Pattern Hair Loss In Women
Androgenetic alopecia, AGA, also known as common pattern hair loss affects approximately 20 million American women. AGA in women is triggered by similar processes to those causing pattern hair loss in men. In both genders, the onset of AGA may occur in early adulthood, though females tend to present signs and symptoms somewhat later than males.
Recent studies suggest that women with some markers of insulin resistance are at significantly increased risk of female AGA. Moreover, a paternal history of hair loss may be a strong predictor of female AGA.
Female pattern hair loss has also been linked with both hyperandrogenism and hirsutism. Most recently, female pattern hairloss has also been linked with polycystic ovarian syndrome, PCOS, though epidemiological documentation of this association is, as yet, not statistically compelling. Nevertheless, the association between PCOS and insulin resistance is well documented.
What actually triggers pattern hair loss in women?
From a susceptibility standpoint, the inheritance pattern in female pattern hairloss is polygenic, and the onset and incidence of the disorder closely parallels that observed in males. The disorder begins in susceptible hair follicles, where dihydrotestosterone, DHT, binds androgen receptor forming a molecular trigger that sets the process of hair loss in motion.
The 5 alpha dihydrotestosterone hormone-receptor complex translocates to the cell nucleus of susceptible hair follicles, initiating a gene activation program that starts the gradual transformation of large terminal follicles to miniaturized follicles. This process occurs within a genetically pre-determined anatomical region, or pattern of the scalp. The hair outside of this pattern remains unaffected. This is why the disorder is called pattern hair loss.
Strikingly, both females and males diagnosed with pattern hair loss have higher levels of 5-Alpha-Reductase, 5AR, in frontal hair follicles compared 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 worked out, but may have contributory relevance as well.
The diagnosis of AGA in women is supported by a pattern of increased thinning over the frontal/parietal scalp with 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 not indicated unless signs & symptoms of androgen excess are present such as hirsutism, severe unresponsive cystic acne, virilization, or galactorrhea.
In most cases, the differential diagnosis of AGA is made based on the patient's history and clinical presentation. Typical differentials include alopecia areata, trichotillomania, and less commonly hair loss associated with disorders such as lupus erythematosis, scabies and other skin manifesting disease processes. Scalp biopsy and lab assay may be useful in elucidating a non-pattern hair loss etiology but, in such cases, should generally only follow an initial clinical evaluation by a qualified treating physician.
Treatment Options
From a treatment perspective, the mono-therapeutic interventions against female pattern hair loss include topical minoxidil, oral spironalactone, oral flutamide and other drugs. Surgical hair restoration can sometimes be an option, however care must be excercised as, in certain persons, the pattern of loss may sometimes extend across much of the entire scalp, rendering hair transplantation less than clinically effective. Recently, botanically derived substances, such as HairGenesis, have also come under investigation as agents potentially useful against the disorder.
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