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diminished
leading to the function being controlled
and/or regulated not controlling
properly causing symptoms of disease
develop. Technically synaptic
neurotransmitter levels prior to
treatment in patients with disease due
to neuron bundle damage are in the
normal range for the population.
The
Bundle Damage Theory and The Monoamine
Theory are not mutually exclusive of
each other. Instead these two theories
can be viewed a complimentary in that
they address different mechanisms of
action leading to neurotransmitter
dysfunction and compromised electrical
flow out of the post-synaptic neuron.
The Monoamine Theory addresses low
levels of neurotransmitters in the
synapse as the etiology of impedance of
electrical flow needed to regulate
function and keep disease symptoms under
control. Whereas, The Bundle Damage
Theory addresses damage to the neuron
structures (primarily post-synaptic)
which impede the flow of electricity
needed to regulate function and keep
disease symptoms under control. With the
monoamine theory and the bundle damage
theory the flow of electrical energy
needed to regulate function is not
adequate. Differentiation of the two
theories lies in the etiology of the
dysfunction. Under monoamine theory
returning neurotransmitter levels to
normal will relieve disease symptoms.
Under the bundle damage theory synaptic
neurotransmitter levels need to be
established that are higher than the
reference range of the population.
It is
the mechanical damage to the
post-synaptic neurons as suggested by
the bundle damage theory and not the
synaptic neurotransmitter levels that is
the primary cause of monoamine disease.
This subset is composed of about 88% of
adult patients and 100% of the elderly
patients with depressive symptoms – the
nonresponders from the depression
studies above.
Neurons are intended to function for
life. Loss of a neuron to apoptosis is
permanent, although in limited areas of
the brain neurons may regenerate to
replace the neurons that have undergone
apoptosis.58 As neurons go
into apoptosis in the post-synaptic
neuron becomes completely non-functional
they tend to go through an agonizing
death where the electrical brilliance
with which they function slowly fades
until the electrical flow through the
neuron regulating function decreases and
stops over time.
The
only way to increase neurotransmitter
levels in the central nervous system is
to administer amino acid precursors
which cross the blood brain barrier and
are then synthesized into
neurotransmitters. Increasing
neurotransmitter levels in the synapse
is analogous to increasing the voltage
in an electrical wire, where by turning
up the voltage you get more electricity
out the other end of the wire. Turning
up the voltage increases the electrical
potential (pressure) of the electrons
entering a partially damaged wiring
connection leading to more electrons
(electricity) flowing out the other end.
In the case of neurotransmitter disease
where the neurons of the neuron bundles
are damaged to the point that the
electricity flowing out of the neuron
bundles is diminished disease develops.
Increasing neurotransmitter levels will
effectively increase voltage in the
remaining viable neurons in the bundle
causing electrical flow out of the
damaged neuron bundles to increase to
the point that normal regulation and/or
control is once again observed. In this
state, from a clinical standpoint, the
symptoms of disease are under control.
Depression cause and risk
factors-pathophysiology The Bundle Damage Theory
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