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References
Note that
this is for general discussion only, info presented here
may or may not be accurate. Please consult your doctor
before
you use anything for hair loss
TOPIC
Shedding
Shedding or
unexplained acceleration in hair loss is commonly reported
by individuals who started a new hair loss regimen or
product. Up till now, there is very little explanation for
this phenomenon. No formal studies or research has been
conducted on this subject. There are "theories" as to why
shedding occurs but we still have nothing conclusive about
this phenomenon.
The following
is a compilation of information pertaining to shedding and
other useful references, provided by Frizz in the forums.
Click here to read the entire post.
The
following is posted by Frizz
===================================
Here is a bunch of useful info for you guys. one is a FAQ
from Dr Lee, a few posts from Dr. Proctor, and a post from
Mike (MKP). i've also posted some searches one can run
regarding minoxidil and shedding, and propecia and shedding.
definitely good reading, i even found out some things i
didn't know!!!
search on minoxidil+baldspot+shedding
results: 2100 posts
http://groups.google.com/groups?hl=en&lr=&ie=UTF-8&oe=UTF-8&q=shedding+minoxidil+baldspot&btnG=Google+Search
search on propecia+baldspot+shedding
results: 3,880
http://groups.google.com/groups?hl=en&lr=&ie=UTF-8&oe=UTF-8&q=shedding+propecia+baldspot&btnG=Google+Search
--------------------------------------------
From: C&D G (muskie@telusplanet.net)
Subject: Re: Shedding question...
View: Complete Thread (3 articles)
Original Format
Newsgroups: alt.baldspot
Date: 1999/11/15
There are alot of peaple who are experianceing shedding here
who want to know more about it. This article is from Dr.
Lee's website,
www.minoxidil.com
F.Y.I.
Buck
SHEDDING AND HAIR LOSS
With its cycle of repetitive planned obsolescence and
rebirth, hair is a unique organ system. It’s of little
wonder that with its
complex and continuous recycling, there can be multiple
clinical disorders based on cycling abnormalities. Although
much is
known about the organization and composition of the hairs
themselves and of the follicles, we still have an incomplete
and
rudimentary understanding of relevant pathways and
mechanisms that regulate follicular function. In this
article, we are
addressing only entities that cause hair loss or shedding,
rather than problems of hypertrichosis or overgrowth of
hair.
The first hair follicles on the scalp form at approximately
the 9th week of gestation. On the average, the human scalp
will have
100,000 follicles and no further follicular neogenesis
occurs after birth. You are born with as many hair follicles
as you are ever
going to have. The same follicles that produced lunago (unpigmented
ultra-fine) hair in the fetus and immediate postnatal life,
eventually produce terminal hair. It is important to note
that during one’s lifetime, the same follicles can
intermittently produce
vellus or terminal hair.
A knowledge of the hair cycle is essential to understanding
hair problems. Hair growth on the human scalp is an
asynchronous
regeneration of the hair follicle in repeated cycles,
referred to as a mosaic pattern of follicular growth. The
growth stage is the
anagen phase. The duration and rate of growth of the anagen
phase normally varies at different body sites, in different
individuals, and at various ages. Scalp hairs have a
relatively long anagen phase typically ranging from 2 to 5
years, but has
been documented to be as long as 10 years. The short-lived
catagen period, usually 2 to 4 weeks in duration, is the
transitional
portion of the cycle. At this time, each terminal hair bulb
moves from its location in the dermis to a more superficial
location by
means of shrinkage and remolding of that portion below the
bulge region where the arrector pili muscle inserts. This
muscle is
not present on true vellus hair and allows terminal hairs to
‘stand on end’. Once a hair has made the transition to the
telogen
phase, its existing hair shaft will not grow any longer. The
hair shaft during the telogen phase is no longer anchored
securely in
the dermis as it was in the anagen phase and can be easily
dislodged with the gentle traction of brushing or shampooing
or
combing. Usually the shedding is unnoticed. Since the hair
can accumulate in the shower drain or on soapy hands,
patients can
erroneously associate washing the hair with causing hair
loss. The telogen hair has a club shaped proximal end within
the hair
follicle and retains the club shape when it is shed. The new
hair produced from the subsequent anagen phase does not
"push
out" the hair from the previous cycle and may on occasion be
found adjacent to the temporarily retained club hair within
the
follicular canal
------------------------------------------------------------------
NORMAL SCALP GROWTH OF TERMINAL HAIRS
Average number of brown/black scalp hairs: 100,000
10% more on blondes
10% less on redheads
Fastest Growth: between 15 and 30 years of age
Slow growth in infants and elderly
Average scalp hair growth: 0.35 mm/day or ~1 cm/month
Hair grows faster in summer than in winter
Month of greatest shed in the Northern Temperate zone:
November
Anagen growth phase: 2 to 5 years
Percentage of hair in anagen phase: 85%-90%
Average daily numbers of hair shed: 50 to 100
Female hair grows faster than male hair
------------------------------------------------------------------
Historically, alopecias have been classified as non-scarring
or scarring. The scarring type is considered permanent
because of
the destruction of the follicle and the presence of fibrotic
changes. The non-scarring alopecias don’t destroy the
follicle and
there are little or no fibrotic changes around the follicle.
