Food and Nutrients in Disease Management
was able to achieve relief of symptoms with dopamine levels in this range. For treatment of patients with Parkinson’s, the therapeutic range of
urinary dopamine is 6000 to 8000 micrograms of dopamine per gram of creatinine. Dopamine levels of this magnitude can be achieved by administration of the amino acid precursor, L-dopa.
Amino acid supplementation can reduce the tachyphylaxis generally associated with pharmacologic interventions. Once the synaptic levels of dopamine are high enough and the fl ow of electricity is
once again adequate to regulate fi ne motor control, clinical resolution of the Parkinsonian tremor and other symptoms are seen.40 As with Parkinsonism, the damage to other neuron bundles of the serotonin/catecholamine pathways
as seen in depression can be dealt with effectively by increasing the neurotransmitter levels higher than is normally found in the system. This has led our group to propose the Bundle Damage
Theory of Depression.
<b>The bundle damage theory</b>
The bundle damage theory states:Neurotransmitter dysfunction disease symptoms, such as symptoms of depression, develop when the electrical fl ow through the neuron bundles that regulate function is compromised by damage to the
individual neurons or the neuron components composing the neuron bundle which conducts electricity to regulate or control function. In order to optimally restore neuron bundle regulatory function, synaptic
neurotransmitter levels of the remaining viable neurons must be increased to levels higher than is normally found in the system, which restores adequate electrical outfl ow resulting in relief of symptoms
and optimal regulatory function.
Bundles of neurons convey electricity that regulates and/or controls numerous functions in the body. If enough of the individual neurons of a bundle become damaged the fl ow of electricity through the bundle is diminished, leading to the function being controlled and/or regulated not controlling
properly, causing symptoms of disease to 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 complementary in that they address different mechanisms
of action leading to neurotransmitter dysfunction and compromised electrical fl ow out of the postsynaptic neuron. The monoamine theory addresses low levels of neurotransmitters in the
synapse as the etiology of impedance of electrical fl ow needed to regulate function and keep disease symptoms under control. The bundle damage theory addresses damage to the primarily
postsynaptic neuron structures that impede the fl ow of electricity needed to regulate function and keep disease symptoms under control. With the monoamine theory and the bundle damage
theory the fl ow 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 postsynaptic 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 postsynaptic neuron and become completely nonfunctional they tend to go through an agonizing death where the electrical brilliance with which
they function slowly fades until the electrical fl ow 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 that 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, whereby turning up the voltage you get more electricity out of 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) fl owing out of the other end. In the case of neurotransmitter disease where the