Frequently Asked Questions about alopecia

The FAQs summarizes the experience of our alopecia email list. It should not be construed as advice to follow. I reserve copyright on this document. No portion should be reproduced for commercial purpose. The views expressed do not necessarily represent those of the University of Louisville. The document has not been edited or examined by the University of Louisville. The author of this document is solely responsible for its content. Individuals are free to distribute the document, as long as it is not altered, and the source is appropriately acknowledged.

Dedicated to my beloved daughter Belinda, an alopecia areata/universalis patient since 2 years of age. —Manuel F. Casanova, M.D.


“This group of perky alopecians has really dashed my hopes for being the centerfold in The New England Journal of Medicine and made me feel a whole lot better about what I have.”

When one of my daughters developed alopecia areata and lost most of her hair several years ago, my perception on the nature and effects of the condition markedly changed. Ever since, I have focused some of my efforts in helping others, primarily children, with the condition. Thus far my most gratifying endeavor has been the creation of a list server and a FAQ (frequently asked questions) on alopecia areata. In sharing the experience of our list server, I initially found a pervasive feeling of helplessness. I realized that alopecia areata was stressful both to parents and children. The new era of managed care has brought forth frustrated parents who do not understand the medical interventions and their side effects, or think that they have lost control over the future outcome of their children. Parents ask themselves how will the condition affect their children physically and emotionally? What can they do to help them? At the same time younger affected children are depressed thinking they may have caused the condition.

This is the nature of the beast and the origin of our FAQ:

  1. to let all of those concerned know they have emotional support,
  2. to provide guidelines about the best ways to handle specific or potential problems. Whether it's information about applying eyeliner, how to extend the life of a wig, or where to purchase a stocking cap for those cold winter nights, this FAQ has been most valuable in providing coping skills for a condition that has no cure at present.
  3. To help our children hold their heads high as they outgrow those formative years otherwise tainted by emotional trauma. I hope the FAQ will remind all of those reading it that what is inside is more important than what is on top of their heads,
  4. For both children and adults with alopecia the FAQ provides information that will enable them to identify problems and act on them so that they do not snowball uncontrollably, and
  5. Although you may have no difficulties talking to family members, discussing problems related to alopecia with friends or stangers may pose some problems. No matter how understanding they may be, they cannot possibly know how you feel. Alternatively other people may be more likely to inform friends and peers of their condition rather than relatives. Perhaps they are afraid to find out about familial traits in that direction. Maybe they don't want to reveal that much of themselves to them. Or maybe they feel more competition to be above average, better than perfect. Not reaching their own unrealistic expectations makes them clam up verbally and emotionally. I hope that by being on the list server, you too, will be able to talk about your condition openly and without any fears.

The free flow of words, usually in the context of a problem, will help you obtain a beter perspective of yourself; your motivations, fears, aspirations, and how to look at the truth of things. Whether the issue be a "problem" from outside, family, self-esteem, lifetime goals, coping, personal shortcomings, or other daily "whatevers", sometimes the mere act of writing something down seems to diminish its burden. Maybe participating within our list server is a variation of the saying, "Grief shared is grief diminished." I don't guess this is all that complicated rocket science, and maybe it's just a means of slowing down to "smell the roses" and taking a good look at what is really important in life. The point is as you go back through your life and face the emotional burdens it helps to defuse the power of negative events. Whatever the mechanisms, it seems to work for me and many of our participants.

In our midst you will find the strength and courage to fight the inner battles we all face. Remember that you have a whole army of supporters now to help you in this quest. Learning about the trials and tribulations of others will help you regardless of whether you have or haven't accepted the condition. Some alopeciacs may not longer be looking for a cure and even if one came along they would let you "take cuts" in front of them. Still, in our list server you will find a place to express your occassional frustrations with people with whom you share a common bond. In essence, the FAQ represents the needs of our alopecia areata community. Our conversations in the list server manifest our desires, hopes and expectations. It is not intended, however, to provide for medical advise. I urge you to read this document thoroughly, apply it as necessary, and contribute to it as appropriate.

The symbol for our support group is the butterfly. It is a very significant symbol of what Alopecians, as a group, go through. As one of our members said, "As the disease begins we are like the caterpillar -feeding- seeking information, what is it, why, what will happen, what can be done, etc. Then we close ourselves into a cocoon, feeling very lonely and lost, alienated from the rest of the world. Within our cocoon we sort out our feelings, learn to deal with this major change in our lives. In our own time and way, we break from our cacoon. We learn to be strong, spread our wings, and learn to help others understand what has happened to us." This life cycle analogy aptly portrays the quest of the alopeciac as an "ugly duckling" dating from a fragile and crumbling stalactite only to realize that in time he/she really was a stalagmite, always reaching for the sky.

