Male pattern baldness, is the most common type of hair loss in men. According to the U. National Library of Medicine NLM , more than 50 percent of all men over the age of 50 will be affected by male pattern baldness to some extent.
One cause of male pattern baldness is genetics, or having a family history of baldness. Research has found that male pattern baldness is associated with male sex hormones called androgens. The androgens have many functions including regulating hair growth. Each hair on your head has a growth cycle. With male pattern baldness, this growth cycle begins to weaken and the hair follicle shrinks, producing shorter and finer strands of hair. Eventually, the growth cycle for each hair ends and no new hair grows in its place.
Inherited male pattern baldness usually has no medical ill effects. However, sometimes baldness has more serious causes, such as certain cancers, medications, thyroid conditions, and anabolic steroids.
Doctors use the pattern of hair loss to diagnose male pattern baldness. They may perform a medical history and exam to rule out certain health conditions as the cause, such as fungal conditions of the scalp or nutritional disorders.
Health conditions may be a cause of baldness when a rash, redness, pain, peeling of the scalp, hair breakage, patchy hair loss, or anunusual pattern of hair loss accompanies the hair loss. A skin biopsy and blood tests also may be necessary to diagnose disorders responsible for the hair loss.
Signs and symptoms Classic male-pattern hair loss begins above the temples and vertex, or calvaria, of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains.
It more often causes diffuse thinning without hairline recession; similar to its male counterpart, female androgenic alopecia rarely leads to total hair loss. The Ludwig scale grades severity of androgenic alopecia in females. Testosterone exists in your body in different forms. This is the form of testosterone most available to act within the body. Testosterone can also be bound to albumin, a protein in the blood. If you have a low level of SHBG, you may have a high level of free testosterone in your bloodstream.
Dihydrotestosterone DHT is made from testosterone by an enzyme. DHT is five times more potent than testosterone. DHT is primarily used by the body in the prostate, skin, and hair follicles. Dihydrotestosterone DHT is made from testosterone by an enzyme called 5-alpha reductase. It can also be made from DHEA, a hormone more common in women. DHT is found in skin, hair follicles, and the prostate.
DHT also acts in the prostate. With too much DHT, a man can develop benign prostrate hypertropy, also known as an enlarged prostate. The existing hair is pushed out of the pore by the new growth and naturally sheds.
Male pattern hair loss happens when the follicles slowly become miniaturized, the anagen phase is reduced, and the telogen phase becomes longer. Over time, the anagen phase becomes so short that the new hairs do not even peek through the surface of the skin. Telogen hair growth is less well-anchored to the scalp, making it easier to fall out. As the follicles become smaller, the shaft of the hair becomes thinner with each cycle of growth. Eventually, hairs are reduced to vellus hairs, the type of soft, light hairs that cover an infant and mostly disappear during puberty in response to androgens.
Users of anabolic steroid drugs, including body builders, have higher levels of DHT. However, they often experience hair loss. The hair on the head grows without the presence of DHT, but armpit hair, pubic hair, and beard hair cannot grow without androgens.
Individuals who have been castrated or who have 5-AR deficiency do not experience male pattern baldness, but they will also have very little hair elsewhere on the body. For reasons that are not well understood, DHT is essential for most hair growth, but it is detrimental to head hair growth.
DHT is thought to attach to androgen receptors on hair follicles. Through an unknown mechanism, it then appears to trigger the receptors to begin miniaturizing. In , researchers found that both plucked follicles and skin from a balding scalp contain higher levels of androgen receptors than those from a non-balding scalp. Some scientists believe that some people have a genetically transmitted susceptibility to otherwise normal levels of circulating androgens, particularly DHT.
This combination of hormonal and genetic factors could explain why some people are more likely than others to lose their hair. It is known that DHT binds to follicle receptors five times more avidly than testosterone, but the amount of DHT in the scalp is tiny compared with the levels in the prostate.
If 5-AR levels increase, more testosterone will be converted into DHT, and greater hair loss will result. Male pattern hair loss can have a negative effect on the self-esteem of a man. To help relieve this, some treatments have already been developed.
