请问哪位大佬有这张图的另一半～求图，谢谢～_百度贴吧
请问哪位大佬有这张图的另一半～求图，谢谢～
请问哪位大佬有这张图的另一半～求图，谢谢～
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保存至快速回贴我想做个大学生生活费与大学生旅游次数的统计分析，用SPSS，，这是定性分析还是定量分析，请问应该用_百度知道
我想做个大学生生活费与大学生旅游次数的统计分析，用SPSS，，这是定性分析还是定量分析，请问应该用
我想做个大学生生活费与大学生旅游次数的统计分析，用SPSS，，这是定性分析还是定量分析，请问应该用什么方法，具体的怎么做，哪位会的大神，请教教我，谢谢啦🙏🙏🙏🙏
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你好，就你给的这个题目的话如果按照作为一个课题的话，定性和定量都可以做，如果做定量，那么可能需要查一些相关资料然后设计一个调查表，调查表的内容应该有定量资料，也有定性资料。如果做定性研究的话，我建议做访谈。所以可能要根据你的研究目的来设计。希望我的回答有帮助，谢谢！
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请问一下已经入手的大侠，日版的黑砖和金砖，操作系统有英文系统吗？
如题，想请教一下，系统是只有日文，还是可以选择英文的，毕竟不太懂那些假名。如果只有日文操作系统，就考虑入国行了。谢谢🙏
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All Rights Reserved.美国脱发协会——关于女性脱发（柆柆编译中——）
转自“美国脱发协会”网站：www.americanhairloss.org/women_hair_loss。
PS：谷歌翻译，有些句子不够通顺。文章太长了，不造什么时候能译完
一、Types of Hair
Loss&脱发类型：
The word alopecia just means
"hair loss" it does not refer to a specific hair loss disease. Any
form of hair loss is an alopecia. The most common alopecia is
androgenetic alopecia (male or female pattern baldness), but it is
not the only hair loss diagnosis. There are many potential causes
of hair loss.
脱发只是意味着“脱发”这个词不指一个特定的脱发疾病。脱发的任何形式是一种脱发。最常见的脱发是雄激素性脱发(男性或女性秃头的),但它不是唯一的脱发诊断。有许多潜在的脱发的原因。
*Introduction
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
脱发可以由许多因素从基因到环境。而性脱发(男性或女性型脱发,AGA)是迄今为止最常见的脱发，皮肤科医生也看到许多其他形式的脱发患者。数百名脱发为主要症状的疾病。
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.
也许最常见的非雄激素型脱发皮肤科医生会看到休止期脱发,斑秃,癣,疤痕脱发，由于化妆品过度使用脱发。其他更罕见形式的脱发可能很难诊断，一些患者可能等上几个月，甚至几年，与众多皮肤科医生正确诊断,并进行协商，直到他们找到一个了解他们的状况。另外,罕见的疾病,几乎没有动机进行研究和开发治疗。通常,即使作出正确的诊断,皮肤科医生可以提供没有已知的治疗条件。
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.
生物学研究头发和头发疾病是一个很小的领域,甚至激素性脱发的研究相当有限。也许全世界20年前有少于100人研究头发的一个主要方式。近年来，可能存在的五倍。这仍然是一个小数量，相比糖尿病的研究,但扩大数字生物学研究人员调查的头发是积极的。
*Effluviums 脂溢性
Effluviums (defluviums) 脂溢性(脱发)
Some hair loss conditions
go by the name "effluvium," which means an outflow. Effluviums
characteristically affect different phases of the hair growth
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
一些脱发情况可以称为“脂溢性”,这意味着一个溢出物。脂溢典型的影响头发生长周期的不同阶段。头皮上的毛囊不不断产生的头发。他们通过一个增长阶段,这周期可以持续两年或以上，然后回归到一个静止期前两个月开始长出新的头发纤维。在任何时间在人类头皮健康,大约80%到90%的头发毛囊的增长。这些积极的毛囊在所谓的毛发生长初期阶段。这让多达10%到20%的头皮毛囊处于休息状态称为静止期,当他们不产生任何头发纤维。
Telogen Effluvium&休止期脱发
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.
休止期脱发(TE)可能是第二个最常见的脱发皮肤科医生看。这是一个很难定义的条件；只有很少的研究了解休止期脱发。从本质上讲,休止期脱发当有一个头发毛囊的数量增长的变化。如果头发毛囊的数量产生显著降低任何理由休息期间,或静止期阶段将会有一个显著增加休眠,静止期阶段毛囊。结果是脱落,或休止期脱发。
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
休止期脱发(TE)出现分散稀疏的头发在头皮上,这可能不是。它可以在一些地区更严重的头皮。通常,头发在头皮稀释超过它的两侧和背部头皮。通常没有发线衰退,除了几个罕见的慢性病例。
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
the hair fibers are still typical telogen hairs.
