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Why
do I have problems with sweating regardless of temperature or exercise?
The possibility of sweat gland problems in alopecia areata is
an area for argument between dermatologists. Tests conducted to
examine sweat gland number and function have shown that people with
alopecia areata can have irregular sweat production. Using what
is called a "silastic imprint method" (a kind of impregnated sticky
tape) density and activity of sweat glands can be determined over
a patch of skin. Two reports suggest decreased sweat gland number
and function in association with alopecia areata (Elieff 1991, Olsen
1994). A more recent report found a slightly lower rate of sweating
in people with alopecia areata compared to age matched control subjects
but suggested that the difference was not significantly different
(De-Berker 1995). There is no specific targeting of the sweat glands
by inflammatory cells, but it is possible that the sweat glands
are malfunctioning as a result of feeling the effects of hair follicle
inflammatory cell infiltrate in close proximity.
Is
hair loss through alopecia areata part of human evolution?
This is a question that has put to me on several occasions recently.
I suspect the question is, in part stimulated by the media, from
newspapers to Star Trek, representing advanced aliens without any
apparent hair. I am not aware of any published material specifically
on alopecia areata in evolution so I can only give my personal view.
We can take this from at least two stand points, hair follicle
evolution and immune system evolution. The hair follicle is a highly
conserved organ. Our therapsid reptilian ancestors (!) have recognizable
hair follicle-like structures with the same basic layout. There
have of course been modifications and adaptions through evolution.
We can point out the obvious such as rhino horns made of compacted
keratin fibers, The brush-like setae of plankton feeding whales
used to filter the water with, sensory hair follicles such as the
vibrissae in rats and mice that have extensive nerve innervation
(human whiskers are not the same as rodent vibrissae!), nails are
just modified hair follicles as are teeth and it would seem even
mammalian eyes were derived from the same, common progenitor as
hair follicles somewhere in our evolutionary history. Our eyes still
contain many common properties with hair follicles.
Humans, with their apparent lack of hair, are not so far removed
from our ancestors as we may like to think. We have not actually
lost any hair follicles, they are merely miniaturized over most
of our body. We have a similar hair follicle density to most land-based
mammals regardless of size. Smaller animals just have smaller hair
follicles and a higher density in their skin. There is a simple
switch involved in the hair miniaturization as we can see from studies
on people in families with congenital hypertrichosis (distastefully
described as "human werewolves") with an extensive hair coat looking
like fur. Hypertrichosis can develop for any individual under a
variety of conditions. It simply requires the hair follicles to
be induced into overdrive as may occur through hormonal changes
and use of some drugs.
People argue about why this miniaturization of hair follicles
in humans occurred. Did wearing of clothes result in hair loss or
did hair loss lead to the invention of clothes? This argument will
continue in perpetuity without any real conclusion. Is hair loss
in general on the increase because we no longer need it? It is possible
but we have no hard evidence to support such a claim. There has
been an increase in androgenetic alopecia in Japan believed to be
the result of a change to a more western diet and the body/hormonal
changes made in response to this alien diet. These changes would
be indirectly related to our evolution and our suitability for the
lifestyle we lead.
Could the antigens in alopecia areata affected hair follicles
be changing in response to our artificial environment and this is
inducing an immune response and hair loss? It may be a possibility.
Reports have been made which hypothesize an over expression of normal
antigens in hair follicles induces onset of alopecia areata. Is
there any advantage of this over expression or is the hair follicle
adversely responding to an alien environment it is not adapted for?
Is the immune system trying to correct this over expression, or
some other modification, as it perceives it as dangerous to the
whole individual? There is no evidence in support but these questions
may indirectly relate to our evolutionary history.
The immune system has evolved to defend ourselves from pathogens.
We can trace its development from the simple, innate defense mechanisms
in sponges through more complex immune systems in reptiles and birds
to the advanced, adaptive immune system of mammals. Alopecia areata
can develop in any mammalian species with a fully fledged adaptive
immune system and hair follicles.
There may be advantages in having an autoimmune condition like
alopecia areata. For example, type I psoriasis has been statistically
shown to be associated with greater resistance to viral, bacterial,
and fungal infections. Apparently having psoriasis confers a more
effective immune defense against these pathogens. For alopecia areata,
the suggestion has been made that there is a significantly reduced
susceptibility towards development of type I diabetes compared to
the general population (Wang 1994). Clearly the genes and/or environmental
conditions required for susceptibility towards onset of alopecia
areata create resistance to development of certain other conditions.
