Background: THE BRAIN
The brain, on an anatomical level,
is an integrated network of nerve cells, support cells (astrocytes,
oligodendrocytes, et al), and is the controller for nerve-endocrine coordinating
functions and its feedback network.
The brain controls the body's
endocrine system through nerve transmission, which centers on the functionality
of the hypothalamus and pituitary gland. This includes the nerve-endocrine
coordination of the pancreas and secretions of the adrenals, thyroid, and
gonads. This, in turn, acts upon the brain and pituitary and on the tissues
throughout the body. This tightly controlled system produces a wide range of
effects for proper functioning of the human organism.
Some hormone effects are used for
development of the organism, from conception through birth. Some are long
lasting. Many are a permanent element for life. Hormones can be initiated during
maturity. Some hormones act later in adult life and can signify
changes in brain function, or are associated with disease states or aging.
Nerve-endocrine functions can also
act upon aspects of human behavior. This integrated system signals you when you
are hungry, or upset. The overall health of this system affects learning,
cognitive reasoning, controls your temperature, allows you to smell fresh-baked
chocolate chip cookies, stimulates growth, oversees your heart rate, and is
necessary for all the life functions enjoyed and needed by the individual. The
Brain, in effect, is the "Chief Operating Officer" of your physical body.
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There are two avenues or pathways to furnish nutrients, oxygen, and
other selective chemicals to the brain. These are via the
Blood Brain Barrier (BBB) and/or the Cerebral
Spinal Fluid (CSF).
The Blood
Brain Barrier is similar, in some ways, to the blood vascular network in
the other parts of the body. The Blood Brain Barrier resembles normal
capillaries, with a few exceptions.
The body's capillaries, outside of
the brain, are more permeable (porous) to fluids, ions, and other molecular
structures because there are very minute spaces between the cells making up the
capillary walls.
The brain's capillary system
(blood brain barrier), on the other hand, are composed of tightly packed cells
or "junctions" which reduce their permeability and eliminates the bulk flow of
solutes through them.
Because of the tight junctions
between the blood brain barrier's capillary cells, there are two specialized
ways that nutrients and other molecules can gain access to brain cell components
and neurons. These pathways are: 1) lipid mediation or 2) catalyzed (active
carrier) transport.
The lipid transport system is
confined to the transfer of small molecules to the brain tissue, and
generally are proportional to their lipid solubility.
The catalyzed transport system
includes both receptor and carrier mediating enzyme processes in order to
provide the brain with nutrients (glucose, amino acids, and nucleosides, etc.)
DIAGRAM #1: The Blood Brain
Barrier - capillary structure and adjacent nerve cell structures.
Another function of the blood
brain barrier is to isolate the brain from toxic products and certain chemicals
that could disrupt the delicate balance of ions, nutrients, and neurotransmitter
substances that are used by the brain's nerve cells.
When Aspartame is ingested and
enters the blood stream, the three toxins of aspartame are "launched" throughout
the body very rapidly.
Following consumption of
aspartame-laced products, the phenylalanine flood overpowers the enzyme systems
of the brain, setting off an induced PKU effect.
This induced PKU affect occurs by
grossly overwhelming those enzymes required to reduce the circulating
phenylalanine for use in other metabolic reactions.
This "overdose" of the competitive
phenylalanine isolate (and aspartic acid) incapacitates the enzyme actions which
controls several types of neurotransmitters (and their precursor amino acids)
reducing dopamine and serotonin production.
The excitotoxin's effects creates
secondary components which are also destructive in nature to the sensitive,
surrounding neural tissues, including a breakdown by-product of phenylalanine
called, diketopiperazine (DKP) which instigates tumor generation, especially
that of the aggressive glioblastoma.
Further neuron insult is added due
to the destruction and mutation of nucleic and mitochondrial DNA from the known
carcinogenic properties of the methanol --> formaldehyde --> formic acid
components.
The other avenue of delivering
nutrients and other necessary molecules to the brain's cell structures is by way
of the Cerebral Spinal Fluid (CSF).
There is a structure called the 'Choroid
Plexus" which is a specialized arterio-venous capillary bed located within the
lateral ventricles of the cerebral hemispheres that secretes the cerebral spinal
fluid. (See Diagrams # 2 and # 3)
The cerebral spinal fluid is a
clear, colorless liquid that circulates around the brain and spinal cord and
baths the tissue with needed nutrients and other constituent molecules.
DIAGRAM #2:
DIAGRAM #3:
The brain is seen to contain four cavities within it. The cerebrum holds
two large Lateral Ventricles that connect at the midline. From here, the CSF
follows the InterVentricular Foramina into the Third Ventricle.
Here, at the Third Ventricle,
another Choroid Plexus adds additional CSF. The CSF then passes through the
Aqueduct of Sylvius, continuing into the Fourth Ventricle, located between the
cerebellum and brainstem. Here, still another Choroid Plexus at the roof of the
Fourth Ventricle contributes additional CSF fluid.
