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itters in thesynapse 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 primarilypostsynaptic 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 damagetheory 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 returningneurotransmitter 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 ofthe 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锟絫he nonresponders from the depression studies above.Neurons are intended to function for life. Loss of a neuron to apoptosis is permanent Jose Canseco Athletics Jersey , although in limited areas of the brain neurons may regenerate to replace the neurons that have undergoneapoptosis.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 whichthey 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 administeramino 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 inan 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 apartially damaged wiring connection, leading to more electrons (electricity) fl owing out of the other end. In the case of neurotransmitter disease where the neurons of the neuron bundles are damagedto 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 neuronsin the bundle Catfish Hunter Athletics Jersey , causing electrical fl ow out of the damaged neuron bundles to increase to the point that normal regulation andor control is once again observed. In this state, from a clinical standpoint, thesymptoms of disease are under control.Etiology of Bundle DamageBundles of monoamine neurons can be impaired from neurotoxin exposures Mark McGwire Athletics Jersey , trauma, or biologicalinsult.56 Neurotoxin exposures are poorly defi ned and ongoing exposures are in contrast tothe MPTP study model of Parkinsonism. The most comprehensive listing located reveals 1179 known neurotoxins.39 Susceptibility of individuals based on genetic predisposition, environmentalinfl uences Glenn Hubbard Athletics Jersey , synergy between chemicals or other predisposing factors suggest that some individuals may experience neurotoxicity from many unlisted substances and at lower than threshold dosesof 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 followingspeculation: Depression The bundle damage锟絪 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 lifetimeeffects 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 reuptakeinhibitors 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 theuse of reuptake inhibitors alone Reggie Jackson Athletics Jersey , 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 betterthan 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 basisof the antioxidant nutrients Dr. David Perlmutter explains in Chapter 28, 锟絇arkinson锟絪 Disease Joe Morgan Athletics Jersey ,锟?and the membrane-stabilizing nutrients Dr. Patricia Kane explains in Chapter 24, 锟絊eizures.锟?IV. PHARMACOLOGYAMINO ACIDSTreatment of depression, as well as any other monoamine neurotransmitter diseases Walt Weiss Athletics Jersey , is not possible through the direct administration of monoamine neurotransmitters. This is due to the fact that monoamineneurotransmitters do not cross the blood-brain barrier, as depicted in Figure 29.1.2,3 Tony Phillips Athletics Jersey ,4,5 The only way to increase the levels of central nervous system monoamine neurotransmitter molecules isto provide amino acid precursors, which cross the blood-brain barrier and are synthesized into their respective neurotransmitters by presynaptic neurons.REUPTAKE INHIBITOR DEPLETION OF MONOAMINEThe 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 drugsthat block reuptake; cocaine and amphetamines block reuptake as well.22 Reuptake inhibitors block CONCLUSIONSThe bundle damage theory creates a framework by which to offer patients new treatments for clinical depression. The theory underscores the<. 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