Therefore, regeneration of the follicle is theoretically
possible. The
division can be arbitrary and can often overlap. The
transformation of a non-scarring to a scarring alopecia has
been identified
in some disorders.
NON-SCARRING ALOPECIAS
Alterations of hair growth
Telogen effluvium
Anagen effluvium
Miniaturization (i.e. Androgenetic Alopecia)
Congenital
Acquired
Follicular mucinosis
Chemical or physical agent
Trichodystrophies-alterations of hair
Congenital
Acquired
Trichotillomania-traction alopecia
Chemical or physical agents
Infectious agents
SCARRING ALOPECIAS
Inflammatory
Lupus erythematosus (chronic type)
Lichen planus pilaris
Planopilaris
Pseudopelade
Scleroderma
Bullous pemphigoid
Epidermolysis bullosa acquista
Folliculitis-secondary to infectious agents
Chemical and physical damage
Granulomatous inflammation
Noninflammatory
Nonscarring pseudopelade
Bullous pemphigoid
Neoplasms-benign and malignant
Many of the causes of alopecia listed above are rare and are
not frequently encountered in any practice. A good
dermatology
textbook will describe the entities. However, it is
important to understand that there are many causes for hair
loss.
Although it may sound contradictory, shedding and hair loss
is not synonymous. First, we must define our terms. Shedding
refers to hair shafts that easily or spontaneously fall out
of the scalp. There are multiple causes of shedding.
Shedding normally
occurs at the end of the telogen phase, but, in pathological
cases, can also occur during anagen. As a rule, shedding
usually
refers to a temporary event and suggests that the hair shaft
will grow back again as thick as before, providing there is
not an
intervening pathological process.
In distinction, hair loss can refer to either the temporary
or permanent loss of hair or a loss not in the number of
hair shafts, but
in the volume and texture of the hair shaft. For example,
permanent hair loss can be caused by a scarring alopecia,
such as
occurs in third degree burns or radiation to the scalp.
Typical of a loss in the volume of hair, but not in the
number of follicles,
would be the miniaturization of the follicle due to male
pattern baldness (MPB).
A complete medical history can almost always determine the
cause of alopecia. If necessary, there are alternative ways
for
determining aberrations of scalp hair cycling. The first is
the ‘hair pull’. This simple technique involves gentle
traction from the
base to the terminal ends of a group of 25 to 50 hairs.
Normally, only a few hairs are dislodged on six to eight
such hair pulls.
Shedding of two to three hairs per pull is pathologic. If
there is increased shedding, the proximal ends should be
evaluated to
determine if there is an intact hair shaft and bulb, which
would indicate either an effluvium (Latin for "a flowing
out") or hair
breakage.
A biopsy of the scalp may or may not be helpful with the
diagnosis of a particular hair disorder. The information it
delivers
about cycling aberrations is merely confirmatory to that
obtained by other simpler, less expensive means, and the
diagnosis of
hair shaft abnormalities cannot be made by a scalp biopsy.
The real value of a scalp biopsy is in the insight it can
offer into
mechanisms of alopecia.
Since this article is being written primarily for the
information of patients affected by pattern baldness, we’ll
limit the subject of
shedding and hair loss due to physiologic processes,
medications, telogen effluvium, anagen effluvium and male
pattern
baldness.