After leaving the Fourth
Ventricle, the CSF essentially flows backward and downward around the midbrain,
exiting the ventricular network below the cerebellum.
Some of the CSF passes downward
into the Spinal SubArachnoid Space (circulating around the spinal cord), and a
portion rises upward, through the Tentorial Notch, spreading over the
hemispheres of the brain.
Re-absorption of CSF is
predominantly assumed through the lymph and blood capillary network of the
subarachnoid space covering the cerebral hemispheres and spinal canal.
VENTRICLE NETWORK:
DIAGRAM #4:
The nutrients supplied by the CSF
are delivered by diffusion into those structures adjacent to the CSF. This leads
to some specialized circumstances.
First, as the CSF diffuses
nutrients (or toxins) to these adjacent structures, there becomes less and less
concentrations of these molecules remaining within the CSF, as it continues
along its track.
If toxins are present within the
CSF, those structures first contacted are far more severely attacked by these
toxins (or excitotoxins), than those bathed in CSF farther away from the
ventricular system and choroid plexus.
Second, diffusion of chemicals is
greatly increased by increases in hydrostatic pressures or flow rates.
Third, inflammation of the
Aqueduct of Sylvius from repeated insults of neurotoxic chemicals contained
within the CSF, can cause narrowing of this duct, resulting in obstruction and
the onset of adult hydrocephalus.
It is in the CSF, where the
phenylalanine and dicarboxylic aspartic acid diffuses, setting off a chain
reaction of repeated excitatory stimuli of surrounding nerve cells and
neuronal structures adjacent to the flow route of the CSF. This eventually leads
to nerve cell necrosis (cell death) in these areas.
The hypothalamus sits adjacent on
either side of the Third Ventricle, where there is a high diffusion rate from
the CSF, leading to sustained and potentially extreme damage to this neuro-endocrine
structure, one of the most vital neural systems in the body.
DIAGRAM #5:
A (simplistic) sequence of events would be the
following:
The transport of excitotoxins
across the blood brain barrier and within the CSF causes several reactions to
occur. The excitotoxins stimulate the nerves to fire excessively. The normal
enzyme actions required to offset the induced, repeated firing of these neurons
are negated by the phenylalanine and aspartic acid.
Furthermore, the energy system
for the required enzyme reactions becomes compromised from: depleted
intracellular ATP stores, the presence of formaldehyde, altered intracellular
Ca+ uptake, damage to cellular mitochondria, destruction of the cellular wall,
and the subsequent release of free radicals. This potentiates oxidative stress
and neurodegeneration.
These toxic by-products initiate
secondary damage, which increases capillary permeability, continuing to destroy
the surrounding nerve and glial cells. This further impedes enzyme reactions,
and promotes DNA structural defects.
Cellular death occurs over the
next 1 to 12 hours. This does not include the long-term or cumulative effects of
formaldehyde adducts and other metabolites. The dead cells leave behind lesions,
or holes, as Dr. Olney discovered with tests he conducted. Evidence indicates
that the following disease states can be clinically identified by their
corresponding anatomic nerve fiber, or nerve bundle damage:
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a) Aqueduct of Sylvius = Hydrocephalus
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b) White matter bundles = Multiple Sclerosis (MS)
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c) Pyramids/Basal Ganglia = Parkinson's Disease
-
d) Lateral corticospinal tracts of spinal cord and
bulbar nuclei =Amyotrophic lateral sclerosis (Lou Gehrig's
-
e) Destruction of hypothalamic regions =Neuro-endocrine
disorders, obesity, psychogenic disorders (behavior, anger) malfunction of
autonomic nervous system, immune suppression, et al. (See Diagram # 5, above)
Above the Fourth Ventricle, lay
the pyramids, and slightly forward are the basal ganglia. With powerful insults
from excitotoxic stimulation, we develop clinical manifestations of Parkinson's
disease (See Diagram # 6). This is further complicated by the depletion of the
neurotransmitter, dopamine, resulting from the obliteration of enzyme sites by
the flood of these excitotoxins.
Parkinson's Disease, itself, is a
complex chronic brain disorder resulting primarily from progressive death of a
specific group of nerve cells in a layer of a region of the substantia nigra
(basal ganglia) in the midbrain.
DIAGRAM #6:
These nerve cells produce a
chemical neurotransmitter called dopamine (which is inhibited by the
phenylalanine/aspartic acid isolates of aspartame). The dopamine enables
communication with receptors on neurons in a region of the brain called the
striatum. Additional dopamine pathways run from the midbrain to the limbic area
and to the cerebral cortex.
The striatum includes three
structures: globus pallidus, putamen and caudate nucleus. (See Diagram 7, below)
The striatum is a part of the
brain involved with regulating the intensity of coordinated muscle activity such
as movement, balance and walking. Insufficient levels of dopamine from the
neurons of the substantia nigra synapsing on neurons in the striatum is believed
to be responsible for the primary symptoms of Parkinson's.
View of Brain structures affected
by Parkinson's (and surrounding structures)
DIAGRAM #7:
As with Parkinsonian, Amyotrophic Lateral Sclerosis (ALS), commonly
called Lou Gehrig's Disease, clearly represents a connection between nerve
damage and the presence of excitotoxic amino acids.