脱落的毛发通常静止期的毛发,它的根可能被一个球形角质包裹。角质化的肿块是否色素或未染色的没有区别；头发纤维仍是典型的静止期的毛发。&
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.
休止期脱发(TE)的人从来没有完全失去他们所有的头皮头发,但严重时头发可以明显薄。虽然休止期脱发往往局限于头皮，在更严重的情况下
可能影响到其他部位，如眉毛或公共区域。
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.
休止期脱发采取任何方式,它都是完全可逆的。毛囊不是永久或不可逆转的影响；只有更多的毛囊比正常情况下应该有静止状态。
There are three basic ways TE can
develop.有三种基本方法休止期脱发可以生发。
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.
1、可能有一个环境的伤害，“冲击”不断增长的毛囊，使它们进入了静止状态一段时间，导致头发脱落，头发弥散性稀疏增加。这种形式的TE可以迅速发展，可能一个或两个月后收到明显冲击。如果触发是短暂的，然后,毛囊会回到它们的增长状态，并很快开始生出新的头发。这种形式的TE通常持续不到六个月，受影响的人一年之内头皮又都有一个正常的头发密度。
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
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.
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
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
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
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
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.
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
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.
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 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
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.
*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. I 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
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
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.
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
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).
*Scarring Alopecia
Scarring alopecia (Cicatricial alopecia )
Scarring alopecia, also
known as cicatricial alopecia, refers to a collection of hair loss
disorders that may be diagnosed in up to 3% of hair loss patients.
It occurs worldwide in otherwise healthy men and women of all
Each specific diagnosis within this category is fairly rare, but
some examples include dissecting cellulitis, eosinophilic pustular
folliculitis, follicular degeneration syndrome (previously called
"hot comb" alopecia), folliculitis decalvans, lichen planopilaris,
and pseudopelade of Brocq, to name a few. Scarring alopecia may
also be part of a much larger condition such as chronic lupus
erythematosus, where many organs of the body can be affected.
While there are many forms of scarring alopecia, the common theme
is a potentially permanent and irreversible destruction of hair
follicles and their replacement with scar tissue.
Most forms of scarring alopecia first occur as small patches of
hair loss that may expand with time. In some cases the hair loss is
gradual, without noticeable symptoms, and may go unnoticed for a
long time. In other instances, the hair loss is associated with
severe itching, burning, and pain, and is rapidly
progressive.
The scarring alopecia patches usually look a little different from
alopecia areata in that the edges of the bald patches look more
"ragged." The destruction of the hair follicle occurs below the
skin surface so there may not be much to actually see on the scalp
skin surface other than patchy hair loss. Affected areas may be
smooth and clean, or may have redness, scaling, increased or
decreased pigmentation, or may have raised blisters with fluids or
pus coming from the affected area.
These visual indicators may help with diagnosis, but it is
difficult to diagnose a scarring alopecia just from the pattern of
the hair loss and the nature of the scalp skin. Often when scarring
alopecia is suspected, one or more skin biopsies are done to
confirm the diagnosis and help identify the particular form of
scarring alopecia. A small biopsy of 2 to 4 mm in diameter is taken
and examined under a microscope. A pathologist or dermatologist
will look for destruction of the hair follicles, scar tissue deep
in the skin, and the presence and location of inflammation in
relation to the hair follicles.
Often, the early stages of a scarring alopecia will have
inflammatory cells around the hair follicles, which, many
researchers believe, induces the destruction of the hair follicles
and development of scar tissue. However, there is some argument
about this among dermatologists, as sometimes a biopsy from a
scarring alopecia-affected individual shows very little
inflammation.
Scarring alopecia almost always burns out. The bald patches stop
expanding and any inflammation, itching, burning, or pain goes
away. In this end stage, another skin biopsy usually shows no
inflammation around hair follicles. Bald areas usually have no more
hair follicles. Sometimes, though, hair follicles, at least those
at the periphery of a bald patch, are not completely destroyed and
they can regrow, but often all that is left are just a few
longitudinal scars deep in the skin to show where the hair
follicles once were.
