Female Pattern Hair Loss

Table of Contents

90% of all Hairloss is Pattern Hair Loss

The most common form of hair loss and balding is known as Adrogenetic Alopecia (AGA), also called Male or Female Pattern Hair Loss, which represents the vast majority of all hair loss cases. Scientists now believe that approximately 90% + of the hair loss seen in Women is caused by pattern hair loss.

Pattern hair loss is a common condition affecting approximately 20 million women in the United States alone. The disorder may begin before age twenty, however more commonly it begins in a person’s 20’s or 30’s.

The hair loss, in general, can be described as mild, moderate or severe and tends to follow a particular pattern in men. (Norwood pattern hair loss chart) In women, it manifests itself as a generalized thinning hair over the entire crown of the head. It is extremely rare for women to lose all of their hair. The amount of hair loss and baldness, as well as the size of the affected areas of thinning hair and balding, tend to gradually increase over time, often over a span of several years or decades.

female pattern hair loss - stop hair loss

The Role of the Enzyme 5-Alpha-Reductase ( 5AR )

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 ( 5AR ), 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.

The Role of DHT in Causing Hair Follicles to Grow Smaller

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 sites (ARS) 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. This process occurs within a genetically pre-determined anatomical region of the scalp. The resultant clinical phenotype may thusly be described as pattern hair loss because the area of loss is segregated within a fairly well defined zone of the scalp.

Hair Loss and it’s Affect on Hair Style Options

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 caliber correlates 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.

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 Di-Hydro-Testosterone (DHT) has been shown to bind to the androgen receptor sites (ARS).

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.