PHYSIOLOGIC SHEDDING
Since it would be normal to have 10 to 15% of all the hairs
on the scalp in the telogen phase, we can expect that 50-100
of
those hairs are at the end of the phase and will readily
shed. The anagen phase is in proportion to the size of the
follicle and can
vary from months to years. Vellus hairs have an anagen
period of a few months. However, regardless of the length of
the
growing period or of the size of the hair follicle, the
length of the telogen phase remains fairly stable, i.e.
approximately 100
days. As a consequence, the anagen/telogen ratio in an area
affected by male pattern baldness is higher than in areas
unaffected or less affected by male pattern baldness (MPB),
so in any given time period, there will be more shedding of
hair
from the areas affected by MPB than there will be in the
remainder of the scalp.
At the end of the telogen phase, the follicle will
re-enlarge and re-organize and begin producing a new hair
shaft. To date, we
do not have any medications that can be used safely to
shorten the telogen phase.
SHEDDING DUE TO CHEMICAL AGENTS
Minoxidil
For the same reasons that minoxidil promotes hair growth, it
can also cause shedding. Despite many years of research and
use,
the exact physiologic mechanisms whereby minoxidil
stimulates hair growth is not known. The stimulatory effect
of minoxidil on
the hair follicle can cause hair that is in the telogen
phase to shed before the end of the normal 100-day telogen
period.
The effect of minoxidil on the hair follicles is dose
dependent. The initial shedding was rarely reported during
use of topical 2%
minoxidil. With 5% topical minoxidil, it was usually not
noticeable, but was infrequently reported. With the use of
currently
available minoxidil concentrations of 12.5%, the initial
shedding is commonly reported. The shedding can be noted
within
weeks of initial use of topical minoxidil.
Since shedding due to the use of topical minoxidil only
effects hair that is in the telogen phase, the increased
shedding should
not last longer than 100 days and should only effect those
areas of the scalp where the topical minoxidil is being
applied.
Finasteride
There have been multiple reports of excessive shedding
several months after finasteride therapy. Typically, there
is a good
response to finasteride to prevent or reverse MPB. Then,
around the 11th to 16th week, there can be sudden shedding,
sometimes on a massive scale. The entire phenomenon fits the
description of a telogen effluvium. It is a common
observation
that post-partum women often suffer the same temporary hair
loss. In the case of finasteride use, the telogen effluvium
appears
to be a reaction to the sudden change in the systemic levels
of the sex hormone, DHT. Often the cause of a telogen
effluvium
are obscure, but has been related to high fevers, stress,
trauma, medications, etc.
The shedding is generally diffuse (global) and can affect
areas of the scalp not usually affected by MPB. So, it would
be
common to note shedding from the sides and back of the head
in addition to the crown, vertex and frontal areas. The
shedding
tends to be fairly symmetrical, but will be more noticeable
in the areas affected by MPB, because there is a higher
ratio of hairs
in the telogen phase than in the other areas of the scalp.
The duration of a telogen effluvium is variable, but rarely
lasts more than a few months and there is invariably
complete
restitution unless another pathologic process also occurs.
As a rule, treatment is not necessary because the hair will
grow back. For most patients, there is no evidence of
residual loss of
hair within a year. However, there have been cases of
patients taking finasteride and reporting repeated bouts of
excessive
shedding. In this situation, it would be advisable to
discontinue use of finasteride in favor of alternative
anti-androgens.
TELOGEN EFFLUVIUM
This is a common type of temporary hair loss and may occur
at any age. The phenomenon represents a precipitous shift of
a
percentage of anagen hairs to telogen, typically 3 to 4
months after an inciting event. The reaction can be to a
variety of
physical or emotional stresses:
Etiologies of Telogen Effluvium
Endocrine
Post-partum
Post or peri-menopausal state
Hypo or hyperthyroidism
Nutritional
Caloric or protein deprivation
Zinc deficiency
Biotin deficiency
Iron deficiency
Drugs
Anticoagulants
Angiotensin-converting enzyme inhibitors
Chemotherapeutic agents
Beta blockers
Lithium
Oral contraceptives
Retinoids (e.g. Accutane)
Hypervitaminosis A
Physical stress
Anemia
Systemic illness
Surgery
High fevers
Psychological stress
In a significant number of patients, no obvious cause is
found for the telogen effluvium. Telogen effluvium is always
potentially
completely reversible and does not lead to total scalp loss.