Treatment Options
Scarring alopecia can involve a lot of damage and permanent hair
loss. For this reason treatment of scarring alopecia should be
quite aggressive. The nature of treatment varies depending on the
particular diagnosis. Scarring alopecias that involve mostly
lymphocyte inflammation of hair follicles, such as lichen
planopilaris and pseudopelade, are generally treated with
corticosteroids in topical creams and by injection into the
affected skin. In addition, antimalarial and isotretinoin drugs may
For scarring alopecias with inflammation of mostly neutrophils or a
mixture of cells, the typical treatment involves antibiotics and
isotretinoin. More experimentally, drugs like methotrexate,
tacrolimus, cyclosporin, and even thalidomide have been used to
treat some forms.
Once a scarring alopecia has reached the burnt-out stage and there
has been no more hair loss for a few years, bald areas can be
either surgically removed if they are not too big or the bald
patches can be transplanted with hair follicles taken from
unaffected areas.
*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.
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
*Infectious Agents
Ringworm .
Ringworm has nothing to do with worms, it is actually a fungal
infection. Ringworm is first and foremost an infectious skin
condition and can occur anywhere on the body, but if it develops on
the scalp it can cause patches of hair loss. When it occurs on the
scalp the professional term for ringworm is "tinea capitis".
Ringworm is the same thing as athletes foot, and the same kind of
fungal infection can affect the nails too. Ringworm of the scalp
usually begins as a small pimple that progressively expands in
size, leaving scaly patches of temporary baldness. The fungus gets
into the hair fibers In the affected area and these hairs become
brittle and break off easily leaving a bald patch of skin. The
affected areas are often itchy, red and inflamed, scaly patches
that may blister and ooze. The patches are usually redder around
the outside with a more normal skin tone in the center. This may
create the appearance of a ring, hence the name, ringworm.
Worldwide, the fungus Microsporum audouini is a very
common cause of ringworm, but increasingly Trichophyton
tonsurans can also cause tinea capitis, especially in Latin
American countries. Other fungi that may cause tinea capitis
include Trichophyton schoenleinii, Trichophyton
megninii in Southern Europe and Africa, and Trichophyton
violaceum in the Middle East. The fungus Microsporum
gypseum can sometimes cause tinea capitis. This fungus is
common in soil and may be transferred to humans by contact with
infected animals. You can also get ringworm from pets that carry
the fungus, and cats in particular are common carriers. Ringworm is
contagious. It can be passed from one person to the next by direct
skin-to-skin contact. You can also catch ringworm through contact
with contaminated items such as combs, unwashed clothing, and
shower or pool surfaces.
Treatment for ringworm varies depending on the particular fungus
involved. Some types of ringworm infection will resolve
spontaneously and so no treatment may be given. Most commonly
though an antibiotic called Griseofulvin is used. Griseofulvin is
very effective against fungi in hair and skin but it is not so good
at treating yeast or bacterial infections. The Griseofulvin
gradually accumulates in the skin and hair. It especially likes to
bind with keratin which is a key component of hair, skin and nails.
The Griseofulvin blocks the fungus from infecting the keratin. More
recently some fungi that cause tinea capitis have been showing some
resistance to the drug Griseofulvin necessitating higher doses and
longer courses of treatment. As an alternative to Griseofulvin,
newer anti-fungal drugs like Terbinafine, Itraconazole, and
Fluconazole can be prescribed.
Folliculitis . Folliculitis is a term for focal
inflammation of hair follicles. It looks like acne with little
rings of inflammation surrounding the opening of a hair follicle.
In the early stages of a folliculitis the hair fiber may still be
present in the middle of the folliculitis, but as the folliculitis
progresses the hair often falls out. When folliculitis is severe,
the inflammation is so intense that it can actually permanently
destroy the hair follicles, leaving little bald patches. There are
forms of folliculitis which are non-infectious such as those caused
by oils and greases applied to the skin that clog up the hair
follicles, but f olliculitis is usually due to a bacterial
infection. Particularly common is an infection of the hair
follicles by Staphylococcus aureus. "Hot tub folliculitis"
is caused by Pseudomonas aeruginosa which grows in
inadequately chlorinated water. It is also possible to have viral,
fungal, or yeast induced folliculitis involving Herpes
simplex, Herpes zoster, Pityrosporum ovale,
Trichophyton rubrum and other causative agents.
Non-prescription topical antibiotics like bacitracin, mycitracin,
or neomycin can be used to treat minor folliculitis. For more
serious infections oral antibiotics such as erythromycin, or
griseofulvin if the infection is fungal in nature, may be used.
