Re: Multiple Sclerosis and Human Evolution

Philip Deitiker (
Wed, 15 Jan 1997 00:00:44 GMT (James Howard) wrote:

>Multiple Sclerosis and Human Evolution
>James Howard

>A few at this newsgroup know that I have developed a new theory
>of human evolution, based on changes in hormones, specifically DHEA,
>melatonin, and testosterone. Basically, my theory suggests that migration
>northwards occurred because of increases in DHEA and decreases in
>testosterone. Now, it is proven that multiple sclerosis is rare in blacks
>and occurs more often in people of northern latitudes. The remainder
>of this post is my explanation of multiple sclerosis (MS). If you read it, you
>will discover that expression of MS may be directly affected by levels of
>DHEA and testosterone. This further supports my theory of human
>evolution, and it further demonstrates that levels of DHEA and
>testosterone are directly involved in differences in the races.
>. . . . . .

Multiple sclerosis is an autoiummune disease, the most probable resaon
that europeans suffer from this disease and africans do not is the

As peoples left africa and moved toward europe the types of diseases
which afflicted the population change from tropical diseases to
disease like influenza, rhinoviruses, tuberculosis. As a result, there
was increased selection for new alleles which were better adapted
toward temperate and artic diseases. It forced the evolution in 50K
years for regional immune system which took hundreds of thosands of
years to develope in africa. As a result, _some_ of the temperate
solutions to temperate diseases have temporarily uncorrected side
affects (correction is long term selection and enviromental
constancy). At the hingepoint of immune misrecognition are a set of
presentation receptors known as HLA (the human equivilant of MHC in
mouse, MHC = major histocompatibility complex), which consists a set
of genes encoding proteins which have the highest known allelic
variation of any known in humans. Why and when does autoimmunity
develope from an HLA allelic potential. If you could answer this
question I assure you that a noble prize will come your way :^).

Here are several possible explanations.
1. If one has 2 (homozygote) for a disease potential allele.
2. A malignant growth and prolonged gamma interferon release
overexpresses a potential allele (in the case with HLA-DRB1)
3. An infection with a pathogen which is using antigen mimicry to
disguies itself (which as it turns out is very common). There are
several good examples for this as triggers for autimmunity. The
immune system is 'tricked' or 'trapped' into self recognition.
4. Degeneration of a tissue for other reasons presents self-antigen as
a trigger. Degradation of cell surface proteins by macrophages which
normally are excluded from the region will release a number of
perceived foriegn trigger petides into solution.
5. Recombination (gene conversion), which happens rather frequently at
HLA loci, produces a novel allele in an offspring which has a high
potency, irregardless of triggers, expression levels, etc.
6. Mutations in a non-coding region result in the constituitive
overexpression either in a tissue line or in development.
Recombination of an overexpressor with a weak self-recognizer may
cause disease.
7. A cancer of immune tissues which result in the destructive and
uncontrolled overexpression of a pathogenic T-cell lines or
... and many, many, more.

Immunosuppresive agents are known to decrease autoimmunity.
Testosterone indirectly increases one of these, adrenaline. Caffeine
and other neural stimulants can result in suppression not aggrivation
of autoimmunity, but there is a long term cost. An example is constant
overstimulation of the adrenergic system may result in subdued
screening for cancer, the stimulation as a result of a small cancer
(self destroyed) may be nothing compared with a cancer permitted to
grow. In the end, the bodies belated defense against a cancer can
result in the triggering of autoimmune disease, irregardless whether
the overexpressed HLA antigen was involved in the destruction of the
Finally there is some reason to correlate multiple sclerosis with
the stress of industrialization, which may be the differential
between its presence in africans vs. europeans. The altered behavior
of individuals in industrialized societies may adversely promote this
condition in suceptible individuals. Thus MS can be alleviated at
times by strategies for dealing with stress. This may have something
to do with situation 4 above, in which oversitmulation and lack of
recuperative sleep, overreliance on adrenergic stimualtes (caffiene,
theophyline, anti-histimines, etc) may cause a slight degradation of
the neural tissues thus allowing the presentation of disease
autodeterminants. Once the disease is presented and memory B-cells are
produced the disease is lifelong no-matter what other events occur (or
otherwise subsidance may take decade(s) even with a lack of new
stimulation). BTW, if I had to weigh the affect of testosterone based
overstimulation and caffeine based overstimulation I would say that
caffiene is probably 10 to 100 times more likely to be the cause
compared to testosterone (since MS has a high prevelance in women).
The oddity of our society is that noone, now, ever questions whether
THC or nicotine have health risks, but caffiene itself may be one of
the largest health risks to modern society and the baby boomers in the
next few years are seeing a very marked increase in many autoimmune
diseases. Because caffiene is socially acceptable drug it is not
questioned. When nictoine was socially accepted it was not questioned.
THC has never been socially acceptable, and of course its fate was