Rarely does more than 50% of the hair become involved in a
telogen effluvium. For more details on telogen effluvium,
please refer to the article found in the Journal Articles on
this website.
ANAGEN EFFLUVIUM
The daily loss of some telogen hairs is entirely normal. It
is always abnormal to shed anagen hairs. The term anagen
effluvium, used to describe the pathologic loss of anagen
hairs, is misleading, as the abnormal anagen hairs in this
condition
are usually broken off rather than shed. An anagen effluvium
is an acute, extreme alteration of growth of the majority of
anagen
follicles, resulting in acute loss of greater than 89-90% of
the scalp hair. The hair is usually dystrophic because of
the
interruption of growth and break off at the level of the
scalp. Unlike the shed telogen hair, the anagen effluvium
hair lost does
not have an attached bulb. These sheds occur 1-2 weeks
following the precipitating cause and result in an acute,
extensive
alopecia that can involve 80-90% of the scalp hair.
The classic and easily recognizable causes of anagen
effluvium of the scalp are radiation therapy to the head and
systemic
chemotherapy, especially with alkylating agents. In
addition, there are a large number of toxic chemicals known
to cause
anagen effluvium such as poisoning by thallium, mercury or
borates. Salts of lead, selenium and arsenic have also been
incriminated.
Regrowth of hair can usually be anticipated if the
precipitating agent is discontinued or removed. Regrowth
after radiation
therapy depends on type, depth and dose fractionation. The
amount of regrowth is directly related to the amount of
damage
inflicted upon the hair follicles.
ALOPECIA ANDROGENETICA
The most common cause of shedding and hair loss is alopecia
androgenetica, also called male pattern baldness, even
though
20% of adult women also suffer from it. The onset is usually
in the third to fourth decades, but the process can begin
immediately after puberty in those most severely affected
and may progress for decades. The basic etiologic factors in
androgenetic alopecia are presumed to be the same in men and
women, although phenotypic expression differs. Men
commonly show bitemporal recession and vertex thinning,
which may progress to an absolute baldness in the affected
areas.
On the other hand, women with MPB generally show
preservation of the frontal hair line and a progressive
thinning on the top
of the scalp, but do not develop frank baldness.
It is well established that both genetic and hormonal
factors play a role in MPB. The genetic factor is by far the
more important.
Perhaps, when the entire human genome is deciphered early in
the third millenium, we will know exactly which gene or
genes
control MPB. Subsequently, there may be gene therapy for MPB.
But for the present, we have only a partial and incomplete
understanding of the pathogenesis of MPB.
The alopecia in MPB is caused by progressive
miniaturization, rather than destruction of involved hair
follicles. In affected
follicles, the percentage of hairs in telogen is increased
and the duration of anagen is decreased. As a consequence,
there is
relatively more shedding in areas affected by MPB. Since
vellus and intermediate hairs have a short anagen phase,
they will
shed frequently. There can be permanent hair loss because
the replacement hair shaft is finer in texture and lacks the
same
volume.
The age of onset and the rate of progression of MPB are
genetically controlled and cannot be predicted. There are
times of
remission and, alternately, times of acceleration. When
there is a period of acceleration, it is often proceeded by
a telogen
effluvium. MPB can proceed with alarming speed and everyone
is familiar with stories of men who went bald ‘overnight’.
Unfortunately (and understandably) the patient will blame
whatever event or treatment coincided with the accelerated
hair loss.
It is the philosophical fallacy of post hoc, ergo propter
hoc, i.e. "after this, therefore, because of this". Since
the dramatic
miniaturization of the follicle occurs within one single
hair growth cycle, these patients are poorly responsive to
treatment and
reversing the MPB is improbable.
The more usual course would be to notice gradual recession
or thinning of the hair. Statistically, this group of
patients responds
better to treatment with minoxidil and an anti-androgen.