Piedra . Piedra (Trichomycosis Nodularis) is a
condition where the hair fibers are infected by a fungus. The
visible indicator of a piedra infection is development of hard
nodules on hair fibers. Indeed, Piedra is Spanish for stone. The
nodules are a concretion of hyphae and fruiting bodies of the
fungus, known as an ascostroma, from which the fungal spores are
released. There are two basic typres of piedra, black piedra and
white piedra, referring to the color of the nodules formed on the
hair fiber. Black Piedra is due to the fungus Piedra
iahortae and is mostly found in tropical countries while white
piedra is due to Trichosporon beigelii and is found mostly
in Europe and Southern parts of the USA.
The infection may affect hairs of the scalp, body and genital
areas. Usually the infection is relatively benign. In parts of
Malaysia, the nodules of black piedra are considered attractive and
traditionally women encouraged its growth by sleeping with their
hair buried in the soil. However, when the infection is severe the
fungus weakens the hair fiber making it easy to break off. This can
result in a patchy - diffuse hair loss. Treatment generally
involves shaving off affected areas or a topical application of
salycylic acid, formaldehyde. White piedra is resistant to azole
based antifungals, but this category of treatments is used for
black piedra. Oral therapy with either ketoconazole or terbinafine
has also been used.
Demodex folliculorum . There is a popular
belief in some communities that Demodex folliculorum contributes to
causing hair loss and that removing Demodex will enable hair
regrowth. Demodex is a little worm-like creature that likes to live
on skin and in hair follicles. Demodex feeds on dead skin and oils,
so it particularly likes to live in hair follicles where there are
lots of both. It is actually very common. We are born free of
Demodex, but during childhood, through contact with others, our
skin can become infected by Demodex. About 70% of adults have some
Demodex in their hair follicles. For the most part, we never know
they are there. They are benign, if repulsive, little creatures.
The most common problem with Demodex is that they may cause
irritation, particularly in the eyelashes. If you have itchy
eyelashes it may be Demodex is the problem. However, this is as
much as Demodex can do to you. It does not cause hair loss.
Seborrheic dermatitis . Seborrheic dermatitis
is not an infectious disease, but it can involve infection.
Seborrheic dermatitis is first and foremost a skin condition, but
it can also involve temporary hair loss if the dermatitis is
located on the scalp or other terminal-haired skin areas. The
dermatitis presents as scaly, sometimes oily, inflamed skin that
can be itchy or even painful to touch. This is an inflammatory
condition the cause of which is not well understood, although there
does seem to be a genetic component and Caucasians, particularly of
Celtic descent, are most susceptible. It seems that the sebaceous
glands attached to the hair follicles begin to produce a very rich
form of sebum. The sebum contains fewer free fatty acids and
squalene but increased amounts of triglycerides and cholesterol. In
part, the trigger for may be androgen steroids. Times of hormone
fluctuation, such as during puberty, can activate the onset of
seborrheic dermatitis. Seborrheic dermatitis can also be observed
in some new born babies when maternal androgens are passed from the
mother to the baby across the placenta. Conditions including
Parkinson's disease, head injury, and stroke can also be associated
with seborrheic dermatitis, and things like stress and chronic
fatigue can make it worse.
The excess, rich sebum production in seborrheic dermatitis can
trigger the proliferation of skin flora. Yeast Pityrosporon
ovale (also called Malassezia furfur) has been shown
to increase in numbers with the intensity of seborrheic dermatitis.
This excessive yeast proliferation causes more irritation and
inflammation. Although all this inflammation is not specifically
directed at the hair follicle, if hair follicles are in the
vicinity of the inflammatory cells then they can still be adversely
affected. Hair follicles find inflamed skin an unhealthy
environment in which to grow. Thus seborrheic dermatitis may
non-specifically cause diffuse hair loss. This hair loss should be
reversible with reduction of the inflammation intensity. Although
seborrheic dermatitis can involve a proliferation of years it is
important to point out that seborrheic dermatitis is not
infectious, you cannot catch seborrheic dermatitis. Where yeast is
involved in seborrheic dermatitis it comes from the affected
individual's own skin. We all have yeasts of various types living
on our skin, the problem in seborrheic dermatitis is that the
yeasts may grow to far greater numbers than normal.
There are several treatments for seborrheic dermatitis. The
simplest treatment involves the use of medicated anti-dandruff type
shampoos to control the skin proliferation and scaling. Several
shampoos might be recommended for alternating use on different days
and each with its own particular activity. Shampoos for seborrheic
dermatitis may contain sulfur, selenium sulfide, zinc pyrithione,
tar, salicylic acid, or oil of Cade. These shampoos have been
available for many years. More recently Azole based shampoos
(Ketoconazole - Nizoral) have been made available over the counter.