Finasteride, or Propecia, was approved for safety and efficacy in , by the U. It is a selective inhibitor of type 2 5-AR.
As androgenetic alopecia progresses and DHT continues to adversely affect the follicles, hairs become thinner, more fragile and often lighter in color with each subsequent life cycle. Eventually, the follicles shut down and will no longer produce hair. Androgenetic alopecia presents differently in men and women. Men typically lose their hair along the hairline, temples and crown.
As hair loss advances, the hairline meets the bald spot at the crown, leaving only DHT-resistant hair on the back and sides of the head. Women show more of a diffuse pattern of hair loss and may experience overall thinning, a widening of the part or patchy hair loss, especially near the temples. As the ears are firmly fixed to the temporal bones, they interrupt the soft-tissue continuity, shore up the soft tissues above and around them, and assume the pull of the soft tissues below.
By contrast, scalp skin is continuous with the skin of the face between the ears and eyes on both sides of the face, so that the weight of the facial soft tissues adds to the pressure in the frontal part of the scalp. The circumstances are similar at the back of the head in terms of effective weights. The weight of the soft tissues below the ear level at the back of the head similarly adds to the pressure in the vertex area as an extra weight compared with the area above the ears.
Anatomy is a determining factor on the magnitude of the downward pull at different parts of the scalp. Middle top of the scalp is supported by the ears in contrast with the frontal and vertex regions. Soft-tissue loads on the frontal and vertex areas of the scalp are more than the soft-tissue load on the middle top.
It comes to the same question again: Why does DHT increase in balding scalp? This is the crux of the matter. Since its introduction, the new theory has been regarded with notable skepticism and resistance. Simplifying a very complicated problem is probably the only disadvantage of the theory. AGA has been one of the biggest and most challenging problems of the humankind.
It has affected so many lives throughout the human history and has been a devastating condition for so many of the afflicted.
It is difficult to settle for any mechanism less than highly complex. However, all natural phenomena that seem to be complex look simpler if viewed from the right standpoint. Disclosure: The author holds a patent on prevention and treatment of male pattern baldness U. Patent No. The Article Processing Charge was paid for by the author.
National Center for Biotechnology Information , U. Plast Reconstr Surg Glob Open. Published online Nov 7. Emin Tuncay Ustuner , MD. Author information Article notes Copyright and License information Disclaimer. From Ankara, Turkey.
Corresponding author. Received Jul 13; Accepted Sep 6. The work cannot be changed in any way or used commercially. This article has been cited by other articles in PMC. Abstract Summary: What is wrong with the current understanding of etiopatho genesis of androgenic alopecia AGA?
The reader would probably agree that the following are generally recognized as safe to claim with regard to androgenic alopecia AGA and contribute to androgenic theory: 5-alpha reductase enzyme activity, which converts testosterone to dihydrotestosterone DHT , increases in balding scalp, 1 DHT increases in balding scalp, 2 , 3 Number of DHT receptors on the hair follicles increases in balding scalp, 4 Blocking conversion of testosterone to DHT delays progression of AGA.
Worst of all, it skimps the most critical question and prevents it from standing forward, which is: Why does DHT or 5-alpha reductase enzyme activity increase in balding scalp? This question requires a solid answer and has priority over the other crucial questions that are as follows: How does DHT cause hair loss while exactly the opposite effect is expected? Why does balding or increase in DHT levels occur only at the top of the head?
Open in a separate window. Footnotes Disclosure: The author holds a patent on prevention and treatment of male pattern baldness U. Different levels of 5alpha-reductase type I and II, aromatase, and androgen receptor in hair follicles of women and men with androgenetic alopecia.
J Invest Dermatol. Regulation of human hair growth by steroid hormones. Testerone metabolism in isolated hairs. J Clin Endocrinol Metab. The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness. Balding hair follicle dermal papilla cells contain higher levels of androgen receptors than those from non-balding scalp.
J Endocrinol.
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