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What
Is Hair, Really?
"The adult human body
averages five million
hairs, of which 100,000
to 150,000 are on the
scalp. Hair is composed
of keratin, the same
protein that makes up
nails and the outer
layer of our skin. The
part seen rising out of
the skin is called hair
shaft or strand. Each
strand consist of three
layers. The outermost
protective layer
(cuticle) is thin and
colorless. The middle
layer, or cortex , is
the thickness. It
provides strength,
determines your hair
color and whether your
hair is straight or
curly.
Hair color is determined
by melanin from your
pigment cells. The more
pigment granules there
are, and the more
tightly packed, the
darker the hair. Two
kinds of melanin
contribute to hair
color. Eumelanin colors
hair brown to black, and
an iron-rich pigment,
pheomelanin colors it
yellow-blonde to red.
Whether hair is mousy,
brown, brunette or black
depends on the type and
amount of melanin and
how densely it's
distributed within the
hair. For example,
deep-black African hair
contains closely packed
melanin in the cortex, a
few in the cuticle. Very
dark European hair,
quite apart from having
more melanin granules
than lighter or blonde
hair, has more melanin
per granule. When
pigment-producing cells
cease to function, the
result is the uncolored
white or gray hair.
In Caucasians, true
blonds typically have
more hair (about 140,000
hair) than brunette
(about 105,000) or
redhead (about 90,000).
Below your skin is the
hair root which is
enclosed by a sack-like
structure called the
hair follicle. Tiny
blood vessels at the
base of the follicle
provide nourishment. A
nearby gland secretes a
mixture of fats (called
sebum) which keep the
hair shiny and
waterproof to some
extent. At the base of
the follicle is the
papilla, which is the
"hair manufacturing
plant." The papilla is
fed by the blood-stream
which carries
nourishment to produce
new hair. Male hormones
or androgens regulate
hair growth. Pubic and
axillary (armpit) hair
are particularly
androgen-sensitive and
grow at lower androgen
levels than hair on the
chest or legs. In boys,
most pubic hair is grown
by age 15, followed by
the development of
armpit hair two to three
years later. In girls,
too, an increase in
androgens at puberty
triggers growth of pubic
and armpit hair. Scalp
hair, not directly
androgen-responsive, is
influenced by local
amounts of a
testosterone derivative,
dihydrotestosterone.
Hair follicles initially
form in utero. No new
follicles are created
after birth, and none
are lost in adult life.
The first hair to be
produced by the fetal
hair follicles is Lanugo
hair, which is fine,
soft, and unpigmented.
This is usually shed in
about the eighth month
of gestation. The first
postnatal hair is vellus
hair, which is fine,
soft, usually
unpigmented, and seldom
more than 2 cm long.
Vellus hair remains on
the so-called hairless
regions of the body,
such as the forehead and
balding scalp. At
puberty, the vellus hair
in some areas is
replaced by terminal
hair, which is longer,
coarser, and pigmented.
Growth starts in the
pubic region; then the
eyelashes and eyebrows
become thicker. Axillary
hair and male facial
hair appear about two
years after growth of
pubic hair begins. Body
hair continues to
develop long after
puberty, stimulated by
male hormones that
paradoxically, also
cause terminal hair to
be replaced by vellus
hair when balding
begins.
Scalp hair fibers grow
from 100,000 to 350,000
follicles which are
reported to occupy the
human scalp; however,
not all the follicles
are productive. In each
producing follicle, the
duration of the hair's
life cycle is influenced
by age, pathology and a
wide variety of
physiological
factors.[1,2] The life
cycle is divided into
the anagen (active),
catagen (transitional)
and telogen (resting)
phases.
The anagen phase is the
period of active hair
growth where protein
synthesis and
keratinization are
continuously occurring.
In normal subjects, this
phase lasts for up to
five years, although
longer durations have
been documented. The
cessation of the anagen
phase is characterized
by a transitory phase
known as catagen. This
phase lasts for two to
three weeks. Following
the catagen phase, the
hair enters the telogen
or "resting" phase. In
normal subjects, telogen
hair is retained within
the scalp for up to 12
weeks before the
emerging new hair
dislodges it from its
follicle.
During the anagen phase,
protein synthesis is the
main distinction of the
hair bulb. In the
telogen phase, the
dermal papilla undergoes
renewal. It is at this
time that structural
characteristics can be
modified. The new hair
should be identical to
its predecessor, but
with advancing age, and
in some pathological
states, a strict copy is
not maintained. In these
circumstances, the hair
may become finer and
shorter, modifying the
esthetic profile. Since
these effects occur over
several hair cycles,
years may elapse before
the affected individual
recognizes the
difference.