Other medicated shampoos may contain fluconazole. All can be
effective in treating seborrheic dermatitis. Some dermatologists
may also prescribe antibiotics to control the skin flora and in
doing so indirectly reduce the inflammation. The inflammation may
be directly treated using a corticosteroid cream or lotion to
control the immune response. Seborrheic dermatitis can be very
persistent once it starts so persistence with treatment is required
and preventative treatment is useful even when the symptoms are
*Hair Shaft Defects
There are a multitude of
conditions where physical damage to the hair fiber results in hair
loss. Sometimes this damage to the hair fiber is due to the hair
being improperly formed by the hair follicles. These conditions are
usually determined by genetic defects. There are also conditions
where physical damage of the hair fiber is caused by something
environmental, most often poor or inappropriate hair care. Hair
loss as a result of physical hair defects are rare compared to
other causes of alopecia, but the most common ones are listed
Loose anagen syndrome . Loose anagen syndrome
or loose hair syndrome involves exactly what the name suggests,
growing hair that is "loose" and easily pulled out of the hair
follicle. Loose anagen syndrome is most often first diagnosed in
young children, more so in girls than boys. Their hair never seems
to grow, they rarely ever need a hair cut, and the scalp hair is
usually thin, especially at the back of the scalp. That the hair is
loose and easily pulled out helps explain why the back of the head
is most affected. The repeated rubbing of a person's head on a
pillow at night pulls out more of the hair on the back of the head,
whereas the front of the scalp has less contact with the pillow and
so the hair is more likely to remain in place. The remaining hair
usually does not grow very long and it can be unruly and difficult
to comb and style. Blond haired children age 2 to 5 years are most
likely to be affected but loose anagen syndrome can appear later in
life as well. The syndrome improves with age of its own accord in
children, but development in older individuals indicates the hair
loss will be more persistent. Why the hair is loose is not known
for sure, but the root sheaths that normally surround and protect
the hair shaft in the skin are not produced properly in people with
loose anagen syndrome. It seems that because the root sheaths are
not fully formed there is a lack of adhesion between the hair shaft
and the root sheath and the hair fiber is poorly anchored in the
hair follicle. There may be a genetic problem behind loose anagen
syndrome and the condition can run in families, but there are also
many isolated case reports with no family history. There are no
known effective treatments for loose anagen syndrome.
Traction alopecia and trichotillomania . In
terms of the mechanical action that causes hair loss, traction
alopecia and trichotillomania are exactly the same. The hair is
plucked out of the skin leaving clear bald patches or diffuse, thin
hair. With traction alopecia the cause may involve things like
tight hat bands, pulling the hair into a tight pony tail, cornrow
hair styles, and anything else that pulls on the roots of the hair.
If traction alopecia continues for a long time and the same hair is
repeatedly pulled out then the hair follicles in the skin can
become so damaged that they stop growing hair permanently.
Trichotillomania is a condition in which the affected individual
plucks out their own hair. Often the hair on the scalp is plucked
to leave bald patches, but the individual may focus on the
eyelashes, eyebrows, pubic hair, or any other hair bearing region.
There is much argument about whether trichotillomania is a habit
like nail biting, or a more psychological problem. Either way,
affected individuals are usually not aware that they are plucking
their hair and when they are made aware of it they often find it
very hard to stop. Some individuals who pluck their hair also then
eat it, a condition called "trichophagia". This is a very dangerous
condition that needs to be treated with some urgency. Hair is not
digestable in the stomach, it can build up into a hair ball. This
can severely irritate the stomach lining leading to severe
ulceration. It is possible to die from trichophagia. Treating
trichotil therapists can probably help more
than dermatologists.
Monilethrix . The condition monilethrix makes
hair fiber look like a string of beads. Along the length of a hair
fiber there are nodes and constrictions making the edge of the
fiber undulate. This hair beading weakens the fiber and people with
monilethrix have diffuse hair loss. Most frequently the hair loss
is at the back of the scalp and neck and can leave the front of the
head relatively unaffected. Monilethrix can also affect hair in
other regions of the body. Under a microscope, the hair fibers can
be seen to have lost their cuticle covering over the nodes while
the constrictions keep their cuticle. The brittle hair easily
breaks once it is exposed above the skin and the fibers rarely grow
very long as a result. Breakage occurs in the weak constriction
points along the fiber. Monilethrix most often occurs in childhood
but young adults can also develop it. It is a genetically inherited
disease and can run in families, although different family members
may be affected to different degrees of severity. The severity of
monilethrix can also change with the seasons. It is often worse in
winter and improves in summer. Monilethrix may spontaneously
improve, although many people have monilethrix for their entire
Overprocessing, cuticle stripping, and bubble
hair . Overprocessing the hair is the most common cause of
physical hair damage by far. Perming, straightening, bleaching, and
dyeing the hair all involve quite harsh chemicals that can
significantly affect the integrity of hair fiber. Using these
cosmetic approaches too frequently or inappropriately can lead to
irreversible damage to the hair fiber. The more hair fiber is
damaged by these processes the weaker it will be and the more
likely it will break off.