Approximately 70% of patients using a 5% topical minoxidil
with an
effective anti-androgen will see a gradual reversal of MPB
with thicker hair growth in 4 to 6 months. An additional 13%
report
no improvement in the amount of hair, but the MPB will not
have progressed. For the remaining 17%, the MPB progresses.
However, it is very likely that the minoxidil/anti-androgen
treatment is slowing the progress of MPB.
There is constant research into the understanding of hair
physiology and pathology. For the present, we have only two
classes
of medications that are proven and safe for the treatment of
MPB. Minoxidil is a non-specific promoter of hair growth.
The
anti-androgens can protect the follicles from miniaturizing
as a reaction to DHT. We are eagerly awaiting new
medications and
better understanding.
----------------------------
From: Peter H. Proctor (pproctor@neosoft.com)
Subject: Re: Shedding-Dr.proctor
View this article only
Newsgroups: alt.baldspot
Date: 1999/04/15
In article <37151b54.0@news.cloudnet.com>
"Tim" <tim@nowhere.com>
writes:
>From: "Tim" <tim@nowhere.com>
>Subject: Re: Shedding-Dr.proctor
>Date: Wed, 14 Apr 1999 17:54:40 -0500
>I am in my 30's, hair loss since 25 almost exclusively in
the temple area.
>Hit a shed phase on Propecia at 3 months. The shed last for
a month and a
>half. The result was that on the top of my head where it
had been ok I lost
>way too much hair. My scalp is clearly visible through my
hair on top now.
>All this in 4 months or so. I had the classic acne and oily
face. Worst of
>all at 4 months I joined the "2%" who suffered "certain
sexual side
>effects". It was bad getting worse.
>My decision was easy - I got off the drug. Since Merck
never said shedding
>was possible I was suspicious. Since I had no decent
diagnosis for the
>increase in loss I was scared. I decided not to gamble any
further. I have
>not seen any regrowth since then (about a month off the
drug). I can say
>that the sexual side effects are gone (whew!). No shedding
(whew!!).
Most people do not experience a noticeable shed of
loss-phase
hair as follicles come out of dormancy under medical
treatment. So it has taken a while for it to become
accepted. BTW, I claim bragging rights for this discovery,
since I saw it in a few patients in the mid-1980's ( one
advantage of treating a lot of people ). It has only been
noted in the Rogaine package insert in the last couple of
years.
Most likely, unlike UpJohn ( who has a decade or two more
experience), Merck has not figured it out yet. This is
possibly because each of their investigators has only a
hundred or so patients. A few incidences of induced shedding
would probably be dismissed as coicidental ( which is what I
thought for a while ). This is particularly since it occurs
before 2-4 months, and thus only involves hair that was
already in the loss-phase when treatment started. And
everybody "knows" that nothing
affects loss phase hair<G>..
It gets even more complicated because there _may_ be a very
few
additional cases in which reflex hyperandrogenicity has
induced additional hair loss with finasteride. This may
happen indirectly in a way which would probably not have
shown up in the clinical trial.
E.g., though I cannot currently point to a defined case, I
can forsee a situation in which someone starts finasteride
and experiences an induced shed of loss phase hair.
Remember, this is a good sign, because it reflects follicles
coming out of dormancy. They then stop finasteride abruptly,
exposing their foillicles to the full fury<G> of reflex
hyperandrogenicity. This is why I advise tapering off this
drug gradually, to let things settle down a bit.
Peter H. Proctor, PhD, MD
http://www.drproctor.com
----------------------------
It depends. And I wish I could give you a better answer.
Maybe this will help: Repeated waves of growth and loss
sometimes do happen in medical treatment. This is because
hair growth often gets a bit synchronized--- it starts to
grow together, so it tends to go through the hair cycle
together.
The most common presentation of this is "crops" of fine hair
which
grow and fall out, with progressive coarsening with each
cycle. The
cropping is enhanced by the fact that medical treatment
decreases the length of the loss phase, where vellous hair
spends half or more of its life-span. This synchronization
tends to damp out after a while.
