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Introduction
 Androgenetic
alopecia, androgenic alopecia, or pattern baldness, has been a part
of the human race for as long as we have historical records. Evolutionary
evidence suggests androgenetic alopecia has been around longer than
the modern human race. Our nearest non-human primate relatives,
orangutans and gorillas can also develop androgenetic alopecia.
Androgenetic alopecia is a very common form of hair loss and could
be described as part of our general genetic phenotype. People who
do not develop androgenetic alopecia are in the minority. We could
even say these non-bald people are the deviants from the norm!
Medicine has long recognized androgenetic alopecia as an inherited
systemic disease associated with sexual development. Ancient Greek
doctors realized that male pattern baldness can develop in men of
any age after puberty. They recorded that young boys castrated before
puberty did not develop androgenetic alopecia regardless of their
genetic family history. However, boys castrated during or after
puberty could develop androgenetic alopecia.
We now know that the reason for their observations is castration
prepuberty stops hair follicles from being exposed to androgens
made by the gonads during adolescence. Castration after puberty
is too late. Once hair follicles have been exposed to androgens
they are fated to become androgen sensitive and androgenetic alopecia
can develop.
Despite its standard name of “male pattern baldness”androgenetic
alopecia is also the most common form of hair loss in women. Androgenetic
alopecia develops as a gradual reduction of scalp hair follicle
size, and reduced time in the anagen active growth phase, leading
to more hair follicles in the telogen resting stage of the hair
cycle. In men, the hair loss is limited to the top of the head and
can involve thinning and/or receding hair lines. In women the presentation
is different with just diffuse thinning over the top of the head
and sometimes thinning over the entire scalp (Olsen 1993). Of course
this is the prime form of hair loss for which treatments are under
development by commercial companies (Schupack 1993).
Epidemiology
Androgenetic alopecia affects between 50 and 80% of Caucasian
men. A rule of thumb is for men in their thirties, 30% have androgenetic
alopecia. For men in their forties, 40% have alopecia and so on
until 80% of men are affected when 80 or more years old. Different
ethnic backgrounds have different susceptibility levels towards
the development of androgenetic alopecia. The Chinese male population
has a similar progressive increase in those affected with advance
in age but in total baldness is much less common compared to Caucasian
males. The numbers of Chinese males affected by androgenetic alopecia
is approximately half that of Caucasian males. American Indians
and African Americans also have a lower incidence of androgenetic
alopecia compared to Caucasians. These frequency differences between
races suggests genetic predisposition is important in pattern baldness
susceptibility.
Hair loss is first observed in women in their late twenties to
early forties, somewhat later in age than first onset in men. Unlike
men the frequency of women affected does not continue to increase
with increasing age. After the fifth decade of life the numbers
of women with androgenetic alopecia does not increase. Androgenetic
alopecia has been suggested to be present in the general female
population at a rate anywhere between 20 to 40%. It is perhaps one
of the best kept secrets that female androgenetic alopecia is so
common. |
