Understanding Hair Loss

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2009

1 de enero de 2009

Understanding Hair Loss The Reason and The Solution

Hair Loss Association

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Introduction

The word "alopecia" is the medical term for hair loss. Alopecia does not refer to one specific hair loss disease -- any form of hair loss is an alopecia. The word alopecia is Latin, but can be traced to the Greek "alopekia," which itself comes from alopek, meaning "fox." Literally translated, the word alopecia (alopekia) is the term for mange in foxes.

Hair loss can be caused by any number of conditions, reflected in a specific diagnosis. Some diagnoses have alopecia in their title, such as alopecia areata or scarring alopecia, but many do not, such as telogen effluvium.

Alopecia can be caused by many factors from genetics to the environment. While androgenetic alopecia (male or female pattern baldness, AGA for short) is by far the most common form of hair loss, dermatologists also see many people with other forms of alopecia. Several hundred diseases have hair loss as a primary symptom.

Probably the most common non-AGA alopecias a dermatologist will see are telogen effluvium, alopecia areata, ringworm, scarring alopecia, and hair loss due to cosmetic overprocessing. Other, more rare forms of hair loss may be difficult to diagnose, and some patients may wait months, even years for a correct diagnosis and undergo consultation with numerous dermatologists until they find one with knowledge of their condition. Plus, with rare diseases, there is little motivation for research to be conducted and for treatments to be developed. Often, even when a correct diagnosis is made, a dermatologist can offer no known treatment for the condition.

Research into hair biology and hair diseases is a very small field, and even research on androgenetic alopecia is quite limited. Perhaps 20 years ago there were fewer than 100 people worldwide who studied hair research in a major way. In recent years, there may be five times as many. This is still a small number compared to, say, diabetes research, but the expanding numbers of researchers investigating hair biology is positive, and eventually should lead to a better understanding and more help for those with rare alopecias.

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Effluviums Effluviums (defluviums) Some hair loss conditions go by the name "effluvium," which means an outflow.

Effluviums characteristically affect different phases of the hair growth cycle.

Hair follicles on the scalp do not continuously produce hair. They cycle through a growth stage that can last two or more years, then regress to a resting stage 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. These active follicles are in what is called the anagen phase. 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.

Telogen Effluvium Telogen effluvium (TE) is probably the second most common form of hair loss dermatologists see. It is a poorly defined condition; very little research has been done to understand TE. In essence though, TE happens when there is a change in the number of hair follicles growing hair. 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 in a few rare chronic cases.

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.

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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.

There are three basic ways TE can develop.

1. There might be an environmental insult that "shocks" the growing hair follicles so much that they decide to go into a resting state for a while. This results in an increase in hair shedding and a diffuse thinning of hair on the scalp. This form of TE can develop rapidly and may be noticeable one or two months after receiving the shock. If the trigger is short lived, then the hair follicles will return to their growing state and start producing new hair fibers pretty quickly. This form of TE usually lasts less than six months and the affected individual has a normal scalp hair density again within a year.

2. The second form of TE develops more slowly and persists longer. The hair follicles may not all suddenly shed their hair fibers and enter a resting telogen state.

Rather, the follicles may enter a resting state as they normally would, but instead of returning to a new anagen hair growing state after a month or two, they stay in their telogen state for a prolonged period of time.

This results in a gradual accumulation of hair follicles in a telogen state and progressively fewer and fewer anagen hair follicles are left growing hair. In this form of TE, there may not be much noticeable hair shedding, but there will be a slow thinning of the scalp hair. This form of TE is more likely to occur in response to a persistent trigger factor.

3. In a third type of TE, the hair follicles do not stay in a resting state but rather cycle through truncated growth cycles. When this happens, the individual experiences thin scalp hair and persistent shedding of short, thin hair fibers.

Causes of Telogen Effluvium: Stress and Diet What are the trigger factors for TE? The short answer is many and varied. Classic short-term TE often happens to women soon after giving birth. Called postpartum alopecia, the sudden change in hormone levels at birth is such a shock to the hair follicles that they shut down for a while. There may be some significant hair shedding, but most women regrow their hair quickly.

Similarly, vaccinations, crash dieting, physical trauma such as being in a car crash, and having surgery can sometimes be a shock to the system and a proportion of scalp hair follicles go into hibernation. As the environmental insult passes and the body recovers, the TE subsides and there is new hair growth.

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Some drugs may also induce TE, especially antidepressants. Often a switch to a different drug resolves the issue.