Peter H. Proctor, PhD, MD
http://www.drproctor.com
----------------
From: Peter H. Proctor (pproctor@neosoft.com)
Subject: Re: Definition of "shedding" and proscar question
View this article only
Newsgroups: alt.baldspot
Date: 1997/02/23
In article <5eomr9@camel2.mindspring.com>
eroberson@mindspring.com
(Bryan Roberson) writes:
>From:
eroberson@mindspring.com
(Bryan Roberson)
>Subject: Definition of "shedding" and proscar question
>Date: Sun, 23 Feb 1997 07:48:24 GMT
>As a relative newbie to the Net and this newsgroup, I'd be
especially
>grateful if someone could provide answers to one or both of
the
>questions below:
>1) What is meant by the term "shedding?" I can assume it
means a loss
>of hair caused by using a new treatment but can anyone be
more
>specific. I've recently begun using Minox and my hairloss
seems to
>have accelerated slightly. How long does this typically
continue? Is
>shedding a problem with Proscar as well?
I answer this question about 2-3 times a week. As hair
follicles come
out of dormancy under the influence of a
hair-growth-stimulator and start to grow a new hair, they
may shed old loss phase hair a little early.
This typically presents as a wave of increased loss
beginning 3-6 weeks after starting treatment and lasting a
few weeks. The loss phase hair was scheduled to fall out in
the next few weeks anyway, so there is no net loss of hair.
In fact, because it signifies follicles coming out of
dormancy, this initial wave of loss tends to be associated
with a good eventual result.
------------------------
From: mike (emkaypee@dodgenet.com)
Subject: Re: Vitamin B5 (Pantothenic Acid) hairloss
View: Complete Thread (16 articles)
Original Format
Newsgroups: alt.baldspot
Date: 2002-01-11 06:19:14 PST
"B5 kid" <me@me.com>
wrote:
>Hi. To keep it short, about 2 months ago I got on high
doses of Vitamin B5
> for very mild acne), about 10mgs. Since about a month, Ive
noticed overall
>shedding and thinning of my hair. Im on minox/propecia, and
have had very
>good results for a couple years with this regimen, with the
usuall shedding
>phases. This is not a normal shedding phase. I'm thinning
like the way I was
>thinning before I got on propecia/minox. I think there is a
correlation
>between the B5 and my hairloss. I'm getting off it right
away. After asking
>a doc, I was told that a drug or vitamin/supplement induced
hairloss or
>shedding is most of the time only temporary, Thank God. Ive
also heard from
>another person who had a similar problem with B5. Overall
shedding and
>thinning. B5 worked pretty good on my acne, but my acne is
so mild, that it
>doesnt really matter. I rather keep my hair.
>
>
Shedding can also be looked at positively. Some people
report shedding experiences with various topicals and this
is just telogen hair coming out because a new anagen cycle
got started again. Considering the positive posts about B-5
and the pubmed studies on showing it to be helpful to
hairgrowth, I would say your shedding is a good thing.
When Revivogen people started putting the OPC's into
Revivogen,all the sudden people start reporting this same
"shedding" you are talking about. OPC's have been tested and
shown efficacious in regrowing hair on both mice and men(mpb).
Actually the other day I started a google
search(alt.baldspot) on
shedding.I was specifically looking for people's comments on
when they started treatment X and then they report
shedding.Shedding is easier to notice than the regrowth for
many people and probably a more accurate indicator of future
hairgrowth.
----------
> Can someone please explain to me the relationship between
shedding and
>hairloss?
Simple really, once you understand the hair cycle and how
pattern loss interacts with it: Regular terminal hair grows
for 2-4 years, goes into a 2-4 month loss phase and then
falls out. Meanwhile, a new hair starts to grow in the same
follicle.
Balding causes miniaturization, which not only makes the
hair finer
and lighter in color, but decreases the time it spends in
the growth phase-- to only a month or so for really fine
vellous hair. The loss-phase stays about the same. Also,
balding follicles tend to stay in the dormant phase even
after the loss phase hair has shed.
Medical treatment does two main things:
1) Reverses miniaturization. So the hair is not only coarser
and lighter, but also spends longer in the growth phase.
2) Brings follicles out of dormancy and starts them growing
hair again. If the follicle does not have a hair in it, we
also call this "growing new
hair". BTW, if the dormant follicle still has a loss phase
hair,
bringing it out of dormancy early can cause this hair to
shed a bit early. This seems to be the source of the
early wave of increased shedding that some people
experience on medical treatment.
Peter H Proctor, PhD, MD
www.drproctor.com
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