Sunday, March 29, 2009

Telling the difference between genetic baldness and everything else

There’s more than one category of hair loss. Can your doctor tell
just by looking at you what kind of hair loss you have? Yes, some-
times. Hereditary hair loss patterns, the most common type of hair
loss in men, have developed into a classical clinical descriptive sci-
ence. Genetic hair loss appears in distinct patterns, and these pat-
terns are almost 100-percent diagnostic for male pattern baldness.
The later section, “Norwood classifications for measuring male pat-
tern thinning” covers the most common baldness patterns. Also,
we discuss the types and causes of pattern balding in the later sec-
tion, “Common Causes of Hair Loss.”
In women, balding patterns also exist (see the section, “Genetic
hair loss in women,” later in this chapter), and a knowledgeable
doctor may be able to tell what’s causing the hair loss just by
looking.
Examining uniform hair loss
A small segment of people lose scalp hair uniformly (diffusely),
rather than losing hair in specific scalp areas. Uniform hair loss
isn’t as easy to detect as other types of hair loss because the hair
is steadily lost all over the head. It’s much easier to detect a bald
spot resulting from hair loss in a specific area of the scalp from
diseases that cause uniform hair loss to the normal genetics of that
particular person.
Hair loss occurs normally and usually occurs at the end of one of
the normal hair cycles that all hair goes through. These hair cycles
are as follows:
 Anagen: The growth stage, which lasts three years on average
but may be as short as a year and as long as seven years).
 Catogen: The stage when the hair prepares to go into the next
phase and undergoes changes in its anatomy, falling out at the
end of this part of the cycle.
 Telogen: The sleep phase when a percentage of the hair disap-
pears (lasts from two to five months on average). About 10
percent of all of the hairs on our head are in the telogen part
of the cycle at any one time.
At the end of the telogen phase, a new hair bud appears, signaling
the beginning of anagen. (Chapter 2 has more about hair growth
phases.)
The hair apparatus starts off producing a baby hair below the skin,
which grows longer and longer until the final terminal hair (a full
mature hair reflective of what we style every day when we comb
out hair) emerges from the pore in the skin. In some adults, the
anagen phase may never start, signaling that the hair follicle may
have died. If a new hair doesn’t grow to replace the lost hair, the
total hair count drops.
Hair grows in natural occurring groups called follicular units (FU). A
single FU contains from one to four terminal hairs and one vellus
hair (a fine hair amidst the clump of terminal hairs). When a hair
isn’t replaced after its telogen phase, the number of hairs in the FU
decreases, but the number of FUs remains the same. So an FU
starting with four terminal hairs may end up with only two or three
terminal hairs as we age or as we undergo some form of balding.
When this happens across the whole scalp, the total hair count
decreases proportionally.
The older the patient is, the more likely it is that doctors see this
uniform hair loss process. About one third of men over age 70 have
this diffuse hair loss, which is called senile alopecia. The name
doesn’t reflect the mental status of those afflicted, but rather it
essentially means that the condition is most common in the eld-
erly. Because hair also becomes finer with age, severe thinning
reflects a loss of both hair bulk (in each hair shaft) and hair densi-
ties. (For more on hair bulk and density, turn to Chapter 2.) There’s
no cure for senile alopecia.
Young men may experience uniform hair loss in the form of a con-
dition called diffuse unpatterned alopecia (DUPA). Doctors believe
that DUPA and senile alopecia are similar but for the age of occur-
rence. DUPA impacts men in their 20s and 30s and doesn’t seem to
be responsive to drugs used to treat the classic type of male pat-
terned hair loss. We cover treatment drugs in Chapter 9.
Identifying dying hair cells
Apoptosis is a cell’s internal “suicide” mechanism that causes cell
death. The phenomenon has recently been studied very carefully,
and what doctors know is that during the transition from anagen to
catagen (that’s the growth phase to the changing phase), some-
thing happens in the hair follicle development.
The cells within the hair follicles communicate with each other,
and certain chemicals secreted in the hair follicle determine which
hairs will survive for another growth cycle and which will die.
Experts believe that the lifespan of each hair follicle — and possi-
bly each follicular unit — is genetically programmed.
Because some of the hair follicles within the FU survive while
others die, there’s some hope that the chemical inducers that
determine the survivors can be identified and manipulated to pre-
vent hair loss. We have identified some of the molecules that stim-
ulate the process but others still need to be isolated. Maybe when
all of the molecules are identified and isolated, we can stop the
balding process from occurring.
Saving dying hair cells
The causes of cell death are complex. Research has shown that the
cells that produce apoptosis-causing chemicals are found in every
part of the hair follicle. It’s possible that different types of hair loss
are influenced by different chemical problems in the pathways that
control cell death.
Although the medical community is identifying many of these
chemical pathways, it’s no closer to finding a cure for apoptosis
than we would like. Interestingly, apoptosis typically doesn’t occur
in cancerous cells, which are thought to be immortal, escaping
their natural destiny of living a given number of cell cycles. For
example, in breast cancer, a gene called BRCA causes the produc-
tion of a particular enzyme that blocks apoptosis. Imagine if it were
possible to bottle that enzyme to use on hair that’s dying off or,
even better, create a cocktail that could make all the cells in the
body immortal! At least we can dream.