The hair cuticle is a very strong outer sleeve of dead and
highly keratinized cells that overlap each other like fish scales
along the length of the hair fiber. The cuticle helps protect the
softer inner cortex structure of the hair fiber from damage. The
overlapping scales of the cuticle may become damaged and "flake up"
if they are exposed to too much processing. For perms,
straighteners, bleaches, and dyes to work the cuticle has to be
opened up so that other chemicals can get to the hair cortex and
either rearrange the chemical bonds in the hair structure, as
occurs with perms and straighteners, or to remove or add hair
pigment, as occurs with bleaching and dyeing. If the chemicals to
open the cuticle are applied for too long, in an unsuitably high
concentration, or too frequently the cuticle may be irreversibly
damaged and even stripped away completely. When this happens the
softer cortex is exposed to the environment. The cortex does not
have the same properties of the cuticle, it has a rough surface, so
at this stage the hair can look dull, "dry" and frizzy. Chemicals
in shampoos, in the water, in air pollution, combined with UV light
exposure can all contribute to further damage and weakening of the
hair cortex. Eventually, the hair may become so weak that it splits
or breaks off completely. More usually, this splitting and breakage
occurs to old hair, that is, towards the end of the hair fiber.
However, if the chemical processing is very severe, it alone can do
so much damage to the hair fiber that the fiber at the root is
severely weakened. If this happens, the hair may beak off at the
skin surface. The result is a diffuse "alopecia".
As well as chemical induced damage, physical processes can also
damage the hair. Aggressive brushing, back combing, and other
grooming techniques that put a lot of physical stress on the hair
fiber can cause the cuticle to flake and strip away. Inappropriate
use of the hair dryer can cause a lot of damage. When you wash your
hair, some water gets under the cuticle and into the cortex. If you
dry your hair with a high heat you heat up the water. This makes
the water expand inside the hair and this literally pushes outwards
to leave spaces in the hair fiber. In severe cases the hair
develops little bubbles inside, a condition appropriately called
"bubble hair". These bubbles make the hair much weaker and likely
to break off. If damaging physical processes are combined with
damaging chemical processes then the problem is compounded.
Physical damage to the hair through overprocessing is difficult
to treat. The best approach is to cut off as much damaged hair as
possible, avoid further chemical processing, be gentle with your
hair and wait for new, undamaged hair to grow in. While there are
cosmetic treatments to help "glue" damaged hair back together, they
only work for a short time and have to be reapplied regularly. The
end result is never as good as the original, undamaged hair.
Trichorrhexis nodosa . One of the most common
hair shaft defects a dermatologist encounters is trichorrhexis
nodosa (also called trichonodosis). Trichorrhexis nodosa is a focal
defect in the hair fiber. When observed under the microscope most
of a hair shaft looks entirely normal. However, in isolated spots
along the length of a fiber swelling and/or fraying can be seen.
These focal defects develop where there is an absence of
Causes of trichorrhexis nodosa can be congenital or acquired.
Congenital trichorrhexis nodosa is very rare, but some people have
naturally weak hair where the cuticle is not properly produced.
Congenital trichorrhexis nodosa is usually hereditary, it runs in
families, and it first develops at a very young age. Abnormal
production of hair fiber that is irregular and brittle can also
occur in metabolic disorders such as those that involve abnormal
urea synthesis, abnormal copper or zinc metabolism, or defective
cysteine or sulfur incorporation into hair fiber
(trichothiodystrophy). Acquired trichorrhexis nodosa is much more
common and develops as a result of excessive hair manipulation and
over-processing. Too much brushing, hairstyles that put constant
stress on the hair, excessive washing, dying, and perming may
disrupt the cuticle in focal areas along a hair shaft.
Trichorrhexis nodosa is particularly seen in people who overuse hot
combs or permanent waves to style their hair. Once the cuticle is
removed from hair fiber then the hair cortex swiftly breaks
Treatment depends on the considered cause of the focal defects. If
the hair production is believed to be abnormal then treatment will
focus on the hair follicle and improving the strength of hair
fiber. Where the defect is the result of excessive grooming the
obvious action is to reduce the amount of hair manipulation. People
are encouraged to stop using brushes, avoid hair styling that
involves chemicals and use only very mild shampoos.