This list will hopefully, help us all to become "Butterflies", help lessen the fear and confusion, and make us realize that real beauty comes from the heart! My biggest reward after participating in our list server has been the experience that the original feeling of despair in some members has been superseded by hope, confidence, and a feeling of loyalty towards the group. I have seen many people come and grow - bet you thought it was a typo, it wasn't. People in our discussions do come and GROW. They learn about their options and grow from the experience. I remember being joined by a 14 year old girl. She was initially scared at dealing with alopecia in a very cruel world. Because of the help she received in the list server she has matured to a point where she can now help others. She received love and now she is giving it back. Isn't that wonderful! Joining our discussion group enabled her to find a little piece of herself, buried sometime before, as she began to lose her hair. Our support was never meant to help her feel sorry for herself. Support meant helping her stand tall and proud, handling her situation with dignity, and feeling human again. Initialy she wasted too much time feeling bad and dragging herself down. Melancholy got to be a bit overwhelming. Time provided this young girl with many choices in how she decided to feel. Crying became pointless. Ultimately it was her conscious choice to get over it. People now congratulate her on how courageous she is handling her hair loss, however, it was her ONLY way out. Still it was HER conscious choice to make. She decided for alopecia to make a positive difference in her life. Given time we all grow to different levels. Looking back I realize that she needed us, just as much as we needed her. She will be on my mind whenever I face my next ailment or crisis. Her experience and those of others is the foundation of our FAQs. As such, this document is not the work of one individual but the collective and unselfish efforts of all of those who have participated, offering their own opinions and experiences. I am deeply humbled and forever grateful to have such wonderful friends and having been a participant in many of their discussions. The friends I have made, sight unseen, I will cherish for a lifetime. They have been strong, funny, ironic, vibrant, acquainted with despair and refusing to surrender to it. Thank you for rushing to help when one of us falls!

In the words of Elton John and Bernie Taupin,


“I hope the day will be a lighter highway
For friends are found on every road
Can you ever think of any better way
For the lost and weary travellers to go

“Making friends for the world to see
Let the people know you got what you need
With a friend at hand you will see the light
If your friends are there then everything's all right.”

I have also listened carefully to the song Wind Beneath My Wings by Bette Midler:

“It must have been cold there in my shadow
To never have sunlight on your face
You were content to let me shine, that's your way
You always walked a step behind
So I was the one with all the glory
While you were the one with all the strength.
A beautiful face without a name, for so long
A beautiful smile to hide the pain.

“Did you ever know that you're my hero
And everything I would like to be
If I can fly higher than an eagle
You are the wind beneath my wings
It might have appeared to go unnoticed
but I've got it all here in my heart
I want you to know I know the truth
Of course I know it
I would be nothing without you.”

The song talks about someone being content to stand in her shadow, letting her take all the glory. For all of you who participated and allowed me to write this document, you are all my special heroes. Time, writing this document, getting to know many of you, have allowed me to smile through the tears. What a gift you have all given me! The initial pain caused by my daughter's hair loss has changed to the wonderful memories of our time spent together. My heart, empathy, compassion and prayers are with all of you.

For facts you may read any alopecia book, listen to your Dr's opinions, read the medical textbooks, search the on-line FAQ's, NAAF materials, or visit the library. For support turn to our list server. This is the place where you can share your feelings, doubts, frustrations, and life encounters with a warm, loving, caring group of individuals who listen to you without judging or criticizing you. Instead, they support you by sharing their feelings, doubts, frustrations, and stories. They will make you laugh and they will make you cry. You will feel as though you "know" them and they "know" you. We are only able to develop that sort of bond and relationship by moving beyond the "strict alopecia topics" (i.e., the one dimensional if "my hair's gone, what now") and sharing a little part of ourselves. Nothing helps more than humor. Many people may find some of the posts within the list server as trivial, ridiculous, non-alopecia related.... but in fact, these are the ones which makes us come alive as people, not just as "alopecia people". If it were not for the distinct flavor and personality of this list and its' most wonderful inhabitants, you would have a very glum outlook on this menacing condition. Instead, the different excursions the list may take makes alopecia a bonding, self-deepening, often humorous condition.

Table of contents


Patient: “I have had alopecia areata since '91. That was the first time I noticed it anyway, it could have been earlier. I had taken a 10 speed bicycle ride from Florida to Texas a year earlier and really don't remember any hair loss.”

Doctor: “AHA! Found what caused your aa! You rode that bike sooo fasssst your hair blew off! Advise......peddling backwards fast so you can catch up to it!!!!!”

Alopecia areata is a fairly common form of hair loss. Approximately 1% of the population will develop alopecia areata at a certain point in their lives. At any given time approximately .1 to .2% of the general population will exhibit the symptoms. This estimate is based on prevalence studies such as the First National Health and Nutrition Examination Survey, conducted from 1971 to 1974 and published in May, 1992. The survey found that of 20,749 individuals studied, 37 could be confirmed as having alopecia areata. Thus, a nationwide prevalence of about 306,000 cases is projected, with estimates ranging from 218,000 to 426,000 (Safavi, Arch Derm 128:702, 1992). In Britain and the United States the sexes are equally affected at all ages.

Clinically alopecia areata is characterized by the sudden appearance of a round or oval patch of non-scarring and painless hair loss with spontaneous remissions and exacerbations. A few patients complain of itching in the scalp before or during the loss of hair. The patches are well-circumscribed and occasionally exhibit the presence of “exclamation-mark hairs” around their margin. Most cases (95%) involve the scalp. Loss of hair from the trunk and extremeties is associated with a more severe course.

The involved skin in alopecic patches remains soft, smooth and almost totally devoid of hair. Patches may appear in analogous fashion to dropping a number of stones at the same time in a clear pool of water. The ripples reverberate around and meet, mix, or bounce off one another. This circular "growth process" has given the idea to a few researchers that alopecia areata is of infectious origin but most believe in an autoimmune etiology (more about this later). Usually the earlier the onset of symptoms the worse the prognosis. Five to ten percent of patients, especially children, end up losing all of their scalp hair (alopecia totalis). When hair is lost throughout the whole body the disorder is termed alopecia universalis. Although the disease itself is non-life threatening, the cosmetic and psychological impact on both patients and parents is tremendous and may lead to a high lifetime prevalence rate of major depression and/or generalized anxiety disorders.

