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Hair Loss Info

Hair loss and thinning hair are common problems in both men and women. Almost all people experience some form of hair loss in their lifetime. For some of these people the psychological effects are by far the worst elements of their hair loss. Though hair loss is often seen as a part of ageing, but when it is premature it brings depression and anxiety. For many people just knowing about the basic reasons for hair loss and understanding how the treatments works (making sense out of something esteroides mexico inexplicable), helps a lot and that, is the primary purpose of the consultation in our center.

Common causes of hair loss seen in our practice are:

  • Pattern hair loss (progressive and permanent)
  • Telogen effluvium (temporary)
  • Alopecia areata (remissions & exacerbations)
  • Post burn hair loss (permanent)
  • Traction hair loss (permanent)
  • Trichotillomania (permanent)

Some hair loss conditions esteroides mexico go by the name “effluvium,” which means an outflow. Effluviums characteristically affect different phases of the hair growth cycle.

What is telogen effluvium (TE)?

The hair follicle is an anatomical structure which evolved to produce and extrude (push out) a hair shaft. Hair is made up of proteins called keratins. Human hair follicles on the scalp do not continuously produce hair but rather in a continuous cyclic pattern of growth and rest known as the “hair growth cycle.”

They cycle through a growth stage (anagen phase) that can last two to six years, and then undergo degradation (Catagen phase 2-4 weeks) and then regress to a resting stage (telogen phase) for up to two months before starting to grow a new hair fiber again. At any time on a healthy human scalp, about 80% to 90% of the hair follicles are growing hair. That leaves up to 10% to 20% percent of scalp hair follicles in a resting state called telogen, when they don’t produce any hair fiber. This is known as the Anagen-Telogen ratio (A/T ratio).

Shedding of the hair occurs only after the next growth cycle (anagen) begins and a new hair shaft begins to emerge. Roughly, we have about 100,000 follicles on the scalp and about 10-20% are in the resting phase. That makes it about 10,000 -20,000 hairs and due to this on average 50-100 telogen hairs are shed every day. This is normal hair loss and accounts for the hair loss seen every day in the shower and with hair combing. These hairs will regrow. Not more than 10 percent of the follicles are in the resting phase (telogen) at any time.

A variety of factors can affect the hair growth cycle and cause increased shedding. Commonly the causes are stress due to any reason – major illness, surgery, injury, childbirth, nutritional deficiencies (especially iron deficiency) etc. TE happens when the ratio of growing to resting hair follicles is altered and more follicles are in resting phase. If the number of hair follicles producing hair drops significantly for any reason during the resting, or telogen phase, there will be a significant increase in dormant, telogen stage hair follicles. The result is shedding, or TE hair loss. TE appears as a diffuse thinning of hair on the scalp, which may not be even all over. It can be a bit more severe in some areas of the scalp than others. Most often, the hair on top of the scalp thins more than it does at the sides and back of the scalp. There is usually no hair line recession, except when TE is superimposed on a developing male pattern or female pattern hair loss.

The shed hairs are typically telogen hairs, which can be recognized by a small bulb of keratin on the root end. Whether the keratinized lump is pigmented or unpigmented makes no difference; the hair fibers are still typical telogen hairs.

People with TE never completely lose all their scalp hair, but the hair can be noticeably thin in severe cases. While TE is often limited to the scalp, in more serious cases TE can affect other areas, like the eyebrows or pubic region. Whatever form of hair loss TE takes, it is fully reversible. The hair follicles are not permanently or irreversibly affected; there are just more hair follicles in a resting state than there should normally be.

What is anagen effluvium?

As a rule the follicle does not shed hair in the growing phase (anagen). Anagen effluvium is a diffuse hair loss like telogen effluvium, but it develops much more quickly and can cause individuals to lose all their hair. The hair follicle along with the bone marrow and most cancers exhibits a rapid cellular turnover. So, when patients of cancer undergo chemotherapy, the chemotherapeutic drug hits the rapidly dividing cells of the cancer. But a collateral damage occurs in the bone marrow and the hair follicles. This is the time when follicles in the growing phase are hit with the chemotherapeutic drug and end up shutting down and causing hair fall which is typically seen in patients undergoing chemotherapy.The onset of anagen effluvium is very rapid. Some individuals who start taking anti-cancer drugs can literally pull their hair out in clumps within the first two weeks. Because these drugs act so quickly and are so potent, the hair follicles have no time to enter into a telogen resting state, as with telogen effluvium, a response to a more moderate environmental challenge.Instead, in anagen effluvium the hair follicles enter a state of suspended animation, frozen in time. The hair fibers fall out quickly, but instead of looking like typical telogen hairs with little bulbs of keratin on the root end, the hairs that fall out are mostly dystrophic anagen hairs with a tapered or sometimes feathered root end.

With chemotherapy medications, the degree of hair loss varies from person to person. Some people may have a mixture of anagen effluvium and telogen effluvium and have more limited hair loss.