Amyotrophic Lateral sclerosis, or
ALS, is a progressive, degenerative disease resulting from damage or destruction
of motor neurons within the brain and spinal cord. Nerve cell destruction
impairs or prevents muscle movement that corresponds to the affected neurons.
The various types of ALS include "bulbar",
which affects the cranial nerves, creating complications with speech and
swallowing, et al. When the damaged neurons extend from the spinal cord to
muscle fibers, this is often termed motor neuron disease. There can also
be various combinations of these degenerative states.
Effects of the excitatory amino
acid, glutamate, have been observed in the brain and spinal cord. There is an
increase of this excitotoxin within the CSF. Additionally, the damaged areas of
the cerebral cortex and spinal cord fail to "uptake" this neurotransmitter
substance, leaving higher amounts in the extracellular space, causing notable
cellular damage due to its excitatory properties.
NOTE: Aspartate (aspartic
acid) is similar to glutamate and reacts with many of the same enzyme
structures.
Also noted, are pathologies
related to cellular calcium (Ca+) channels, which are altered by the presence of
glutamate or aspartate. Calcium changes may cause further deterioration by
triggering secondary antibody effects that react to this damage. Cellular damage
will cause the release of oxidizing agents, resulting in high, free radical
exposure that even further damages the nerve cells. Mitochondrial damage is
compounded from this surge in free radical generation.
DIAGRAM #8:
Multiple Sclerosis (MS) is a
disease that affects the myelin (myelin sheath), which is the insulation or
coating of some of the nerves of the brain, spinal cord, and of the periphery.
Damage has also been identified that affects a part of the nerve fibers called
the axons. Oligodendrocyte damage and cell loss also occurs.
Nerve cell damage takes place
within the "white matter" of the brain, where the neurons have myelin sheaths,
giving this part of the brain its color.
Demyelination of the central
nervous system (white matter) are hallmarks of this disease. This is normally
(but not always) accompanied by optic neuritis, asymmetrical muscle weakness, or
fatigue.
Evidence seems to point to an
immunological disorder, as a response to an inflammatory process in the brain
(and/or spinal cord).
Although many scientists have not
identified a definitive cause of Multiple Sclerosis, many hypothesize that MS
may be of a triggered immunological origin. These authors' investigative
research into known scientific endeavors, biochemical facts, and available data,
leads to the following deduction. Hopefully, this will prompt further
investigation into the etiology of MS by non-industry funded researchers.
IF MS is an "immunological"
response, then the following need be considered:
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A reduction in glutathione synthesis will impair
antioxidant defenses.
-
Glutathione is virtually eradicated (not
available) following the ingestion of aspartame and its resulting metabolic
reactions.
-
T-Cells (immune response cells) are dependant upon
intracellular glutathione,
-
Functionality of the T-cells is impaired during
this period.
-
Deamination results from methanol toxicity -->
formaldehyde --> formic acid and can be highly mutagenic for nucleotides, DNA,
RNA transcription processes.
-
Pharmaceutically manufactured isolates (alone or in
concert with additional excitotoxic food additives/environmental toxins)
creates an excitotoxic response to include:
-
increased cell damage from oxidation,
-
mitochondrial damage (incl. a reduction in
available ATP),
-
imbalance of inter/extracellular amino acids and
their precursors,
-
increased intracellular Ca+ or
disruption of gated processes,
-
release of damaging free radicals,
-
excessive nitric oxide (NO) production,
-
displacement/release of free iron within the
brain,
-
mutagenic effects from formaldehyde or
generalized cellular DNA mutations,
-
subsequent inflammatory response as a result of
this cellular damage
-
Evidence reveals that
Methanol has long been the agent most well know
to cause auto-immune antibodies to "attack" the pancreas and myelin sheaths of
neurons.
-
The structures damaged in MS are the white fibers
of the CNS. These structures are in intimate contact with the cerebral
spinal fluid immediately after the fluid is formed by the Choroid Plexus.
Therefore, the white matter receives massive doses of dicarboxylic amino
acid neuro-excititoxins which are delivered to the brain from the CSF.
It is proposed that, regarding MS
diagnosis' (and possibly other potential auto-immune diseases of the central
nervous system), this sequence of damage from aspartame would elicit an
inflammatory reaction. This leads to a generalized (and possibly defective)
immune response against the neurons that have sustained damage, alteration, or
exhibit other "non-familiar" DNA changes.
In some cases, the immune system
itself may have been damaged by the formaldehyde's mutagenic effects or affected
by brain chemistry/enzyme changes, creating a flawed system. This could cause
the body to attack and catabolize its own nerve (or other) cells. Destroyed
neurons will eventually be absorbed, leaving lesions or holes where they once
had been.
Abstinence from aspartame appears
to relieve the clinical presentation of excitotoxic-induced MS.
This immune process defect may (in
part) also explain the rise in cross-chemical sensitivity syndrome.