Alopecia areata is unusual during the first year of life, one third to one-half of all cases start by age 20, and only 25% of the cases occur after age 40. Twenty to thirty percent of patients develop a single episode. The statistics show that some optimism will not hurt since in 60% of cases the first patch exhibits hair regrowth during the first year. In one third of patients the initial patch never exhibits evidence of regrowth. Some studies suggest that the percent of patients who develop extensive disease (alopecia areata to either totalis or universalis) is anywhere from 16.7% to 19%. Recurrences are possible even after a 20 year remission.

It is currently accepted that alopecia areata is caused by an auto-immune response of your own body. Research yields the theory that a gene or genes from our parents gives us a pre-disposition for this condition, yet it doesn't appear at birth. Rather, the theory holds that sometime after birth, we are exposed to an "insult" (Fortune favors the brave!). This insult may be a virus or disclosure of a previously secluded protein for which our immune system defends itself. Here's the problem: the portion of protein exposed by this insult closely resembles an intrinsic protein sequence within the hair follicles' cells. The end result is that the immune system attacks the hair follicle in a case of mistaken identity. The resultant inflammatory reaction is non-specific and other structures surrounding the hair follicle also die. This includes sweat glands as well as the cells that provide the pigment to the hair. Surrounded by more and more inflammatory cells, the hair follicle retreats into the higher layers of skin. It then starves itself by not being able to get nutrition, and sheds its shaft (the hair) thus entering an extended period of dormancy.

Some believe the predisposition to the disease and the subsequent physical insult is not always enough. These people believe that emotional or stress problems can trigger the disease. This may offer an explanation as to why stress reduction, hypnotherapy, etc., have been of some help to a few patients. I am personally skeptical. There seems no doubt that emotions can affect the immune system, but perhaps after being triggered, the condition runs freely on its own. Sometimes this process abates temporarily and hair regrows, sometimes not.

There is an overlap between alopecia areata and other organ specific autoimmune disorders. Some of these include atopy (e.g., seasonal rhinitis, bronchial asthma, and atopic dermatitis), thyroiditis, Addison's disease and vitiligo. Case reports have also claimed an association with pernicious anemia and myasthenia gravis. The generation of these auto-antibodies appears to be gender related. It is now known that females with antithyroid antibodies are at increased risk for developing severe hair loss. There is undoubtedly an increased familial incidence of the disorder (about 20% of cases) which is more likely genetic rather than environmental. In familial cases the severity of involvement in relatives bears no prognostic significance to individual patients. Current therapy relies on attempts to modulate the immune system. Thus far, corticosteroids, contact sensitizers and UV radiation have failed to alter the course of the illness.


“I've been through just about all degrees of (hair) loss over the years, … there's probably some colloquialism about ‘tempting fate’ that would apply here, so maybe I should get back to counting my blessings instead of indulging in fear.”

“The chemical shorthand for gold (and for alopecia universalis) is AU. Surely, there must be some value in that … beyond that I shine.”

Alopecia areata is the 'umbrella term' that refers to patchy hair loss, total (or near total) loss on the scalp (a. totalis) and combined loss of scalp, facial and body hair (a. universalis). These terms are useful to indicate the extent of hair loss but they are more descriptive than clinical.

Using these terms can sometimes be difficult - it is not always clear in which category a person belongs. It really isn't important to force a definition when one is in that vague in-between area. Some of our patients have made transitions from patchy to totalis followed by regrowth. Similarly, some patients with totalis have patches of hair loss elsewhere in the body while others with "universalis" have scattered hairs still present in some parts of their body. At what point did they change from areata to totalis, or from totalis back to areata or universalis? Technically it is a matter of percentages and that is really not important to us. Like one of our members said, "I have one hair that periodically grows on my chin (of all places) and another that mysteriously appears on my knee. And yet another single hair periodically grows on my left big toe. Does this make me AT as opposed to AU?" The distinction is sort of like splitting "hairs" (or hair as the case may be!).

For clinical research purposes it is very necessary to define the group being studied. It is a great concern of researchers to have uniform standards when studying alopecia areata so that results from one study can be relevant when comparing results from another study. One of these parameters is severity or extent and clinicians have often taken an arbitrary cut-off when designing their studies- those that have less than 25% hair loss are either mild or moderate, those that have more than 25% hair loss are staged as severe. In the future such criteria will be superseded by factors that are at the molecular level such as HLA markers.

Other terms used in describing different subtypes of alopecia areata include:

which literally translated from the Greek means snake and referes to the winding or bow-like spread of hair loss around the margins of the scalp. It is most commonly seen as a band affecting the back and sides of the head (otherwise known as the occipital and temporal regions).
describing a reticular or grid-like hair loss. Patients with reticular alopecia have many patches involving most of the scalp. Due to the infrequency of this subtype and its similarity to hair loss of different causation a skin biopsy is usually ordered to clarify the diagnosis.
form is seen after recurrent bouts of hair loss followed by partial regrowth. In affected regions, short hair often intermixes with longer hair. The appearance of the scalp is one of thinning rather than a bald patch. Again, because of similarities with other types of hair loss, a skin biopsy may be ordered to clarify the diagnosis.

