PARKINSON’S PUZZLE

Dr. Michael Colgan

English physician James Parkinson first described the symptoms of Parkinson’s in 1817.1
He called it the shaking palsy,” but had no idea of its cause or how to treat it. It took
another 150 years to solve the mystery.
In 1913, Friedrich Lewy discovered pink taining, round globs in areas of dying nerve cells.
Combined with four main physical symptoms, resting tremor, loss of balance, rigidity, and
slowness of movement, these Lewy bodies used to be a definitive diagnosis for Parkinson’s
disease.
Today, some researchers consider Lewy bodies a separate phenomenon, the underlying
factor in what is termed Lewy Body disease.2 These globs of damaged cells also occur in
the brains of Alzheimer’s patients, Parkinson’s patients, in other dementias — and in some
apparently healthy people. This increasing complexity of sub-categorization compromise in
Parkinson’s is not a mark of great scholarship.
The rest of Parkinson’s has been split into grab-bag lots. There is idiopathic Parkinson’s
with, supposedly, no known cause. Not very helpful. There is genetic Parkinson’s, mostly
related to an autosomal dominant gene which codes for a protein called alpha-synuclein.3
Autosomal simply means that it occurs on a gene that does not determine sex. Dominant
means that offspring have a 50% chance of inheriting it. This gene defect confers a
tendency to develop Parkinson’s in about 5–10% of cases. But only about half of those
showing the genetic markers ever develop the disease. Also, the rate of Parkinson’s in
identical twins is no higher than among fraternal twins, so we are pretty sure that at least
90% of all cases of Parkinson’s are caused by life events or environmental trauma.4,11-15
Some folk are going to be annoyed with me for dismissing so much research in a single
page. I acknowledge that it would take a whole book just to cover this one matter in detail.
All else I can say here is that we have been watching this scene unfold for the last 30
years. It reminds me of the unworkable compromises of the Ptolemaic Universe, which,
nevertheless, held sway for a thousand years. Ptolemy’s scheme fell immediately when
subjected to the greater brainpower and much simpler model of Galileo and Newton, which,
in turn, fell immediately with the genius of Einstein. We tend to forget that we are no
smarter than all the medieval scholars who believed in Ptolemy.
I want to suggest an explanation of Parkinson’s that better fits the science. The structural
damage and the symptomatology of the disease are simply a part of the multiple-system
brain damage of usual aging, damage that affects almost all of us. As I explained in
Chapter 1, the symptoms of this brain damage that become dominant, and trigger a
particular diagnosis, denote merely the structures most affected. 5-10
In the medical fog surrounding Parkinson’s, however, the usual diagnosis follows the
symptoms. The treatment advised is almost always diagnosis-specific, symptomatic relief of
the shortage of dopamine using the drug levodopa (L-dopa). Unfortunately, unless you treat
the whole brain, there is little hope of stopping or even slowing down its degeneration.

SUBSTANTIA NIGRA DAMAGE

There is a smidgeon of logic behind levodopa. In 1919, a Russian neurologist, Tretiakoff,

discovered that patients with symptoms of Parkinson’s had lost dark-colored neurons in an
area of the midbrain now called the substantia nigra (black body), shown below. 15,16
This area is part of the ancient mammal brain, which mediates balance and control of
voluntary movement. But it was not until the 1960s that researchers showed how
Parkinson’s symptoms, especially tremor and loss of balance, are caused by progressive
death of substantia nigra neurons which supply our brains with the essential
neurotransmitter dopamine. The drug levodopa floods the brain with dopamine.
In a normal brain, levodopa would produce a frenzy of over-activity. By the time a
Parkinson’s case has come to notice, however, there are not enough dopamine-producing
cells left for the brain to over-react. The drug does help the remaining cells to function a bit
longer, but does zero to prevent further cell death or slow the progress of the disease.
Levodopa is always too little, too late.
Nigral neurons die off with age in almost every one of us. The most accurate predictor of
Parkinson’s, by far, is simply how long you have lived. Between ages 55 and 65, the
incidence triples. And by age 75, it increases almost nine-fold.3 Parkinson’s is simply part
of the damage of the brain with age that would eventually get all of us, were we not to die of
something else beforehand. To prevent it or inhibit its progress, you have to treat the whole
brain.

RATE OF LOSS OF NIGRAL CELLS

You have roughly 400,000 nigral neurons at birth, and that is nearly your lot for life. You do
get some more by neurogenesis, but as yet no one knows how many or how to stimulate
their growth. The average healthy brain loses up to 20,000 nigral cells per decade after age
25. So, in 50 years, by age 75, you have lost up to 100,000 nigral cells, about 25% of your
supply. By then you are getting shaky. Whether Parkinson’s symptoms become apparent
before we die of something else depends on the rate of nigral cell loss. We can slow that
rate right down.
At first, the victim may notice only slight symptoms, such as hand tremor on picking up a
cup of tea, and dismiss them as stress or fatigue. By then about 15–20% of the nigral
neurons are already dead, and it is time to treat the disease aggressively. Otherwise, it
progresses inexorably to hand tremor at rest, shaking of the limbs, muscle wasting, loss of
bone mass, loss of balance, rigidity and slowness of movement, difficulty in initiating
voluntary movement, and finally loss of speech and movement altogether.
We know now that this silent, symptomless degeneration is happening to all of us. There
are more than one million Parkinson’s patients in the US alone. Prevalence of the disease
is increasing rapidly throughout the Westernized world. Our initial advice to patients with
beginning Parkinson’s is to see their physician about a formula similar to the one given
below.
There is one extra wrinkle. For about 20 years now, we have been collating reports that
coffee inhibits Parkinson’s. We were interested because the caffeine in coffee belongs to a
chemical group called xanthines. One important xanthine in the human brain is adenosine,
which we have discussed in relation to adenosine triphosphate, the energy molecule.
Caffeine inhibits some adenosine receptors, causing dopamine levels to increase.
Until the last five years, the research was spotty. Now we have some good data. Webster
Ross and colleagues at the University of Hawaii analyzed the data from a 30-year follow-up
of 8,000 Japanese Hawaiian men. Those who never drank coffee showed a massive five
times the risk of developing Parkinson’s. 17
A large follow-up study by Alberto Ascherio and colleagues at Harvard analyzed the records
of 135,000 people of mixed ethnicity.18 They found that men who drank coffee regularly
cut their risk of Parkinson’s almost in half. The lowest risk occurred with moderate coffee
intake of 1–3 cups per day. Beyond that level, risk rises again. We are now confident that
coffee is protective against Parkinson’s.
Colgan Institute Formula against Parkinson’s. (Under the supervision of your physician
only.)
Taken daily in the am with food
Rasageline 25 mg
Acetyl-L carnitine 1000 mg
R+ lipoic acid 600 mg
N-acetyl cysteine 600 mg
Cytidine–diphosphate choline 300 mg
Co-enzyme Q10 300 mg
Docosahexaenoic acid 1000 mg
To learn more click here to go to the Colgan Institute website.
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