This section is just the
tip of the iceberg in terms of what can cause hair loss, but other
than androgenetic alopecia, most forms of alopecia affect
relatively few people in the general population. 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 over-processing. The average non-hair
specialist dermatologist may never see any of the other hair loss
conditions in his or her clinic during their entire career!
However, this can create a problem for those who do have a rare
form of alopecia. It may be hard to get a proper diagnosis if the
dermatologist they consult with has no experience with their
condition. For some people with rare hair loss conditions, a
correct diagnosis may take months, sometimes even years, and
consultation with numerous dermatologists until one is found 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,
there is no known treatment for the condition that a dermatologist
can offer the individual. 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.
Women's Hair
Loss女性脱发
Mistakenly thought to be a strictly male disease, women
actually make up forty percent of American hair loss sufferers.
Hair loss in women can be absolutely devastating for the sufferer's
self image and emotional well being. Unfortunately, society has
forced women to suffer in silence. It is considered far more
acceptable for men to go through the same hair loss process.
*Introduction
Mistakenly thought to be a
strictly male disease, women actually make up forty percent of
American hair loss sufferers. Hair loss in women can be absolutely
devastating for the sufferer's self image and emotional well
Unfortunately, society has forced women to suffer in silence. It
is considered far more acceptable for men to go through the same
hair loss process. Even more unfortunately, the medical community
also treats the issue of women's hair loss as if it were
nonexistent. Since hair loss doesn't appear to be life threatening,
most physicians pay little attention to women's complaints about
hair loss and essentially tell their patients that "it's no big
deal", and that "you'll just have to live with it."
Of course what these physicians don't seem to realize is that
the psychological damage caused by hair loss and feeling
unattractive can be just as devastating as any serious disease, and
in fact, can take an emotional toll that directly affects physical
The American Hair Loss Association recognizes that hair loss is
women is a serious life altering condition that can no longer be
ignored by the medical community and society as a whole.
*Types of Women Hair Loss女性脱发的类型
Hair loss can be temporary or long lasting. Temporary hair
loss can be easy to fix when its cause is identified and dealt
with, or difficult when it is not immediately clear what the cause
is. Hair loss that could possibly have been temporary, may become
long lasting as a result of an incorrect diagnosis. The potential
for such misdiagnoses is perhaps the most frustrating aspect of
hair loss for women. The information in this section will help you
identify the cause of your hair loss and ideally lead you and your
doctors to the right treatments for your particular kind of hair
loss, sooner, rather than later.
Alopecia is the medical term for excessive or abnormal hair loss.
There are different kinds of alopecia. What all hair loss has in
common, whether it's in men or women, is that it is always a
symptom of something else that's gone wrong in your body. Your hair
will remain on your head where it belongs if hormone imbalance,
disease, or some other condition is not occurring. That condition
may be as simple as having a gene that makes you susceptible to
male or female pattern baldness or one of the forms of alopecia
areata, or it may be as complex as a whole host of diseases.
Fortunately, hair loss may also be a symptom of a short-term event
such as stress, pregnancy, and the taking of certain medications.
In these situations, hair will often (though not always) grow back
when the event has passed. Substances, including hormones,
medications, and diseases can cause a change in hair growth,
shedding phases and in their durations. When this happens,
synchronous growth and shedding occur. Once the cause is dealt
with, many times hairs will go back to their random pattern of
growth and shedding, and the hair loss problem stops.
Unfortuantely, for some women, hair loss becomes a life long
*Causes of Hair Loss脱发原因
Dihydrotestosterone (DHT), a derivative of the male hormone
testosterone, is the enemy of hair follicles on your head. Simply
put, under certain conditions DHT wants those follicles dead. This
simple action is at the root of many kinds of hair loss, so we'll
address it first.
Androgenetic alopecia, commonly called male or female pattern
baldness, was only partially understood until the last few decades.
For many years, scientists thought that androgenetic alopecia was
caused by the predominance of the male sex hormone, testosterone,
which women also have in trace amounts under normal conditions.
While testosterone is at the core of the balding process, DHT is
thought to be the main culprit.
Testosterone converts to DHT with the aid of the enzyme Type II
5-alpha reductase, which is held in a hair follicle's oil glands.
Scientists now believe that it's not the amount of circulating
testosterone that's the problem but the level of DHT binding to
receptors in scalp follicles. DHT shrinks hair follicles, making it
impossible for healthy hair to survive.
