Food and Nutrients in Disease Management

neurons of the neuron bundles are damaged
to the point that the electricity fl owing 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 fl ow 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.

<b>Etiology of Bundle Damage</b>

Bundles of monoamine neurons can be impaired from neurotoxin exposures, trauma, or biologicalinsult.56 Neurotoxin exposures are poorly defi ned and ongoing exposures are in contrast to
the MPTP study model of Parkinsonism. The most comprehensive listing located reveals 1179 known neurotoxins.39 Susceptibility of individuals based on genetic predisposition, environmental
infl uences, synergy between chemicals or other predisposing factors suggest that some individuals may experience neurotoxicity from many unlisted substances and at lower than threshold doses
of known neurotoxins, and so was not considered. Under the bundle damage theory it is assumed that neurotoxins are the leading cause of monoamine bundle damage leading to the following
speculation: Depression The bundle damage’s theory of repeated insult during a lifetime can explain the lack of effi cacy seen in the treatment of elderly with reuptake inhibitors who presumably have greater cumulative lifetime
effects from neurotoxins and other events that cause neuron damage. In the end these patients need to have neurotransmitter levels established that are much higher than can be achieved with reuptake
inhibitors alone.With repeated insult more damage occurs, which is cumulative. When the damage is at the point where the neurotransmitter levels needed to control disease symptoms cannot be achieved with the
use of reuptake inhibitors alone, from a clinical standpoint it appears that the drug is not working.This may explain why about 90% of adults treated with reuptake inhibitors achieve results no better
than placebo.The bundle damage theory may also explain why developed countries have a higher rate of depression as the population is exposed at a higher rate to neurotoxins.
Since insult exposure may be ongoing in patients with depression, optimizing nutritional status is important. Improving neuronal ability to minimize and recover from toxic insult form the basis
of the antioxidant nutrients Dr. David Perlmutter explains in Chapter 28, “Parkinson’s Disease,” and the membrane-stabilizing nutrients Dr. Patricia Kane explains in Chapter 24, “Seizures.”

<b> IV. PHARMACOLOGY</b>

AMINO ACIDS
Treatment of depression, as well as any other monoamine neurotransmitter diseases, is not possible through the direct administration of monoamine neurotransmitters. This is due to the fact that monoamine
neurotransmitters do not cross the blood-brain barrier, as depicted in Figure 29.1.2,3,4,5 The only way to increase the levels of central nervous system monoamine neurotransmitter molecules is
to provide amino acid precursors, which cross the blood-brain barrier and are synthesized into their respective neurotransmitters by presynaptic neurons.

REUPTAKE INHIBITOR DEPLETION OF MONOAMINE

The National Institute of Drug Abuse presents a detailed discussion on its website on how reuptake inhibitors deplete neurotransmitters.22 Medicines used to treat depression are not the only drugs
that block reuptake; cocaine and amphetamines block reuptake as well.22 Reuptake inhibitors block
<b>CONCLUSIONS</b>

The bundle damage theory creates a framework by which to offer patients new treatments for clinical depression. The theory underscores the importance of minimizing toxic exposures, through
avoidance where possible, through diminished uptake, and through adequate nutrients. Similarly patients who have inadequate substrate for neurotransmitter synthesis may need cofactors, nutrients
involved in sulfur pathways, and amino acid precursors. Patients may also receive benefi t from amino acid precursors beyond what can be obtained from diet alone.
There are three primary considerations in the use of amino acids for treating depression.First, proper levels of amino acids should be administered with the drugs to prevent depletion of
neurotransmitters. Second, proper use of amino acids will keep the drug functioning properly, avoiding tachyphylaxis. Third, the use of amino acids may cause a drug side effect to become
active. In summary, amino acids hold more therapeutic potential and less potential for harm when
administration is physician-guided.

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