More persistent insults can result in more persistent TE. For example, a chronic illness may lead to TE. Arguably, the two most common problems are chronic stress and diet deficiency. Many dermatologists believe chronic stress can gradually exert a negative effect on hair growth and lead to persistent TE. Research with animal models has provided evidence to back up this claim. There does indeed seem to be a link between stress, a change in hair follicle biochemistry, and more hair follicles entering a telogen resting state.

Whether dietary problems are causing TE in North America is hotly argued among dermatologists. A lack of a mineral, vitamin, or essential amino acid can certainly cause TE, such as with people in third world countries where diets can be completely deficient in one or more nutrients. Animal experiments also provide supporting evidence.

In first world countries the average diet is rarely completely deficient in a particular vitamin or mineral. However, some dermatologists claim that with a reduction in red meat intake and a preference for vegetarian diets, some individuals are not getting a balanced intake of all the nutrients required for good hair and overall body growth. In particular, there are claims that women may be deficient in their iron intake. Why women specifically? Because women lose iron at regular intervals as a result of menstruation.

Some dermatologists believe that as we now eat less red meat, a key source of iron, some people are not eating enough iron and TE is the result. Other potential deficiencies of the modern North American diet -- such as a lack of zinc, amino acid L-lysine, or vitamins B6 and B12 -- have also been suggested to contribute to TE. When dietary deficiencies are suspected, supplements may be taken. However, supplements themselves can cause problems. Our bodies can only process so much iron each day. At high doses, iron is toxic and this can itself cause hair loss. At really high doses, iron supplements will cause death. Vitamin A supplements can also cause a TE reaction in some individuals, as excessive vitamin A can also be toxic.

TE can occur on its own or as part of another disease. The early stages of androgenetic alopecia (male or female pattern baldness, AGA for short) are effectively TE. Early AGA is characterized by an increase in resting telogen hair follicles. Someone in the early stages of AGA may have up to 40% of their scalp hair follicles in telogen.

TE can also be a symptom of other conditions, such as inflammatory conditions like alopecia areata. Hair follicles are particularly sensitive to thyroid hormones and about one third of individuals with a thyroid disorder have TE. Exposure to toxins can also cause TE as one of many symptoms.

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Treatments for Telogen Effluvium How TE is treated depends on what has activated it. For short-term TE that can be linked to a trigger like surgery, the best response is to sit tight and wait for the follicles to recover of their own accord.

For persistent TE, if the causal factor can be isolated, then the best method is to remove it. For example, if stress is the problem, stress reduction is the long-term answer. If a dietary deficiency appears on a blood test, then supplements can work.

A deficiency in thyroid hormones can be treated with hormone supplements.

However, often a specific causal factor cannot be identified. If this is the case, there are few treatment options. Most dermatologists resort to prescribing minoxidil, a direct hair growth stimulator. Minoxidil can work well for some individuals with TE, but if the underlying cause is still present, then minoxidil must be continued to block redevelopment of TE. With removal of the trigger, minoxidil use can be stopped.

Before leaving the subject of TE, here are a few words about natural hair shedding.

Everyone sheds hair and you may see more hair shed at certain times of the year.

Studies show that humans, at least in Northern Europe away from the equator, shed more hair in the fall and to a lesser extent in the spring.

This temporary increase in the number of telogen hair follicles and shed hair is probably due to changes in hormones in response to changes in daylight exposure.

Studies in mink and other mammals show that daylight exposure significantly alters prolactin levels and that prolactin has a significant effect on molting. As with mink and other mammals, humans probably have much the same molting response. Such hair loss should be temporary.

Anagen Effluvium 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. Anagen effluvium is most frequently seen in people taking cytostatic drugs for cancer or those who have ingested toxic products like rat poison.

Substances of this type inhibit rapid cell proliferation. This is a desirable factor if you are trying to block the development of a cancer, but the cells of hair follicles are some of the most rapidly proliferating, noncancerous cells the body has. Hair fiber from scalp hair follicles grows at up to 0.4mm a day and that rate of growth requires a lot of cell proliferation. Cytostatic cancer drugs and various toxins and poisons inhibit rapid cell growth, including the proliferation of cells in the hair follicles. The result is a sudden shut down of hair fiber production.

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The onset of anagen effluvium is very rapid. Some individuals who start taking anticancer 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 cytostatic anti-cancer drugs, 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.

Some experimental drugs to block drug induced hair loss are under development, but the same fear applies. The treatments to stop hair loss may also protect any cancer cells in the skin.

