AGA in Women

AGA in Women
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Androgenetic alopecia, AGA, otherwise known as common pattern hair loss affects around 20 million American women. AGA in women is triggered by similar processes to those that cause pattern hair loss in men.  In both genders, it starts in early adulthood.  However, it is not as common among women as in men.

Recent studies imply that women with some markers of insulin resistance are more prone to  female AGA.  Furthermore, a paternal history of hair loss may be an indication of female AGA.

Female pattern hair loss has also been connected with both hyperandrogenism and hirsutism. Most recently, female pattern hairloss has also been associated with polycystic ovarian syndrome, PCOS, though epidemiological documentation of this association is, as yet, not statistically compelling. Nevertheless, the connection between PCOS and insulin resistance is well documented.

What actually triggers pattern hair loss in women?

From a vurnerability standpoint, the inheritance pattern in female pattern hairloss is polygenic, and its onset and incidence of the disorder also can be observed among males. The disorder begins in resceptive hair follicles, where dihydrotestosterone, DHT, binds androgen receptor that forms a molecular trigger, settings the process of hair loss in motion.

The 5 alpha dihydrotestosterone hormone-receptor complex translocates to the cell nucleus of susceptible hair follicles, which intiates a gene activation program that starts the gradual conversion of large terminal follicles to miniaturized follicles. This process happens within a genetically pre-determined anatomical region, or pattern of the scalp. The hair outside of this pattern stays unaffected. This is reason why it is known as pattern hair loss.

Noticeably, both females and males diagnosed with pattern hair loss have higher levels of 5-Alpha-Reductase, 5AR, in frontal hair follicles in contrast to occipital, back of the scalp behind the ears.  Other predisposing factors such as differential cytochrome P450 levels in susceptible versus non-susceptible hair follicles are less well clearly calisthenics, but may have contributed as well.

The diagnosis of AGA in women is supported by a pattern of augmented thinning over the frontal/parietal scalp that has greater density over the occipital scalp, a retention of the juvenile hairline, and the presence of miniaturized hairs in the effected zone of loss. Most women with AGA have normal menses and pregnancies. Extensive hormonal testing is usually can not be indicated unless signs & symptoms of androgen excess shows that include hirsutism, severe unresponsive cystic acne, virilization, or galactorrhea.

As a general rule, the differential diagnosis of AGA is made entirely on the patient’s history and clinical presentation. Typical differentials such as alopecia areata, trichotillomania, and less commonly hair loss connected with disorders such as lupus erythematosis, scabies and other skin manifesting disease processes. Scalp biopsy and lab assay may be useful to elucidate a non-pattern hair loss etiology but, in such cases, should generally only follow an initial clinical evaluation by a trained treating physician.

Treatment Options

Treatment can come from topical minoxidil, oral spironalactone, oral flutamide and other drugs. There are some instances when surgical hair restoration is an option.  However care must be work out as, in certain persons, the pattern of loss may sometimes extend across much of the entire scalp, which renders hair transplantation under clinically effective. A more recent technology that could treat the thinning of the hair is HairGenesis.