Some cancer treatment centers try to block the hair loss using a cold therapy. More popular in Europe than North America, cold therapy involves covering the scalp with ice packs or using a special hood filled with cold water while the anti-cancer drugs are given. The cold sends the hair follicles into suspended animation prior to contact with the drug. This stops the hair follicle cells from taking up the drug and being damaged by it. The result is much less drug-induced hair loss. However, doctors worry that any cancer cells in the skin may also avoid the anti-cancer drugs if cold therapy is given during drug treatment.

Depending upon the type of anti-cancer medication used, one can see complete regrowth to partial regrowth to no regrowth. On completion of an anti-cancer drug treatment course, a person may start to see new hair growth within a month. The hair follicles are not destroyed, so there should be a normal hair growth density. Typically the hair which grows back may have a different character – like the original straight hair may become curly hair.

What is androgenetic alopecia (AGA)?

It was Hippocrates who first made the connection between hair loss and male hormones. He noted that eunuchs did not go through the balding process. It took us almost 2400 years to realize that Hippocrates was correct in his assumption. However, it took a Psychiatrist by the name of Dr Hamilton who actually managed to connect testosterone, genetics and balding.

The etiology is genetic (inheriting the gene from either parent) and thepathogenesis is androgen (male hormone) mediated, Alopecia is a general term for loss of hair – Androgenetic alopecia means loss of hair induced by genes and male hormone. So, for a person to get AGA there has to be genetic predisposition, sufficient levels of male hormone and adequate time for these two factors to work together.

How do androgens (male hormones) cause hair loss?

Hamilton first noted that androgens (testosterone, dihydrotestosterone) are necessary for the development of male pattern baldness. The amount of androgens present does not need to be greater than normal for male pattern baldness to occur. If androgens are present in normal amounts and the gene for hair loss is present, male pattern hair loss will occur.

Testosterone converts to Dihydrotestosterone(DHT) with the aid of the enzyme Type II 5-alpha-reductace, which is present in the hair follicle cells (outer root sheath and dermal papilla). Dihydrotestosterone (DHT) is a derivative or by-product of testosterone binds to the androgen receptors (receptors exist on cells that bind androgens). These

receptors have the greatest affinity for DHT followed by testosterone, estrogen, and progesterone. After binding to the receptor, DHT goes into the cell and interacts with the nucleus of the cell altering the production of protein by the DNA in the nucleus of the cell. Ultimately growth of the hair follicle ceases.

While the entire genetic process of male pattern baldness is not completely understood, we do know that DHT shrinks hair follicles, and that when DHT is suppressed, hair follicles continue to thrive. Hair follicles that are sensitive to DHT must be exposed to the hormone for a prolonged period of time in order for the affected follicle to complete the miniaturization process (Miniaturization is the hormone-driven biological process in which hairs shrink in size over time, eventually leaving a bald scalp). Today, with proper intervention this process can be slowed or even stopped if caught early enough.

If androgens are present in normal amounts and the gene for hair loss is present, male pattern hair loss will occur. Axillary (under arm) and pubic hair are dependent on testosterone for growth. Beard growth and male pattern hair loss are dependent on dihydrotestosterone (DHT). Finasteride acts by blocking this enzyme and decreasing the amount of DHT.

In men who develop male pattern baldness the hair loss may begin any time after puberty when blood levels of androgens rise (physiologic – as part of developing secondary sexual characteristics). The first change is usually recession in the temporal areas which may or may not include a thinning crown. Hair in these areas including the temples and mid-anterior scalp appear to be the most sensitive to DHT. This pattern eventually progresses into more apparent baldness throughout the entire top of the scalp, leaving only a rim or “horseshoe” pattern of hair remaining in the more advanced stages of MPB. For some men even this remaining rim of hair can be affected by DHT.In some areas of the scalp, most or all of the follicular units have the genetic predisposition to be immune to the effects of DHT. As a result, these areas might never become miniaturized, and so hair will remain on these parts of the scalp for the person’s entire life. This happens most often in the back and sides of the scalp, aptly known as the “permanent zone,” while the front and top of the scalp are the first areas to experience thinning and baldness.

Do the androgens affect all hair follicles on the body in the same way?

The androgens have somewhat of a paradoxical effect on the hair follicles on hair follicles on different parts of the body. This response is based on the inherited androgen sensitivity in individuals.

The hair follicles of the face, especially in the beard and mustache area, respond positively to the male hormone. This is typically seen at puberty, when follicles producing fine vellus hair start producing thicker terminal hair. Male pattern baldness is generally characterized with the onset of a receding hairline and thinning crown. Hair in these areas including the temples and mid-anterior scalp appear to be the most sensitive to DHT. This pattern eventually progresses into more apparent baldness throughout the entire top of the scalp, leaving only a rim or “horseshoe” pattern of hair remaining in the more advanced stages of MPB. For some men even this remaining rim of hair can be affected by DHT. Therefore the same hormone (androgens) can have different effects on follicles in different parts of the body.