While, the development of anagen effluvium is rapid, the recovery is also equally rapid. Because the follicles are just frozen in time, they are ready to grow once the factor causing the anagen effluvium has been removed.

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. However, some people notice a change in the nature of the hair fiber produced. Some people find their hair changes from straight to curly or vice versa, or sometimes there is a change in hair color. These changes may be permanent.

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Alopecia areata

Alopecia areata (AA) is probably the third most common form of hair loss dermatologists see, after androgenetic alopecia and telogen effluvium. The lifetime risk for AA is nearly 2%, or two in every 100 people will get AA at some point in their lives. It is not contagious; you can't catch AA from someone who has it.

Researchers believe AA is an autoimmune disease such as rheumatoid arthritis, but in this case the individual's own immune system attacks hair follicles instead of bone joints. Just why or how AA develops is not clear. For whatever reason, the immune system is inappropriately activated and attacks hair follicles. Research using several disease models shows certain types of lymphocytes play a primary role in the hair loss. They seem to attack the hair follicles, mistakenly thinking that somehow they are a threat to the rest of the body.

AA can affect men, women, and children. It often appears as well-defined circular bald patches on the scalp. Many people will get just one or two patches, but for some the hair loss can be extensive. Unfortunately, children who develop AA before puberty are most likely to develop more extensive and persistent hair loss.

Hair loss that spreads to cover the entire scalp is called alopecia totalis. If it spreads over the entire body, affecting scalp, eyebrows, lashes, beard, pubic hair, and everything else, then the condition is called alopecia universalis. If the alopecia is just limited to the beard area in men, it is called alopecia barbae.

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The inflammation involved in AA focuses on the roots of hair follicles deep in the skin. As a result there is very little visible at the skin surface. There is no redness and often no pain, although a few people do find their skin itchy or painful to touch in the very early stages of AA development. Usually, though, there is no sensation -just a patchy shedding of hair.

The hair loss can be quite sudden, developing in a matter of a few days and it may happen anywhere on the scalp. The patch is usually smooth bald skin with nothing obvious to see beyond the absence of hair. Unlike other autoimmune diseases, the target of the inflammatory response in AA, the hair follicles, are not completely destroyed and can re-grow if the inflammation subsides.

People with just one or two patches of AA often have a full and spontaneous recovery within two years whether or not they receive treatment. However, about 30% of individuals find the condition persists and becomes more extensive, or they have repeated cycles of hair loss and re-growth.

Traditionally, AA has been regarded as a stress-induced disease. Unfortunately that view persists today, even among some dermatologists, even though very little scientific evidence supports the view.

AA is much more complicated. Extreme stress might trigger AA in some people, but recent research shows that genes can also be involved. There are probably several genes that can make an individual more susceptible to developing AA. The more of these genes a person has, the more likely they will develop AA. Some researchers believe there are a wide range of contributing factors that make someone more susceptible to developing AA. Hormones, allergies, viruses, and even toxins might contribute. Probably several factors combined are involved in the activation of AA in any one individual.

Treatments for Alopecia There are a range of treatments for AA, but none are effective for everyone and some people with AA don't respond to any treatment. Because some of the available treatments have a high risk of side effects, they are often not used for children.

The most common AA treatment involves the use of corticosteroids. Corticosteroid creams applied to the bald patches are popular with the average dermatologist, although this treatment approach is only successful for the very mildest cases. A more potent approach is to inject corticosteroid solutions into the bald patches. This can work well for some people, but close monitoring is required to ensure that side effects, such as skin thinning at the site of injection, do not occur.

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In extensive cases, systemic corticosteroids (those taken in pill or other form to affect your body) are used, though not continuously since they can cause significant side effects like bone thinning. But short-term "pulse therapy" often has good results.

More specialized treatment approaches involve the application of contact sensitizing chemicals to the skin. These cause an allergic reaction that can help promote hair growth. That may sound counterintuitive but it seems to work. A variety of experimental approaches are currently in laboratory and clinical trials. One group of drugs being tested are "biologics," which have bits of protein that interfere in a very specific way with the activity of immune cells. Biologics are injected systemically to damp down the immune activity and allow hair to regrow. The results of these trials are awaited with much interest.

Unfortunately, people with more extensive, long-term AA find the treatments currently available do not work well. For these individuals the only practical answer is a wig and lots of emotional support. It can be depressing not to have hair, especially for children, who don't want to be different from their classmates at school, and women. In North America and many other countries of the world, you can access a network of support agencies for people with AA. Details are on the National Alopecia Areata Foundation website (http://www.naaf.org).