Pathogenic infections or diabetes are life threatening events whereas
alopecia or psoriasis are not. This may suggest an evolutionary
advantage to keeping such traits as alopecia areata and may even
indicate why alopecia areata might spread through a population.
There has been debate about autoimmune disease and how in general
it may be on the increase. Similar arguments have been put forward
about allergies/atopy. In principle, there is some relation between
the two. Allergy can be described as an unwanted over-reaction to
an exogenous (external) antigen and it can be traced in evolutionary
terms to our need to respond to gut parasites and respiratory/mucosal
infections. Autoimmune disease is an unwanted over-reaction to an
endogenous (internal) antigen. The immune system must be able to
respond to any dangerous pathogen and so must be able to target
almost all antigens - including our own. Evolution has developed
several mechanisms to ensure tolerance to our own self antigens
but clearly these mechanisms can break down under certain circumstances.
Our immune system was developed for operating under the extreme
conditions our ancestors had. The western world in terms of diet,
medicine and sanitation is very alien and not an environment it
is adapted for. The basic suggestion is our immune system has less
to react against in our modern world and sometimes becomes "restless"
(that's as best as I can describe it) leading to unwanted activity.
The potential for continued hair loss and/or hair follicle miniaturization
in our future evolution is possible but there is no obvious advantage
to hair removal and certainly no apparent advantage to active removal
by the immune system. The advantages of having hair may be gradually
diminished as we exert ever greater control over our environment.
Hair may no longer be important for heat control with the invention
of central heating. However, nasal hair and eyelashes still play
a significant role in protection from dust and infection, although
with advances in medicine these too are much less important in our
health.
I doubt that hair loss through alopecia areata is directly linked
to hair follicle removal as part of our evolution. Alopecia areata
may be indirectly linked to evolutionary traits in the hair follicle
and immune system that have developed in mammals and a lack of adaption
to our increasingly artificial environment. However, the trait of
alopecia areata may confer associated advantages on the individual
protecting them from other, potentially more serious conditions.
Why
is alopecia areata research so slow?
A combination of factors make for slow progress in alopecia areata
research. Concerted attempts to understand and define alopecia areata
have only truly begun in the last 15 years or so. Much of the stimulus
can be attributed to the National Alopecia Areata Foundation. This
means that alopecia areata research is so much further behind compared
to research on, for example, vitiligo or psoriasis. We have a lot
of catching up to do in our understanding of alopecia areata. Only
a few research groups focus predominantly on alopecia areata research.
There are perhaps only 20 groups worldwide who have a key interest
in this disease. Finally, lack of money for research is the fundamental
problem. Much more research could be done and at a faster pace but
that requires more money to pay for salaries and laboratory equipment.
The
future of alopecia areata research
There are three main avenues of alopecia areata research.
- a) Genetic research
- b) Research into the causal mechanisms of alopecia areata
- c) Research into new or improved treatments
a) Almost all gene research is currently carried out in
the USA. At the moment the research is at a preliminary stage where
scientists are exploring which genes are common between people with
alopecia areata. The main focus of research are the genes which
code for MHC (class II). Unlike the gene success stories such as
cystic fibrosis where the problem can be traced to action of one
single, aberrant gene, alopecia areata is probably the result of
a combination of genes working together. This may help to explain
why there is such variation in the way alopecia areata can occur
in different people. Not surprisingly this will make analysis of
gene interaction more difficult. Genetic research is a long term
project which has so far defined some of the alleles more common
in people susceptible to alopecia areata development. But as for
using this information to develop more effective treatments, the
research will probably not bear fruit for several years.
b) Molecular and cellular research into how hair follicles
are inhibited from growing hair is the main preoccupation of academic
research. Work from other fields such as other autoimmune diseases
and general hair biology is also relevant here. Of chief concern
is to provide evidence that the immune cells and/or antibodies really
are affecting the hair follicle.
c) New and improved therapies are primarily under development
by clinical dermatologists and occasionally commercial companies.
Because of the commercial aspect, new drugs and treatment trials
are usually shrouded in secrecy. However, considering the increase
in interest in alopecia areata shown by private companies recently
there will may be a few developments in this area over the next
few years. |