Note: An interesting case report appeared published in the Am J Dermatopathol 1999 Feb; 21(1):46-50. The article written by S. Kossard was entitled "Diffuse alopecia with stem cell folliculitis: chronic diffuse alopecia areata or a distinct entity?:

A 34-year-old woman presented with an 8-year history of slowly progressive diffuse nonscarring alopecia with loss of hair density. Scalp biopsy specimens showed increased miniaturized follicles and an asymmetric wedge-shaped lymphocytic infiltrate concentrated on the stem cell-rich region at the point of entry of sebaceous ducts and at bulge-like regions of multiple follicles. Several hair bulbs emerging at the stem cell compartment also were inflamed, but the hair bulbs in the deeper dermis and subcutis were spared. I speculate whether these findings may represent a stem cell folliculitis similar to the reaction pattern previously observed in graft versus host disease and in androgenetic alopecia. The additional presence of peribulbar lymphocytic inflammation could indicate that the patient had a variant of alopecia areata. The clinical presentation of a slowly progressive diffuse alopecia without progression to clinically recognizable alopecia areata and the prominent lymphocytic inflammation involving the stem cell compartment may prompt a reexamination of similar cases currently classified as chronic diffuse alopecia areata. The concept that lymphocytes can inhibit stem cell function without destroying the stem cells themselves needs consideration.

describes a type of hair loss that resembles a triangle.
variant is diagnosed when the hair loss surrounds a birthmark.

When the condition affects the beard it is known as alopecia BARBAE. As one of our members said, "Sometimes I look like I have shaved while totally drunk." The beard is involved in about 10% of men.

In biblical times a name was supposed to say a little of who you were. A name even defined a person's destiny. Take for example the name Jesus, it is synonymous with Savior. -Although somewhat unrelated and jokingly, I always thought that the name itself (Jesus) gave away the punch line to the story.- I think there is some truth to the fact that names provide a little about a person's destiny. You see, once a diagnosis (a name for a medical condition) is received it is repeated time and time again. The name dwells within you, the diagnosis becomes a Mantra, an exercise in self-hypnosis. Names are definite and don't necessarily adapt to many of the things we learn or have learned about the condition. Once you give or receive a name, it may mark the beginning of the end. It is unfortunate that many patients are slaves to the power of the word. It shouldn't come as a surprise that these same patients accept what others say of them rather than who they are. One of the things that is hard for some people to understand is that contrary to names, people have the capacity to progress in who they are. Are you always an alopeciac? Do you TAKE TIME to enjoy being a good mother/father, friend, cook, golfer, etc.? Given enough time (aging) anybody can qualify as being an alopeciac, but how many will qualify as having been a good parent or a good friend? I think that splitters, those that believe in areata/totalis/universalis are the gnostics of the world. When you put "medical truth" above faith, you deny a person of his/her humanity. In our case salvation is attained by accepting who we are rather than reading labels.

In summary,the term alopecia areata has survived most attempts by the medical community to broaden it almost to the point of non-existence. Not only do we have alopecia areata but we must consider totalis, universalis, ophiasis, reticular, diffuse, triangular, perinevoid, barbae, etc. In a certain sense alopecia universalis stands for a severe form of the condition, while alopecia areata is a less severe condition. There are studies suggesting that certain people may have a selective vulnerability to the more severe forms of the disorder. I personally believe that there are no real points of demarcation. Transitional forms can regularly be seen and outcome is the same for all of them (mainly unpredictable). Usually there are periods of clinical standstills followed by sudden exacerbations. If anything, the glorified latin nomeclature does justice to the marked variability of the disorder especially in chronic cases. Nothing in the medical terminology is sacrosant or distinctly procrustean. As a matter of fact we can create our own terminology. How about dividing the condition into positive and negative symptoms? Positive symptoms would be those distinguished by the appearance of an abnormal phenomenon (e.g., inflammatory cells in a biopsy, abnormal CD4/CD8 lymphocyte ratio, hyperactive thyroid, atopy), while negative symptoms are those characterized by absence or diminution of normal function (e.g., lack of skin pigmentation, depression, social [mal]adjustment, amount of hair loss?). We could probably say that the negative symptoms are the more enduring and those that underlie most of the "disability". In essence I don't believe in merely attaching labels that pan out to be meaningless or worse, pejorative. If this has been the case in alopecia areata it is because the medical profession has found that the presentation of the condition is diverse, its cause unknown, and response to treatment unsatisfactory. If anybody believes that they can dissect apart AA from AU solely on the amount of hair loss, HLA subtyping, etc., they should perform a good epidemiological study with statistical methods based on cluster or discriminative function analysis to see whether their populations are trully heterogeneous. In the discussion of lumpers vs. splitters I get off my soapbox by reminiscing that in all of my medical readings I have learned more about what alopecia is not rather than what it is. I now understand a lot better the condition in social and cultural terms than from the medical standpoint. Maybe alopecia areata is not a disease and that's the reason we haven't been able to find a cure. If anything we should find a cure for our society. Maybe people should stop victimizing and persecuting others simply because they are different.


Clinicans usually classify hair loss as scarring and nonscarring. In scarring alopecia, the hair follicles are involved by inflammation. The attendant fibrosis and loss of hair follicles prevents any potential regrowth. Scarring is manifested by a pale, glazy and smooth scalp. Scarring types of alopecia include infections, systemic diseases (e.g., lupus erythematosus, sarcoidosis, scleroderma, dermatomyositis), and physical or chemical trauma (e.g., freezing, burns, trauma, radiation, acids, alkali). In noscarring alopecia, the hair follicles are preserved or resting. Snoozzzzzzzze. This explains the reversible nature of many of these disorders. Among the nonscarring types of alopecia (accounting for over 90% of cases) that produce localized hair loss are alopecia areata, telogen effluvium, androgenetic alopecia (male pattern baldness), tinea capitis/scalp ringworm, and trauma (hair pulling and traction). Other causes of nonscarring alopecia with diffuse involvement include systemic diseases like lupus, hypo and hyperthyroidism, and nutritional deficiencies (e.g., iron, protein, biotin, zinc).