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Understanding Hair Loss by www.best-hair-loss-solution.com Congenital Hypotrichosis Hypotrichosis is the term dermatologists use to describe a condition of no hair growth. Unlike alopecia, which describes hair loss where formerly there was hair growth, hypotrichosis describes a situation where there wasn't any hair growth in the first place.

Hypotrichoses (plural) then are conditions that affect individuals right from birth and usually stay with them throughout their lives.

The majority of hypotrichoses are due to genetic aberrations or defects of embryonic development.

There are hundreds of types of genetic hypotrichoses. Often, affected individuals have other physical or mental problems beyond a lack of hair. Conditions such as Graham-Little syndrome, Ofuji syndrome, cartilage-hair hypoplasia, Jeanselme and Rime hypotrichosis, Marie Unna hypotrichosis, and metaphyseal chondrodysplasia, among many others, can involve the symptom of hypotrichosis.

With the rapidly improving understanding of the human genome, our comprehension of why and how genetic defects cause hair loss and other symptoms is growing. But, while we may understand the genetics and the biochemistry behind hypotrichoses, treating them is very difficult. Most conditions involving hypotrichosis have no known treatment.

A few forms of hypotrichosis are worth mentioning, either because they are relatively common or because they are interesting in terms of understanding hair follicles.

Congenital Aplasia Aplasia cutis congenita, or congenital aplasia, is a developmental defect where, for reasons not understood, the skin does not fully form as an embryo develops. A baby may be born with a patch of skin that is like an open wound or an ulcer. Often this defect occurs at the back of the scalp, at the center of the "whorl pattern" of hair growth. If the defect is small, the skin will scab over and the baby is left with a scar.

Sometimes this happens in the womb and all that can be seen at birth is a patch of scalp where there are no hair follicles. However, if a baby is born with a large congenital aplasia, it usually requires an operation to cut out the affected area and close up the skin. This is often done with some urgency, since the open wound is a site of potential hemorrhage and infection. The quicker the defect heals, the better.

Triangular Alopecia Triangular alopecia (alopecia triangularis) is a condition similar to congenital aplasia.

It is usually apparent from birth and tends to affect a triangular patch of skin and hair above the temples. For unknown reasons, the skin fails to grow hair follicles in this area in a few people. While babies are not born with open ulcers as with aplasia cutis congenita, the long-term result is much the same -- a bald patch where hair does not grow. The affected area can be surgically removed or implanted with hair follicles taken from elsewhere on the scalp.

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Congenital Atrichia Congenital atrichia or papular atrichia is a unique condition in terms of the hair loss pattern. It was the first human hair loss disease researchers determined was caused by a single gene defect. Although the condition is generally regarded as a hypotrichosis, it is not strictly so. People with congenital atrichia can be born with a full head of hair like any normal baby. But in early childhood they lose all their hair, and it never regrows.

Normal hair follicles rely on chemical communication between two basic cells types: modified keratinocytes, which form the outer skin epithelium, and modified fibroblasts, called dermal papilla cells. These two cell groups must "talk" to each other through biochemical signals to ensure that hair growth and cycling occurs. The cells must stay in close contact with each other to keep the process going. One cell population cannot grow hair without receiving signals from the other cell population.

The mechanism of congenital atrichia is not fully understood, but it seems that as the hair follicles enter their first resting (telogen) state in early childhood, the two cell types get separated from each other. The epithelial cell component of the hair follicle retracts, as it should when hair follicles go into the resting phase of the hair cycle.

Normally the dermal papilla cells would also go with the retracting epithelial cells, keeping in close contact, but in congenital atrichia they don't.

Instead the dermal papilla cells get left behind deep in the skin and too far away from the epithelial cells to talk to them. Without this communication a new anagen growth phase cannot occur and hair never grows again. While congenital atrichia is genetic and runs in families, it is a gene defect that can spontaneously develop in some embryos born to parents who do not have the condition. Some people diagnosed with alopecia universalis have congenital atrichia instead.

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Research into hair biology and hair diseases is a very small field, even research on androgenetic alopecia is quite limited. However, recent years have seen a growing interest among clinicians and scientists to work on these problems to understand their mechanisms and to develop new treatments.

Perhaps 20 years ago there were less than 100 people worldwide who studied hair research in a big way. Now (2004), there are perhaps 500. Still a very small number compared to, say, diabetes research, but the expansion in numbers doing research on hair biology is "a good thing" and eventually it should lead to a better understanding and more help for those with rare alopecias.

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