Like skin cells, hair
grows and is shed
regularly. Shedding
anywhere from 50 to 100
hairs per day is
considered normal. The
average rate of growth
is about 1/2 inch a
month. It is now known
that hair grows fastest
in the summer, slowest
in the winter, speeds up
under heat and friction,
but slows down when
exposed to cold. Hair
grows the best between
the ages of 15 to 30.
But, hair growth begins
to wind down sometime
between the ages of 40
and 50. Progressive hair
loss begins naturally in
both sex about age 50,
accelerating in the 70s.
About 40 percent of
Caucasian men lose hair
to some extent by age
35."*
"By far the most common
form of hair loss is
determined by our genes
and hormones: Also known
as androgen-dependent,
androgenic, or genetic
hair loss. It is the
largest single type of
recognizable alopecia to
affect both men and
women. It is estimated
that around 30% of
Caucasian females are
affected before
menopause. Other
commonly used names for
genetic hair loss
include common baldness,
diffuse hair loss, male
or female pattern
baldness."*
What is the cause of MPB?
"The rate of hair
shedding in androgenic
alopecia is speeded up
by three forces:
advancing age, an
inherited tendency to
bald early, and an
over-abundance of the
male hormone
dihydrotestosterone (DHT)
within the hair
follicle. DHT is a
highly active form of
testosterone, which
influences many aspects
of manly behavior, from
sex drive to aggression.
The conversion from
testosterone to DHT is
driven by an enzyme
called 5-alpha reductase,
which is produced in the
prostate, various
adrenal glands, and the
scalp. Over time, the
action of DHT causes the
hair follicle to degrade
and shortens the anagen
phase. Though the
follicle is technically
still alive and
connected to a good
blood supply--it can
successfully nurture a
transplanted follicle
which is immune to the
effects of DHT--it will
grow smaller and
smaller. Some follicles
will gradually die, but
most will simply shrink
to the size they were
when you were born which
produce weaker hairs.
With a steadily shorter
anagen growing cycle,
more hairs are shed, the
hairs becoming thinner
and thinner until they
are too fine to survive
daily wear and tear.
Balding hair gradually
changes from long,
thick, coarse, pigmented
hair into fine,
unpigmented vellus
sprouts."*
"Current research also
indicates an
immunological factor in
balding. Basically, the
immune system begins to
target the hair
follicles in the hair
loss area. The current
theory is that the rise
in male hormones such as
DHT during puberty
INITIATES this process.
This is why many drugs
which lower male hormone
levels do not completely
stop and reverse the
hair loss process. One
other target of
treatment is to
manipulate the messenger
chemicals in the body
that tell follicles to
initiate anagen and
telogen phases. Super
Oxide radical is
believed to be one of
the messenger substances
causing hair to enter
telogen (resting phase),
while nitric oxide is
one of the messenger
substances causing hair
to enter anagen (growth)
phase. These treatments
use topical treatments
to stimulate nitric
oxide levels while
decreasing Super Oxide
Radical levels using
Super Oxide Dismutase (SODases).
Many of the drugs
currently being
researched and studied
by the FDA are SODases."**
"However, the sebaceous
gland attached to it
remains the same size.
As the hair shafts
become smaller, the
gland continues to pump
out about the same
amount of oil. So as
your hair thins, you
will notice that your
hair becomes flatter and
oilier.
Other physiological
factors might cause hair
loss. Recently, a group
of Japanese researcher
reported a correlation
between excessive sebum
in the scalp and hair
loss. Excessive sebum
often accompanying
thinning hair is
attributed to an
enlargement of the
sebaceous gland. They
believed excessive sebum
causes an high level of
5-alpha reductase and
pore clogging, thus
malnutrition of the hair
root.
Although this condition
could be hereditary,
they believe diet is a
more prominent cause.
The researchers note
that Japanese hair was
thick and healthy, with
a small gland and little
scalp oil, until the
occidental habit of
consuming animal fat
crept into their diet
after World War II. This
change has led to a
significant height
increase in the Japanese
population, but it has
also resulted in more
Japanese men losing
hair. To some extent,
their observation makes
sense since problems
with greasy hair have
often been noted as much
as six months to a year
prior to when thinning
hair becomes noticeable,
but this might be just
one of the symptons, not
underlying cause, more
research is needed. Most
doctors agree that if
you have a oily scalp
with thinning hair,
frequent shampooing is
advised. Shampooing can
reduce surface sebum,
which contains high
levels of testosterone
and DHT that may reenter
the skin and affect the
hair follicle."*
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