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WHAT REALLY CAUSES MULTIPLE SCLEROSIS:
AN EXECUTIVE SUMMARY
In young adults, in temperate Western climates, multiple
sclerosis is the most common disease of the nervous system.1
Globally, some 2.5 million people suffer from this illness.2
Multiple sclerosis is a progressive disease for which there is no
recognized conventional cure. It is associated with inflammation
and ultimately the loss of myelin from the surface of nerves.
This process of demyelination causes disruption to nerve transmission
that can affect many body functions. It eventually
leads to the patches of nerve scarring, known as 'sclerosis,'
that give multiple sclerosis its name.3
Multiple sclerosis occurs more often in some families than
chance alone would dictate. The average person living in the
United States, for example, has roughly a 1 in 750 chance of
developing multiple sclerosis.4 However, the children, brothers,
sisters, or non-identical twins of somebody who already suffers
from the disorder have a risk of getting it that ranges from
about 1 in 100 to 1 in 40. In the case of identical twins, this
risk increases to 1 in 3.5 Of course, if genetics were the only
causal variable, the sibling of an identical twin with multiple
sclerosis would always get the disorder. More specifically, in a
large Canadian study of 5,463 multiple sclerosis patients, attending
10 different clinics, the disorder was found in 7 pairs of
27 monozygotic (identical) twins, that is in 25.9 percent of them,
and in 1 of 43 dizygotic (fraternal) twins, or 2.3 percent.6 The
risk of a first-degree relative of a multiple sclerosis patient
developing
the disorder was between 5 and 15 times higher than
that of the general population.7 Indeed, in Vancouver, British
Columbia,8 first-degree relatives of multiple sclerosis patients
were found to have a risk of developing the disorder that was
30 to 50 times greater than that of the general population.
viii
What do these figures really mean? Well in schizophrenia, the
lifetime risk of developing the disease for relatives of a victim of
the illness are roughly as follows:9 grandchildren (5 percent);
uncles and aunts (2 percent); half siblings (6 percent); siblings
(8 percent); siblings with one schizophrenic parent (17 percent);
children (13 percent); fraternal twins (18 percent); identical
twins (48 percent), and the offspring of two schizophrenics (47
percent). Clearly, genetics play a much stronger role in deciding
who becomes schizophrenic than they do in controlling who
develops multiple sclerosis. Even so, there appear to be not
one, but four or perhaps more genetic aberrations involved in
schizophrenia.10
There can be no single genetic key to multiple sclerosis. Incidence
and mortality for the disorder have highly non-random
distribution patterns, typified by well developed global zones.
The incidence and mortality rates for multiple sclerosis are
not constant, but fluctuate markedly. They are probably falling,
for example, in North America and Western Europe, but
rising in many Mediterranean countries. Beyond that, migration
is likely to increase or decrease the risk of developing
multiple sclerosis. Every one of these characteristics is inconsistent
with a dominant role for genetics in the etiology of
this disease.
Similarly, virologists, neurologists, and numerous other researchers
have spent a century or more searching for a causal
pathogen in multiple sclerosis.11 However, it is apparent that
no such pathogen exists. If it did exist, it would have to infect
women roughly twice as often as men, except where the disorder
was rare. In these latter regions, it would cause illness
in females at a rate of about six times that seen in males. It
would also be much more infectious in certain families. This
pathogen would pose more of a threat to adolescents than to
young children, but it would almost never infect Lapps or Inuits.
ix
Nevertheless, it would cause multiple sclerosis in predictable
global belts of infection in which prevalence declined both toward
the equator and westward into Asia. In short, the genetic,
epidemiological, and geographical evidence makes it very likely
that virologists and neurologists will spend the next century
looking for this elusive pathogen, with no more success than
that accompanying their work in the last one hundred years.
Taken as a whole, the available scientific and alternative evidence
suggests that multiple sclerosis patients suffer from
chronic inflammation caused by diets that contain inadequate
antioxidants, omega-3 deficiencies, excess sugar, and foods that
fail to significantly reduce oxidative stress. In addition, gluten,
cow's milk, or some other allergen further promotes autoimmune
disease. The coup de grâce, however, is a thyroid hormone
deficiency that causes an abnormal need for dopamine.12
Dopamine is very susceptible to oxidative stress and can break
down to form toxins such as dopachrome and other chrome
indoles. These, in turn, kill oligodendrocytes,13 the cells needed
to repair the damage to myelin caused by chronic inflammation.
Beyond this, a shortage of triiodothyronine in multiple
sclerosis patients appears to reduce their ability to produce
new oligodendrocytes.14 Therefore, myelin deteriorates and the
symptoms of multiple sclerosis worsen. Wilcoxon and Redei
have shown that such associated thyroid malfunctions in adults
may be triggered by environmental challenges early in life.15
This process is termed fetal programming.
If the three step hypothesis presented in this book is correct,
then it is possible to prevent and reverse multiple sclerosis.
However, to achieve such goals requires societal and individual
commitment. This volume concludes with an outline of the
strategies that are needed. These include promoting antiinflammatory
diets16 and methods for avoiding the allergens
that trigger inflammatory cascades and associated chronic
x
autoimmune disease.17 Also discussed are orthomolecular
techniques for mitigating the negative impacts of the neurotoxins
associated with the oxidation of excess dopamine and
for stimulating the body to produce higher levels of antioxidant
enzymes, such as glutathione peroxidase.18 In summary, this
book provides new evidence on the causes of multiple sclerosis
and offers approaches for reversing its impacts.