Announcing the Cure for Parkinson’s Disease
Looking for doctors to try a new treatment and send observations
(Pardon the length of this document.  You cannot describe a useful brain
theory in a sound bite.)
Some theory (Part 2)
This comes in 7 parts.  Do not apply any of this information without reading
all 7 parts.  Each part will have words at the end saying "continued in
Parkinson’s Disease Cure’ Part [#]" for those whose servers might truncate
these documents.

Table of Contents
Introduction................................................................
...........................Part 1
Some of my theory helpful to understanding this
treatment....................Part 2
Some of my theory helpful to understanding this treatment
(cont.).........Part 3
The
Treatment...................................................................
....................Part 4
The Treatment
(cont.).....................................................................
.......Part 5
Why announce it this way on the
Internet?.............................................Part 6
Why approach Parkinson’s disease
first?................................................Part 7
Some theory
Sleep = Withdrawal = Placebo Effect
It is impossible for any cure to be found with the current methods of
seeking out biological treatments.  A cure for any neurological problem
could never be possible with a maintenance medication.  No cure could be
found by trying one or two doses of a medication a day and looking for
improvement in rats or people.  No cure is possible when changing the levels
of any chemical in the brain so far out of the normal range that would be
found in a healthy brain as is the case with most pharmacological treatments
used today.
All neurological disorders are either caused by a communication of stress at
such a level that the process that causes withdrawal is overwhelmed or are
caused by a breakdown in the process behind withdrawal itself.  (The
differences in the various disorders is a result of the geography in the
brain where stress may be concentrated.  All thinking problems are created
as an aberration of one process related to communication in the brain.)
(Because of a re-identification of stress, my use of the word "stress" is
somewhat different than that of the scientific community.)
This version of the treatment requires medication with a history of being
very safe when used at dosages much higher than required by this treatment.
The doctors (in a lucky deduction using bad logic) believe that the person
with Parkinson’s Disease is suffering from a deficiency in dopamine because
of their success using L-Dopa and because of questionable brain chemical
measurement techniques.
(If greater levels of a chemical in a nerve site cause the site to become
more reactive to that chemical over time, then a measurement of a trend in
the brain to have less of a certain chemical might really be an indicator of
a problem caused by too much of that chemical in the past leading to greater
reactivity to that chemical.)
(If L-Dopa has a "therapeutic range,"  how could they confidently make any
guesses about the brain needing more dopamine.  If the brain needed more
dopamine, it would improve with any increase up to a certain level and not
just when a range of medication is given that raises the dopamine levels up
much further than they would be found in a healthy brain.)
When you understand the language the brain uses to communicate with itself,
it becomes clear how the brain does its work, controls most things and makes
its decisions site by site and not by raising the levels of chemicals
throughout the entire brain.  The brain’s ability to inhibit or excite the
firings in an entire area of the brain has to do with mechanisms behind
focus.
(The graphic artist, for instance, develops an ability to focus on the lines
of the subject by learning to send inhibitory chemicals throughout the brain
without increasing levels of the chemicals that inhibit the centers for
visual perception.  The artist is not aware of doing this but just finds the
"zone" where focus is increased.  This state is difficult to explain because
it comes with inhibition of the language centers of the brain.)
The medical community is making some big mistakes in theory (and therefore
they "understand" very little about why things work or don’t work) because
of using the response to various maintenance medications as the foundation
for much of their basic science.
Response to many medications is really a happy accident that comes with
increasing an inhibitory chemical to the right range where it affects the
stressed area of the brain that has become too responsive to that same
chemical.  The antidote is the poison.   The parts of the brain experiencing
stress (and communicating that stress throughout the rest of the system) are
firing a greater number of times per unit of time.  The decision is not
clear (both on and off) in a site that is not able to respond to excitatory
chemicals at any volume without "flickering" (stuttering, tremor…).  Add a
little inhibitory chemical and the part causing the problem goes into a
coma.  Without firing it does not communicate stress throughout the system
and the system appears to be working better.  But receptor sites that were
not having a problem before might begin to have a problem with an increase
in inhibitory chemicals.  These sites were not as inhibited so not as
sensitive to the chemicals as were the problem sites.  It takes a certain
volume of chemical or a certain amount of time for these to become problem
sites like the sites that were put into a "coma."  This is the reason for
therapeutic range with medications that tend to inhibit the nervous system.
(Most anti-depressants, anti-psychotics, sedatives, barbiturates...)  There
is a wide range of different sensitivities to chemical brain messengers
caused by a variety of processes that have been witnessed and are still to
be understood.  These various sensitivities could be created by a nerve cell
synapse changing the number of receptors to various chemicals in proportion
to each other,  by the cell retaining some of the chemicals for different
lengths of time after absorption (half-lives), by growth and atrophy (a
dendrite grows and delivers a greater amount of chemical to a smaller and
now more sensitive receptor site dealing with a greater concentration of
certain chemicals), by a greater number of nerve fibers sending messages to
one place, and by processes within the nucleus of the nerve cell that can
only be imagined at this time.
