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Interestingly, recent studies suggest that women with some markers of insulin resistance are at significantly increased risk of female AGA.   Moreover, a paternal history of AndroGenetic Alopecia seemed to be a stronger predictor of female AGA compared to women with normal or minimal loss of hair.

Female AGA has also been linked with hyperandrogenism and hirsutism and, most recently, also with PolyCystic Ovarian Syndrome (PCOS), even though epidemiological documentation of the latter association is not necessarily statistically compelling. Nevertheless, the association between polycystic ovarian syndrome and insulin resistance is well documented. 

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 frontal 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 and symptoms of androgen excess are present such as Hirsutism, severe unresponsive cystic acne, Virilization, or Galactorrhea.

Read more about hairloss in women.

From a susceptibility standpoint, the inheritance pattern in both sexes effected by AGA is polygenic (meaning that the pattern hairloss is caused by multiple genes linked to hair loss). Interestingly, the onset and incidence of the disorder in women closely parallels that observed in males. The disorder begins in susceptible hair follicles, where Di-Hydro-Testosterone (DHT) has been shown to bind to the androgen receptor in susceptible hair follicles. This hormone-receptor complex translocates to the cell nucleus, initiating a gene activation program thought to be responsible for the gradual transformation of large terminal follicles to a miniaturized phenotype (the hair follicles begins a negative growth cycle, getting smaller and smaller over time.)

This process occurs within a genetically predetermined anatomical region of the scalp. The resultant clinical picture may thus be described as pattern hair loss because the area of loss is segregated within a fairly well defined zone of the scalp.

Pattern hair loss is believed to result from the conversion of Testosterone to a problematic hormone known as Di-Hydro-Testosterone (DHT) by an enzyme called 5-Alpha-Reductase (5AR). The DHT binds to specific points in the hair follicle known as Androgen Receptor Sites (ARS). One may think of this as an electrical plug going into an electrical wall outlet. 

Unfortunately, when this attachment occurs in susceptible scalp hair follicles, it causes a negative change in the growth pattern of the hair. The follicle and accompanying structures begin a process of miniaturization, that is getting smaller. As a result, the hair in those follicles also shrinks in diameter and the hair growth cycle becomes shorter.

The result is smaller, thinner, virtually invisible hairs and a shrinking area of scalp coverage - a process which is called male or female "pattern hair loss".

Strikingly, both females and males diagnosed with pattern hair loss have higher levels of 5-Alpha-Reductase (5AR) and androgen receptors in frontal hair follicles compared to occipital follicles (hair follicles anatomically located outside the typical pattern of loss). Other predisposing factors such as differential cytochrome P450 levels in susceptible
versus non-susceptible hair follicles are less well known, but may have contributory relevance as well.

The formulations of HairGenesis™ work by interrupting this negative cycle and the activity of the enzyme 5-Alpha-Reductase, thus preventing damage to the hair follicle caused by DHT. Therefore, a healthier hair follicle is better able to produce a healthier and stronger hair.

In either gender, the differential diagnosis of AGA is typically made based on the patient's history and clinical presentation. The common differentials include Alopecia Areata (AA), Trichotillomania, and Loose Anagen Syndrome. Less typically, the cause of hair loss may be associated with disorders such as Lupus Erythematosis, scabies or other skin manifesting disease processes. Scalp biopsy and lab assay may be useful in determining a non-pattern hair loss etiology but, in such cases, should generally only follow an initial clinical evaluation by a qualified treating physician.

Thinning hair typically reduces the styling options one may choose. When a person begins to suffer the affects of male or female pattern hair loss, one has fewer choices, shorter styles and less flattering hair cuts. Conversely, by using a hair loss treatment such as HairGenesis™, which has been clinically demonstrated to correct pattern hair loss, one may regain a degree of hair style flexibility. This is because individual hair cailber corrolates to overall hair density. In other words, as an analogy, if a person has ten thousand hairs that become twice as thick, it is essentially as good as having twenty thousand hairs.

From a treatment perspective,  the mono-therapeutic interventions against female pattern hair loss have included topical Minoxidil, Oral Spironalactone, Oral Flutamide and other AntiAndroGenetic compounds.

In men, Finasteride is indicated whereas the potent Anti-Androgen Spronalactone is not. Finasteride, as used in Propecia™ and Proscar™, is a Type 2-selective 5-Alpha-Reductase inhibitor, and was approved in 1997 as the first oral pharmacologic therapy for the treatment of men with Andro-Genetic Alopecia (pattern hair loss).

Recently, botanically derived substances have also come under investigation as ingredients potentially useful against this pattern hairloss.  Because these botanical substrates have been shown to operate via different mechanisms of action from one another, a unique approach has been employed with an eye toward synergizing carefully chosen herbal and botanical compounds into a successful, safe and effective formulation.

Through many years of on-going research and ingredient testing and usage, this has led to the development of HairGenesis™.  In placebo controlled, double blinded research, HairGenesis, containing both Type 1 5-Alpha-Reductase inhibitors (5AR) and Type 2 5-Alpha-Reductase inhibitors has shown remarkably successful results in treating thinning hair and pattern hair loss in both men and women.

The results of this significant work has been outlined in a peer-reviewed, published IRB monitored, FDA-regulated IRB research study.  In the published report, HairGenesis™ was described as having been successfully tested in treatment subjects over the course of a 22 week trial.

Historical and basic science data for the compounds and complexes found in the formulations of HairGenesis™ further support the hypothesis that Hair Genesis™ offers a   both safety and a high rate of efficacy in appropriately selected subjects. Follow up clinical studies are being planned. 

Evolutionary improvements to the HairGenesis™ treatment line are ongoing as research and development of this revolutionary concept in using natural ingredients instead of drugs gains wider acceptance and desirability.

For those wishing to develop a deeper understanding of the processes involved in this subject, we have provided a selection of relevant research data covering important elements of hair growth and the disorders associated with hair loss:

Hair Loss: Causes, Clinical Manifestations, And Available Treatments

Androgen Disorders Related to Pattern Hair Loss

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