Telogen effluvium

The normal hair undergoes a growth cycle with several phases. The active growth phase is called anagen and the resting phase is called telogen. Normally 80 to 90% of your hair is in the anagen stage. People with telogen effluvium have shifted their growth cycle in such a way as to precipitate many of the anagen hairs into the telogen phase. If you keep track of the amount of hair lost in your hair brush, pillow, and bathtub a person with telogen effluvium will probably lose some 400 per day. This amount is 4 to 5 times what is considered normal. The hair loss in telogen effluvium is diffuse and often barely perceptible to the clinican. Usually it takes for a 25% loss of hair (diffuse) in a normal individual before hair loss is noticeable.

In alopecia areata, hairs have similarly been shifted to the telogen resting stage. Contrary to the case of telogen effluvium, the shift occurs in a well circumscribed area. A biopsy specimen will also show that the trigger mechanism for both conditions is different. The base of the hair follicle in alopecia areata will show inflammatory cells, but the same will be absent in the telogen effluvium biopsy.

It may be noteworthy to point out that stress may be a the precipitating factor for the shift of anagen hairs to their telogen phase. Two to three months after a severe illness (especially one with bouts of fever) or childbirth, scalp hair may be shed in abundance. Other reported stressors include hemorrhage (including blood donation), crash dieting or malnutrition, emotional stress and certain drugs. Among the drugs associate to telogen effluvium are aminosalicylic acid, amphetamines, bromocriptine, capatopril, carbamazepine, cimetidine, coumadin, danazol, enalapril, etretinate, levodopa, lithium, metoprolol, propanolol, pyridostigmine, and trimethadione. Unless these drugs or stressor are repeated, hair tends to grow back.

Telogen effluvium is more commonly seen in women than in men. It is classically described following childbirth or withdrawal from the pill. It begins from less than a month to 4 months post partum. Hair shedding may last for as long as a year. Treatment with different hormones (e.g., estrogen, progesterone), zinc, biotin, and even minoxidil 5% have provided no consistent effect.

Women may also complain that they never recover their full length of hair but this may be due to the normal aging process. As you get older the time your hair spends in the anagen phase seems to shorten. Consequently the length of your hair will shorten with ageing.

Other causes of diffuse hair loss include:

If no cause is immediately obvious, the work-up should include a skin biopsy, CBC (complete blood cell count) (with hemoglobin), ESR (erythrocyte sedimentation rate), ANA (antinuclear antibody), serum iron, and thyroid function tests. The thyroid panel should include total and free T4, T3 and thyroid stimulating hormone (TSH). For females with suspected androgenetic alopecia levels of DHE-SO4 and free testosterone are included. Theodore J. Daly of Garden City Dermatology, New York routinely orders the following laboratory tests for patients where he suspects alopecia areata: TSH, T4, antithyroid antibody, antimicrosomal antibody, ASO, anti DNAse B titer, anti-reticulin antibodies, antigliadin antibodies, ANA, ds-DNA.

Androgenetic alopecia (also known as common baldness, male pattern baldness, androgen-dependent alopecia, premature baldness, diffuse alopecia of females).

This is the most common type of alopecia with an onset after puberty. Over the age of 40 it affects some 50% of men and roughly an equal number of women. It is said to follow an autosomal dominant inheritance pattern but some clinicians differentiate between patients with an early onset of symptoms (less than 30 years of age) and those in which the same pattern develops later in life. Usually the younger the patient is at the onset of symptoms, the more severe the eventual loss of hair. Certain racial groups have a much lower incidence of androgenetic alopecia, e.g., Chinese, Japanese, Native Americans, and some black Africans.

While hair loss in men tends to be manifested at the vertex, in women it tends to be more diffuse. Women with androgenetic alopecia rarely become complete bald. Hormonal factors appear to play a major role in its development. Men castrated before puberty do not develop androgenetic alopecia regardless of any genetic risk factors. They only develop the baldness if given testosterone. Then, if the hormone (testosterone) is discontinued, the baldness does not progress, but unfortunately, it does not reverse either. In women there is usually a delay until after a period of hormonal imbalance (e.g.,menopause, institutions or discontinuation of oral contraceptives, the postpartum period),thus suggesting a protective effect for estrogen. Some women also tend to have greasy skin, acne, and sometimes, evidence of polycystic ovarian disease. Sometimes androgentic alopecia can be initiated at times of hormonal change (e.g., institution or descontinuation of hormonal contraceptives). Still results of tests measuring testosterone, gonadotropins, and estradiol in women with androgenetic alopecia have been quite variable (most results show normal levels).

Clinically, androgenetic alopecia is characterized by a miniaturization of hair and its follicle. Individual hairs are reduced in diameter or thinned out. The hairs become smaller and eventually unpigmented. Skin biopsies have shown an abnormality of the growth cycle, with a large proportion of individual hairs in the resting (telogen) phase. In addition, some biopsies reveal a moderate chronic inflammatory reaction around the hair follicle and its surrounding structures. The condition usually manifests itself as a bitemporal recession of the hair line in males. The remaining hairs become finer and less manageable for the patient. Some patients may also notice increased oiliness and a tingling sensation of the scalp.