The excitatory brain messengers have a more complicated effect on the system
and they operate with a very different algorithm or pattern.  They are not
just the opposite of the inhibitory chemicals.  Medications that deliver
mostly excitatory chemicals to the brain (some medications are both by
increasing some excitatory chemicals along with some inhibitory chemicals)
include amphetamines, methylphenidate, L-Dopa…
First, I have to explain that, in the language that the brain uses to
communicate with itself,  it is a mistake to consider a nervous site to be
excited or stimulated if the on and off firings have a faster cycling
(number of firings per unit of time).  A site that is firing rapidly is
actually inhibited:
When a nervous site is not firing it is making no decisions.  It is asleep
(in micro terms), in a coma, dead… it is not thinking when it is off.  When
it is firing it is awake, alive, thinking (in micro terms dealing with very
small units of time of relative change in behavior).  There are very big
differences in the sensation of firing and not firing and no consciousness
during the time of not firing.  A small period of time relative to the
amount of time firing is a period of transition where the cell is still
having sensation but that sensation is rapidly changing to a period of
non-sensation.  The end of the firing is the dying or death (an extremely
small period of time) that corresponds with the burst of inhibitory chemical
down the line that stops another cell from firing (or rather votes on
whether that cell will fire a certain way or not).  In order to have any
sensation or thought the nervous sites need to be excited.  The longer the
unbroken time of excitation and firing, the greater the "yes" decision or
stimulation or excitation down the line.  The larger the number of stops in
a period of time the greater the "no" decision or inhibition or agitation or
discomfort or stress down the line of communication.

(Nervous cells are voting mechanisms.  The message sent down the line by one
nerve fiber can be overruled by the vote of the messages sent by other nerve
fibers.)
It has taken an enormous amount of logic to find this part of the theory and
I will only give my conclusions now.  The mathematical logic getting me to
these conclusions is quite complicated and this has to be as readable as
possible.  Let the results of the treatment on people in need be the proof
rather than arguing these new theories based on the peer-pressure activity
of sticking with current scientific community assumptions.   I only go into
this now because it is important to see how easy it might be to make the
wrong conclusions by trying to understand the nervous system without having
the right theory to begin with.  Current techniques in scientific method
will not get you to the answer because there is a flaw in scientific method.
Here is the important difference in the behaviors of the different classes
of brain messengers:
Inhibitory messengers always create greater inhibition at any increase in
volume.  These chemicals either sedate the nerves that are affected or they
create a greater number of switches from on to off during a unit of time
when the nerve is firing (the agitation that is a form of inhibition
previously confused with being a state of greater excitation).
Any increase in inhibitory chemicals serves to create greater inhibition.
Too much inhibitory medication will lead to sleep or coma or death.  Too
much inhibitory chemical will not cause the cell to fire longer or become
more stimulated in any way in which the brain communicates.
Excitatory chemicals are very different.  They operate with a
"circuit-breaker" or "overflow switch."  Too much excitatory brain messenger
results in a shutting off of the site probably due to more than one process.
(One of these processes is caused by the ion channel sweeping inhibitory
chemicals into the cell along with excitatory chemicals until the cell stops
firing.)
"No" messengers = "No" Too much "No" messenger still = "No"
"Yes" messengers = "Yes" But too much "Yes" messenger = "No"
Because of this characteristic and the fact that inhibitory chemicals tend
to have longer half-lives in the system, the system will tend to move
towards greater inhibition throughout life.  People and animals become
slower as they age.
This system makes a lot of sense in evolutionary terms.  An organism needs
to always be wary of stimulus in order to survive.  Shyness is protective.
The stop lasts longer than the start and has the strongest vote.   Possible
dangers must be processed before acting.  Impulsive action towards stimulus
leads to greater danger.
Understanding these differences leads to greater understanding of all life.
These differences in response to these chemicals is inherent in all behavior
and perception and language and culture and emotion…
This theory explains why:
Hot is hot.  Too much hot is more hot or pain or the absence of feeling.
Cold is cold.  Too much cold becomes hot (dry-ice burn).
(Too much hot does not become cold.)
Dark is dark.  Too much dark is still dark.
Light is light.  Too much light can cause blindness or dark.
(Too much dark does not become light.)
People tend to say things like "it’s too good so it must be bad" but not say
things like "it’s too bad so it must be good."  Grandiosity is different
because parts of the brain dealing with social connections stop working and
amnesia (inhibition) about the down or depressing or stressed or agitated
thoughts lead to an over-confident and less-aware state.
Too much sweet can taste bad but too much ugly taste is unlikely to taste
sweet.
There is a coordination in the system of these different realms of
perception:  "Dark" is aligned with "Bad" is aligned with "No" is aligned
with "Fire" is aligned with "Sour" is aligned with pain and tension is
aligned with fear and anger…
"Light" is aligned with "Good" is aligned with "Yes" is aligned with
"Cool/cold" is aligned with "Sweet" is aligned with pleasure/sex and
relaxation is aligned with happiness and calm…
Cool water poured on the back elicits an emotional response that is
stimulated, awake, an upright posture like that during sex, eyes open
(light), with laughter…  (Very cold water might get on opposite reaction
because of too much stimulant creating an inhibitory response.)
Hot weather causes slumped posture, droopy eyes (dark), drowsiness,
depression…   or the change occurs quickly when a loud noise creates a fast
version of this inhibited response with a startle/fear response of forward
flinching posture, eyes closed, blackout/confusion, muscle tension, a
tendency for feeling warm rather than cold during the moment of fear.
(Parkinson’s disease is a slow progression into this same inhibited state:
the body posture is like that of startle/fear - flinching forward, hands
forward, head down, tiredness, muscle tension, sweating, depression.)
No animal would be designed to seek pain over pleasure as a road to health.
Health comes from seeking pleasure and not pain.  But there is a catch here.
The mechanisms behind pleasure are also the mechanisms behind withdrawal.
We know that pleasure aids the placebo effect.  We haven’t noticed, until
now, that placebo effect is one with withdrawal.
When the body is taking care of itself, it takes care of itself best in an
environment of pleasure.  But we can’t recreate that exact same process with
medication.   Medication does not work with the same subtlety as the brain.
Medication can enhance the placebo effect but only while enhancing the
withdrawal experience at the same time.
[CONTINUED in ‘ Parkinson’s Disease Cure’ Part 3]