely abruptly lose hair in a classic Hamilton-IV pattern with a deep bi-temporal depression and that their hair loss may get better when its suspected origin is put to a halt. Female hair loss, hirsutism, and acne may react with anti-androgen medications, validating the concept of androgen reliance in women with pattern hair loss.

Some observations however, have inquired about the task of androgens in pattern hair loss among women. Norwood gave details on families where pattern hair loss among women seem to have been acquired separately from male balding and in a case, female pattern hair loss happened in a young female who was deficient in the number of circulating androgen or other manifestations of androgenization after puberty. Finasteride, a 5 reductase inhibitor, is successful in treating baldness among males but in a restricted randomized trial, have not succeeded to halt the abrupt hair loss in postmenopausals with pattern hair loss and androgen levels that are standard.

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