Hormones play a huge role in regulating both hair growth and hair loss. This blog will focus on androgenetic alopecia (AGA), and the role hormones play in it.
In androgenetic alopecia, the hair follicle is the target tissue, but for the sake of being thorough in a discussion about hormones and hair loss, we should also mention the hair follicle is not only targeted by androgen hormones. Other endocrine system hormones like estrogens, glucocorticoids, thyroid hormones, amongst twelve others that are released have an impact on hair growth as well.
Hair follicles, the target for AGA, are amazingly intricate physiologic units of cells that not only produce hair but are capable of performing numerous functions at once. For example, they can metabolize hormones including androgens, estrogens, and prostaglandins. When a healthy scalp hair follicle is in the growing phase, the hair follicle can synthesize hormones like CRH, ACTH, cortisol, melatonin, and prolactin. Beyond this, amongst other things, hair follicles also express erythropoietin and its receptor. So, from this brief snapshot, you can see that the hair follicle is very elaborate and can be affected by many physiological, hormonal changes. Recognizing the complex nature of each follicle is essential to grasp why Androgenic Alopecia is not as cut and dry as one may think.
Androgenetic Alopecia in Men
As the name suggests, androgenetic alopecia is derived from the words androgen and genetics because they both play a role in this type of hair loss. With Androgenetic Alopecia, years ago testosterone got the blame, but we know that the real culprit in men is the substance DHT (dihydrotestosterone). DHT is a metabolite of testosterone and has a higher affinity for the androgen receptor (AR receptor). A receptor is a protein molecule that receives chemical signals from outside a cell.
So at the cellular level, when those DHT chemical signals bind to an androgen receptor, this launches the genes that gradually transform large, terminal hair follicles to smaller more vellus follicles. Not only are the follicles miniaturized, but the anagen (growing phase) of the follicle is shortened. We know that men diagnosed with androgenetic alopecia differ from men without AGA. They have higher levels of cellular 5-alpha-reductase than men without AGA. Cellular 5-alpha reductase is the enzyme that converts testosterone to DHT resulting in higher levels of DHT inducing miniaturization. Not only this but there are higher quantities of androgen receptors in the balding scalp than in the nonbalding scalp. And as we just discussed, we know that DHT binds to androgen receptors, even better than testosterone, resulting over time in fewer large, terminal hair follicles and more follicles in the miniaturizing and vellus state.
There seems to be confusion among the public as to how genetics impacts AGA, and scientifically there is still more to learn. The androgen receptor that the DHT binds to (leading to follicle miniaturization) is on the X chromosome, and for men, they inherit the X chromosome from the mother, which may be why people tend to think androgenic alopecia stems from only the maternal side of the family. However, this is not the full explanation. AGA is inherited genetically from more than one source, meaning both maternal and paternal genetics are involved, so it is polygenetic.
Also, not all males will exhibit symptoms even though they carry several forms of the gene, so there is something called variable penetrance at play. In other words, the gene does not exhibit the same manifestation in two different people, which is why you might have AGA, but a brother with your same biological parents may not experience any miniaturization. And even beyond this, there are several other chromosomes identified which can give genetic susceptibility for developing alopecia. As a result, we say that the inheritance of AGA in males in polygenetic with variable penetrance.
Androgenetic Alopecia in Women
The etiology or cause of inherited hair loss in women is not as straightforward as it in in men. Even the name Androgenetic alopecia for women has now mainly been replaced with the term Female Patterned Hair Loss to help distinguish the different etiological features of this process in women versus men and reflects the lack of evidence to support a hormonal contribution in all cases of the condition.
The hallmark feature of FPHL is the progressive transformation of terminal hair follicles (large, thick, pigmented) to vellus hair follicles (short, thin, nonpigmented) with a shortened anagen growing phase. This results in a miniaturization and thinning of hair usually over the top of the head with preservation of the hair line, but some women exhibit thinning all over their scalp.
The mechanism which causes the changes in the female hair follicle in FPHL is not completely understood, and the degree to which androgens and genetics contribute to FPHL in most women is less clear. To sum things up, from what we presently understand, the scientific reason this happens is not as simple in women as in men.
What role do androgens play in FPHL?
Androgens exert their effect on hair using circulating testosterone obtained from the adrenal glands or ovaries. Only free testosterone can enter cells and undergo conversion to DHT, although the role of this growth and effect on the female hair follicle is less clear than for men.
What we are learning is that most women with FPHL do not have elevated testosterone levels, unless they experience hyperandrogenism. Hyperandrogenism, also known as androgen excess, is a medical condition characterized by excessive levels of androgens (such as testosterone) in the female body and the associated effects of the elevated androgen levels. So, for example in the face of a patient with hyperandrogenism like polycystic ovarian syndrome (PCOS) women have a higher testosterone and DHT levels and may develop early-onset FPHL.
Some proposed explanations for FPHL in the face of normal androgen levels could be an increased sensitivity of hair follicles to androgens and an influence of estrogens on the development of this condition. After menopause statistically there are growing numbers of women with FPHL which suggests a possible role for estrogen. However, studies have demonstrated conflicting evidence as to whether estrogens stimulate or inhibit hair growth.
While we know that genetics influence the susceptibility of men developing AGA, not much is known regarding the genetic basis and inheritance pattern of female pattern hair loss, so inheritance is not thought to play nearly as big of a role in women with FPHL.
Resolving Hair Loss at HT&RC
If you are a male noticing a pattern of continued hair loss and concerned you have AGA, contact our office to discuss your concerns and treatment options with Dr. Gray. Likewise, if you are a female experiencing generalized, rapid hair shedding with thinning, contact us to schedule a consultation. We can provide a workup for an underlying systemic illness, medication exposure/change, lifestyle modification, or change in hair care practices. The diagnosis of FPHL is a combination of a detailed inquiry into your history, including family, social, and medical histories, as well as a comprehensive physical examination with appropriate testing.
Every hair loss situation is unique. Dr. Gray is not content to merely treat the symptoms of hair loss. He brings the expertise to identify the therapies which proactively treat the underlying causes of each individual case. Each patient is highly involved in the planning and monitoring of appropriate treatment, whether surgical or non-surgical. When you're ready for your consultation with Dr. Gray, please contact us.