Several medical conditions have been associated to androgentic alopecia. A thorough work-up for an endocrine type abnormality may be necessary if patients exhibit irregularities in either menstruation or lactation, acne, or virilizing hair growth. Laboratory work up may disclose pathological ovaries (polycistic ovary syndrome), adrenals, or pituitary. Among the laboratory tests recommended for all balding females are thyroid function tests, serum levels of dehydroepiandrosterone sulfate, testosterone, androsteneidione, and sex hormone-binding globulin.

In some women with abnormal androgen metabolism, antiandrogen drugs (e.g., cyproterone acetate) have been prescribed with some success. The drugs prevent the progression of the hair loss but only produce mild to moderate regrowth. Side effects prevent the use of hormonal therapy in males. Surgical intervention is directed at redistributing hair from the side and back of the head into the balding areas. This procedure entails multiple punch biopsies with removal of hair plugs and their transplantation to affected areas. Other surgical techniques attempt to reduce the size of the bald area by excising an elliptical area of skin from the vertex and stretching the adjacent skin. Repeated interventions may be necessary. Some information regarding wigs are provided in other sections of this document.


“Last Saturday I was in the library working on a midterm when I almost passed out (2x in a row). It was unexpected and severe, and a woman at the library helped me get to a doctor. To make a long story longer...I have no family history on either side of thryoid disorder. My mother, however, told me tonight that she has known her thyroid has had *low* activity levels that she has never been treated for in the past. I also want to mention now that I had my thyroid tested (during a CBC--complete blood count) about six years ago, and received no callback that anything was wrong. I saw my doctor for a follow-up appointment and she said that my thyroid function is indeed low. I have been prescribed medicine that I will have to take for the rest of my life.

“After researching hypothyroidism (as opposed to hyperthyroidism) via the web, I made some startling discoveries. The symptoms vary, and often go unnoticed, ranging from dry skin and nails, losing hair in patches or all over, and constipation, to weight gain, tiredness, fatigue, and sometimes even mental illness and psychosis. This condition is so often overlooked, and perhaps because it occurs most often in women, it is misdiagnosed as a mental condition.

“I have had all of these symptoms to one degree or another at various stages of my life. Also included as symptoms are bouts of severe weakness (which go away within minutes or hours, and may leave one feeling like it's all mental, ie. crazy), a feeling of being *unbalanced*, forgetfulness, and cold sensitivity. I was treated by two different doctors over the past few years, and one even prescribed an antidepressant (which I later flushed down the toilet because it made me sick). Both doctors were male (but this may not mean anything) and treated me like a *stressed out female*.”

Approximately half of hypothyroid patients suffer from hair loss. The alopecia is generalized and characterized by thinning of hair rather than bald patches. The hair itself becomes dull, coarse, and brittle. This is a systemic disorder and hair all over the body appears to be affected; including the beard, pubic hair, etc. Some researchers have reported that the hair cycle of hypothyroid patients is shifted to the telogen (resting) phase- a phenomenon similar to that observed in alopecia areata and telogen effluvium. Another similarity betwen these conditions resides in the fact that these patients exhibit brittle nails with longitudinal and transverse ridges. Many years ago researchers thought that loss of the lateral third of the eyebrows (Hertoghe's symptom) was characteristic of the condition. This change has now been reported in thallium toxicity, lupus, seborrheic dermatitis, and some patients with alopecia areata.

The most common cause of primary hypothyroidism is autoimmune in origin. Laboratory tests have shown the presence of a circulating antithyroid antibody. This antibody can be found in some patients with alopecia areata. The end result is a more severe type of hair loss with a poorer prognosis. Besides loss of hair, some of the manifestations of hypothyroidism include; fatigue, lethargy, cold intolerance, cramps, muscle stiffness, weight gain, cold hands and feet, dry skin, low body temperature (below 97.8F) --sufferers feel the cold deep inside, low blood pressure, constipation, and unexplained fatigue (particularly upon rising and in the afternoon; more energy at night).

Thyroid effect many body functions. Many women have a family history of thyroid disease, particularly on their maternal side. Menstrual problems are common among low-thythroid patients; irregular cycles, painful cramps, heavy bleeding, PMS, endometriosis, infertility, ovarian cysts, etc. Some clinicians suggest that PMS may be a form of thyroid disease.

The diagnosis is based on thyroid function tests primarily the measuring the levels of TSH total T4, free T3, and T3. However, blood tests are not always reliable. For instance, the Center for Disease Control regularly sends out blood samples oto 7 per cent of all laboratories in the U. S. Between 8 and 25 per cent of tests yield erroneous results. If you have the symptoms but not the laboratory results, have them done again at another laboratory!

The following is an instructive story from one of our participants:

“My 13 year old son was tested twice for his thyroid by two different dermatologist and was told :"nothing wrong". This really bugged me as he had all the classic symptoms of hypothyroidism. We are currently with an immunologist and he also deals with people with chemical sensitivities. We took my sons basal temperature for a week every morning same time before he got out of bed and found that his temp was between 94 and 97 which is very low. He had his cortisol tested which was 3.2 (very low) should be 4.2 to 10. He is currently on a low thyroid hormone (1mg). I can see a marked improvement in his well being. His skin is not dry anymore. The eczama on his arms and legs have gone and he is not as sluggish anymore.”