The hormonal process of testosterone converting to DHT, which
then harms hair follicles, happens in both men and women. Under
normal conditions, women have a minute fraction of the level of
testosterone that men have, but even a lower level can cause DHT-
triggered hair loss in women. And certainly when those levels rise,
DHT is even more of a problem. Those levels can rise and still be
within what doctors consider "normal" on a blood test, even though
they are high enough to cause a problem. The levels may not rise at
all and still be a problem if you have the kind of body chemistry
that is overly sensitive to even its regular levels of chemicals,
including hormones.
Since hormones operate in the healthiest manner when they are in a
delicate balance, the androgens, as male hormones are called, do
not need to be raised to trigger a problem. Their counterpart
female hormones, when lowered, give an edge to these androgens,
such as DHT. Such an imbalance can also cause problems, including
hair loss.
Hormones are cyclical. Testosterone levels in some men drop by 10
percent each decade after thirty. Women's hormone levels decline as
menopause approaches and drop sharply during menopause and beyond.
The cyclic nature of both our hair and hormones is one reason hair
loss can increase in the short term even when you are experiencing
a long-term slowdown of hair loss (and a long-term increase in hair
growth) while on a treatment that controls hair loss.
The following are the most common causes of women’s hair
Andogenetic Alopecia
The majority of women with androgenic alopecia have diffuse
thinning on all areas of the scalp. Men on the other hand, rarely
have diffuse thinning but instead have more distinct patterns of
baldness. Some women may have a combination of two pattern types.
Androgenic alopecia in women is due to the action of androgens,
male hormones that are typically present in only small amounts.
Androgenic alopecia can be caused by a variety of factors tied to
the actions of hormones, including, ovarian cysts, the taking of
high androgen index birth control pills, pregnancy, and menopause.
Just like in men the hormone DHT appears to be at least partially
to blame for the miniaturization of hair follicles in women
suffering with female pattern baldness. Heredity plays a major
factor in the disease.
Telogen Effluvium
When your body goes through something traumatic like child
birth, malnutrition, a severe infection, major surgery, or extreme
stress, many of the 90 percent or so of the hair in the anagen
(growing) phase or catagen (resting) phase can shift all at once
into the shedding (telogen) phase. About 6 weeks to three month
after the stressful event is usually when the phenomenon called
telogen effluvium can begin. It is possible to lose handful of hair
at time when in full-blown telogen effluvium. For most who suffer
with TE complete remission is probable as long as severely
stressful events can be avoided. For some women however, telogen
effluvium is a mysterious chronic disorder and can persist for
months or even years without any true understanding of any
triggering factors or stressors.
Anagen Effluvium
Anagen effluvium occurs after any insult to the hair follicle
that impairs its mitotic or metabolic activity. This hair loss is
commonly associated with chemotherapy. Since chemotherapy targets
your body’s rapidly dividing cancer cells, your body’s other
rapidly dividing cells such as hair follicles in the growing
(anagen) phase, are also greatly affected. Soon after chemotherapy
begins approximately 90 percent or more of the hairs can fall out
while still in the anagen phase.
The characteristic finding in anagen effluvium is the tapered
fracture of the hair shafts. The hair shaft narrows as a result of
damage to the matrix. Eventually, the shaft fractures at the site
of narrowing and causes the loss of hair.
Traction alopecia
This condition is caused by localized trauma to the hair
follicles from tight hairstyles that pull at hair over time. If the
condition is detected early enough, the hair will regrow. Braiding,
cornrows, tight ponytails, and extensions are the most common
styling causes.
*Oral Contraceptives
Since the "pill" was approved by the FDA in 1960, oral
contraceptives have become one of the most popular forms of birth
control used today.
Millions of women are prescribed the pill each year in this
country, but very few are aware that oral contraceptives are a
common trigger of hair loss for many who use them.
The "pill" suppresses ovulation by the combined actions of the
hormones estrogen and progestin or in some cases progestin alone.
Women who are predisposed to hormonal related hair loss or who are
hypersensitive to the hormonal changes taking place in their bodies
can experience hair loss to varying degrees while on the pill or
more commonly, several weeks or months after stopping the pill.
The American Hair Loss Association recognizes that for the most
part oral contraceptives are a safe and effective form of birth
control. The AHLA also recognizes that the "pill" has been
clinically proven to have other health benefits for some women who
use them. However, with that said, the AHLA believes that it is
imperative for all women especially for those who have a history of
hair loss in their family to be made aware of the potentially
devastating effects of birth cont