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The
most common form of hair loss is determined by our genes and
largely influenced by our circulating hormones. Androgenetic
hair loss (AGA) typically called pattern hair loss is the
single most common form of alopecia and affects both men and
women. It is thought that over 60 million American men
and 20 million American women suffer from AGA. The disorder
can be inherited from either the mother's or father's side
of the family and is highly variable in its expression.
About 50% of those with a parent who has experienced AGA can
expect to inherit some degree of pattern hair loss as well.
AGA in men can start at an early age but usually will become
evident in the late 20’s to late 30’s. Interestingly,
it has been shown that approximately 20% of 20 year olds,
30% of 30 year olds 40% of 40 year olds and so on experience
some degree of pattern hair loss.
Hair
Genesis offers a solution.
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The
Hair Loss Process
Women
with this trait develop thinning hair, but rarely become completely
bald. The condition is referred to as Ludwig pattern androgenetic
alopecia and can manifest in the teens, twenties or thirties.
There is no cure for either the male or female form of this
disorder, although medical treatments have recently become
available that may help some people. One treatment involves
applying a lotion, minoxidil, to the scalp twice a day. Another
treatment for men is a daily pill containing finasteride,
a drug that blocks the formation of the active male hormone
in the hair follicle.
The
Hair Loss Process
(The DHT Theory)
(The most widely accepted theory)
The speed at which hair loss occurs in AGA
is primarily dependant upon four factors:
1) Progression in age.
2) Genetic tendency to pattern hair loss
3) The prevalence of circulating dihydrotestosterone (DHT)
4) The susceptibility of the target hair follicle to DHT
DHT is a highly active form of testosterone,
which influences many aspects of human development, from sex
drive to aggression. In both males and females DHT is
a naturally occurring hormone which assists with sexual development
during fetal development and also during puberty. DHT
which is synthesized in the prostate, various adrenal glands,
and the scalp is catalyzed from testosterone by one of two
5-alpha reductase isoenzymes, commonly referred to as Type
I and Type II 5AR. Type I 5AR is thought to be much more prominent
in the scalp than Type II. DHT which results from 5AR binding
with testosterone is the androgenic hormone thought to be
most responsible for pattern hair loss in women as well as
men.
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DHT has a very high affinity for the
androgen receptor and is estimated to be five to ten times
more potent than testosterone. This can be thought of
as a key fitting in a lock. Other androgens that may play
some role in pattern hair loss include androstenedione, androstanedione
and DHEA. During AGA associated hair loss, DHT has been shown
to contribute to a process of reprogramming certain hair follicles
on a cellular and molecular level. Clinically, this
reprogramming results in hair follicles which become progressively
thinner, finer and more susceptible to breakage than healthy
unaffected hair.
As noted, hair follicles at the front, top,
and upper back of the head in most men are genetically programmed
to become susceptible to this process at some point in life.
Those hairs which cover the sides and bottom back of the head
typically are not influenced by these phenomena, which is
why most men do not lose hair in these areas. The retention
of hair in these anatomical locations has been recognized
since the time of Hypocrites. In fact, this zone of
hair is known as the Hypocratic wreath.
Pattern hair loss can be a fairly lengthy progression.
As the hair becomes effected by AGA a the growing cycles for
hair growth are typically reduced. In the absence of
a DHT inhibitor applied either systemically (in the bloodstream)
or locally (applied to the scalp), or both, each time your
hair cycles, the follicle and accompanying structures including
the visible hair will become thinner, shorter, and ultimately
completely miniaturized.
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With progressively shorter anagen growing cycles,
more hair is either resting in telogen (resting phase) or
growing in a weaker, finer state. Ultimately, the remaining
hair becomes finer and thinner as well. The sebaceous gland
(gland producing sebum – natural oil) attached to the hair
follicle remains approximately the same size. As the hair
shafts become smaller, the gland continues to pump out about
the same amount of oil (sebum). So as susceptible hair begins
to thin, one commonly notices that the hair becomes flatter
and oilier.
End stage pattern hair loss is largely dependant
upon genetic factors but can progress across several decades
before reaching complete presentation. AGA is clinically
divided into a number of levels. In men these levels
are referred to as the Norwood scale of baldness ..
In women the scale is called the Ludwig scale of female hair
loss .
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