Before the advent of sophisticated laboratory tests for thyroid hormones, physicians commonly diagnosed hypothyroidism based on two things -- basal body temperature (that is the temperature of the body at rest) and Achilles reflex time (reflexes are slowed in hypothyroidism). The problem with relying totally on thyroid hormone levels is that *mild hypothyroidism* is the most common form and doesn't show up in the blood tests so it goes undetected until it becomes moderate to severe.

Basal body temp should be between 97.6 - 98.2 (or 36.4 - 36.7 celsius). Women who still have *periods* must specifically tests themselves on days 2/3/4 during their menstrual cycle. For men and postmenopausal women any days are fine. In contrast, high basal body temperatures (above 98.6 F or 37.0 C) are less common, but "may" be evidence of hyperthyroidism.

When testing basal temperature:

  1. Use a glass (not digital - sorry) mercury thermometer.
  2. Shake the thermometer "down" to below 95.0 F (or 35.0 C) and place it next to your bed BEFORE going to sleep.
  3. As soon as you wake up, place the thermometer under your armpit for a FULL 10-minutes. Try not to move and keep your eyes closed. It might help you to keep your eyes closed if you can set a timer to go off in 10-minutes (egg timer, snooze button).
  4. AFTER 10-minutes, read and write down the temperature and date. If you are a woman having a period, also write down which day it was in your cycle -- day-2, etc. (Day-1 being the first day of menstruation.)
  5. Record your temperature for at least 3 mornings, preferably at the same time of day. If you happen to be a person who works nights, and/or typically is "up all night", then take your temp when you wake up. *Morning* is not a key word -- *resting temperature* IS. But, it should be at near the same time of "day".

Treatment is directed at replenishing those thyroid hormones that are scarcely available. Thyroxine usually forestalls thyroid gland enlargement making surgery (to relieve obstructive symptoms) unecessary. Especially in the elderly or patients with heart disease, hormonal therapy should be instituted quite cautiously in order not to tax the function of the heart. Unfortunately, replacement therapy while preventing the further loss of hair, often fails to reverse the original hair loss or provides for incomplete regrowth. One final caveat regarding replacement therapy is that Synthroid is the commercial compound that is sold as an identical hormone to that produced by the thyroid gland. In the information packet for the patient that accompanies the Synthroid pills the following statement is provided, "Partial hair loss may occur rarely during the first few months of Synthroid therapy, but it is usually temporary."

Some alternative approaches to a healthy thyroid gland include supplementing your diet with up to 12 kelp tablets a day (or eat sea vegetables (in particular, kombu, arame and dulse) and use iodized salt when you cook. Also, go easy on foods that suppress thyroid function (goitrogens) which can interfere with the production of thyroid hormones, particularly when eaten raw (cabbage, radishes, rutabagas, turnips and others such as peaches, peanuts, soybeans, and spinach).

There is some anecdotal evidence that the need for thryoid supplementation may be diminished in women taking progesterone. According to Jonh Lee, MD in "What Your Doctor Didn't Tell You About Menopause" estrogen may act as a competitive inhibitor for the binding of thyroid hormone to its receptor as both compounds have phenol rings.

You may obtain more information on hypothyroidism from:

The Broda O. Barnes, M. D., Research Foundation
P. O. Box 98
Trumbull, Connecticut 06611
(203) 261-2101
FAX (203) 261-3017

Although the Barnes Foundation provides for education and distribution of information regarding thyroid conditions, they have a vested interest in using their own diagnostic urine test and in networking patients to physicians using their methods.

You may also obtain information from The Thyroid Foundation of America at phone #800-832-8321 or fax 617-726-4136.


“When my thryoid level is too high, you can fry an egg on me (scrambled, sunny side up, you name it; hot, hot hot!), I have more tachycardia, I sleep less and awake too early. On the bright side for me, I had much more stamina, energy and drive throughout the day and into the evening. Downside, too much thyroid can cause serious cardiac problems and bone loss.”

A disease characterized by cyclical bouts of a hyperactive thyroid manifested clinically by an increased metabolism, i.e., nervousness, insomnia, tremors, frequent bowel movements, excessive sweating, and heat intolerance. The expression of symptoms may vary depending on the age of the patient, duration of the disease, and the presence of any other concomitant organ disease (e.g., heart failure). It is said that younger individuals suffer from nervous symptoms, while older ones manifest cardiovascular and muscular problems.

Many skin changes have been reported in hyperthyroidism. Characteristically the skin of the legs and feet is raised, thickened and may become hyperpigmented and itchy. The fingernail may separate from the nailbed with a curving upwards of its distal portion. This has been observed especially on the ring finger. Hair loss of a diffuse nature is seen in almost half of the patients. The scalp hair becomes fine and soft. One to two percent of hyperthyroid patients suffer from alopecia areata while 5 to 10% suffer from vitiligo. Contrariwise, a study in children 16 years and younger found a 20% incidence of SUBCLINICAL hyperthyroidism in patients with alopecia areata (Millgraum et al. Alopecia areata, endocrine function and autoantibodies in patients 16 years of age or younger. J Am Acad Dermatol 17:57-61, 1987).


“My hair is continuing to wave goodbye. I'm not waving back as there's no joy in Mudville tonight.”

“For me it has been fifteen years with alopecia! Jeez, where did time go??”

One of the difficulties with alopecia areata is the great variability in relation to prognosis, treatment response and association with other conditions (e.g., atopic states, autoimmune disorders). There is no way anybody can predict what will happen with disease progression. The condition seems to have a mind of its own. The old saying, "It will get worse before it gets better" doesn't apply to alopecia. The condition seems to get better or worse only if it wants to. A Dermatologist gaving you a prediction should go into the fortune telling business and give up his profession.

Please don't ask yourself why does my hair fall out while others seem to recover? Should we all die at the same time? Should we all become sexually mature simultaneously? Why are some people prone to obesity and yet others thin? Tall or short? External events, internal events, a biological clock, the good Lord? Nobody has an answer. Taking into account the above mentioned considerations, and with some trepidation, there are some aspects of the medical literature well worth mentioning.

Ikeda wrote an article almost three decades ago where she classified alopecic patients into different subtypes. I may summarize some of her findings by saying that the younger the patient at the onset of his/her condition, the worse the prognosis and the higher the probability of progressing to totalis or universalis. Of those patients who developed the condition before puberty, 50% eventually progressed to alopecia totalis/universalis. This stands in contrast to those patients who developed the condition after puberty, in whom only 23% developed totalis. Other bad prognostic indicators have variably been suggested, including:

  1. chronicity (the longer you have a bald spot the less of a chance for recovery- some Dermatologists believe that any patch over 1 year bears a poor prognosis),
  2. association with other autoimmune (including allergies) and endocrine conditions,
  3. the ophiasis type of alopecia where a posterior patch spreads over the ears following the hairline and,
  4. the presence of nail defects, e.g., ridging, pitting. Usually the more severe or extensive the alopecia the more likely the presence of nail defects. There are many exceptions to this generalization as I have seen patients with severe nail involvement and minimal alopecia and some AU patients with no nail involvement.

In females, there is at least one study suggesting that the presence of antibodies directed against the thyroid bears a poor prognosis. Anecdotally, I may also add, that patches in the back of the head and baldness following the hair line appear to be more recalcitrant to any form of treatment. There is only sparse and inconclusive evidence trying to correlate disease severity and family history (incidentally, the estimated risk for a child of a parent with alopecia areata to develop significant hair loss has been estimated as 2%). This is not to say that you should lose all hope if you have any of the above predispositions. I have read case reports of patients with alopecia universalis where hair regrowth ensued after complete immunosupression for a transplant. If you ever examine under the microscope a scalp biopsy of a patient with alopecia areata, you will find that the follicle remains behind (often filled with a connective tissue cell called fibroblast). This means that for some reason hair production has been "switched off" and more importantly, that there should be a way of switching it back on again. As one of our friends said, sometimes we have to be thankful for whatever regrowth we get. It is just encouraging that the follicles are truly alive.

A table in the book "Atlas of Clinical Dermatology" (2nd edition) by Anthony du Vivier (Mosbey-Wolfe, 1993) summarizes the factors indicating a guarded prognosis as follows:

Although a prognosis on future outcome is impossible to predict, the results of a hair pull test may be indicative of your present state of disease activity. In this test, a Dermatologist grabs and then lightly pulls on some 8 adjacent hairs. Normally, none of the hairs come out. For purposes of the exam up to two hairs pulled out are considered normal and six or more as abnormal. An abnormal test around the alopecic patch suggests that it will keep growing. If the abnormal test is also observed in otherwise unaffected scalp, the alopecic process may spread. If the results are negative everywhere, the worse may be over.

In summary, the fundamental symptom of alopecia areata is hair loss- this is always present and specific for definition purposes. It may start early on, and as in the case of my daughter, there seem to be predictors of poorer outcome from the earliest of stages. A Dermatologist told me that by 9 years of age my daughter may become universalis. It is foolhardy, at the present point in time, for me to consider both conditions as different. I believe that alopecia universalis is the later evolution of alopecia areata. It seems to me that areata, totalis and universalis are more or less conspicous points along a continuum of presentations. There are certainly a variety of routes by which the disorder may take its downhill course- slowly and insidiuosly or acutely with a vengance. More often than not the progression is characterized by remissions and exacerbations. The literature says that the longer a patch of hair loss remains (usually 5 years as the cut off) the worse the probability for its growing back again. Still, this is only true in a statistical sense, as some patients may "improve" after even longer periods of time. I distinguish between improvement rather than recovery because Dermatology is a medical field characterized by diagnosing things that can be seen on the skin (not when they are absent). Biasing the prognosis of alopecia solely on the amount of hair loss is abusive and renders the whole concept liable to improper usage. Prognosis should be based not only on the fundamental symptom (hair loss) but also on the presenting situation (accessory symptoms) and course taken by the illness. Prognosis should not be based on the cross sectional picture presented to the clinician but rather on the longitudinal course of the condition...Still, after all is said and done, how do statisticians factor in dumb luck, fate, and the curiosity of the gods into prognosis? A good logo for our alopecian community would be a roller coaster. There will be ups and downs in our lives with alopecia. One day we may be in full force conquering alopecia only to be followed by another day where the hair loss may be in control of our lives. Some people may regain a full head of hair (I call these periods hollidays) while others progress to totalis or universalis. Yet, it doesn't matter where we join this roller coaster or how long we have been on board, just hang on! Remember that having no hair is just part of the ride. Likeness or differences, being alopecia areata, totalis or universalis, we all share the same ride. The important thing is not classifications but rather facing the adventure, accepting the challenge and coming out better because of it.

The University of Louisville is not responsible for the contents of these individual pages; comments on this these individual pages should be directed to Manuel F. Casanova.