SURVIVAL FACTOR IN NEOPLASTIC AND VIRAL DISEASES
By
WILLIAM FREDERICK KOCH, Ph.D., M.D.
Chapter 13
CLEAVAGE OF THE HOST-CELL PATHOGEN INTEGRATION
Let the host cell and its functional Carbonyl group — FCG — and the activating ethylene linkage be represented by the above formulas:
or by a chain of its polymers.
Whether dehydrogenation takes place at the point of integration of the pathogen and the FCG system, or at the farthest end to begin the destructive oxidation of the pathogen, depends on its structure. At any rate, the most exposed and most active hydrogen atom would be attacked. In the virus pathogen, this would be a terminal unit of the virus, since viruses are built up as by a polymerization process, that is: by the addition of a free radical of each unit to a pole of a double bond or free radical of the other unit already laid down. Therefore, the last added unit would be most exposed and dehydrogenation would take place at the carbon atom alpha to a double bond in this outer unit as at (f) or (a). A free radical so produced would add molecular oxygen to make a peroxide free radical, and this would cleave the molecule into two parts, each of which would carry a Carbonyl terminal. The double bonds of this Carbonyl group would activate the hydrogen on the carbon atom alpha, thereto and dehydrogenation would lead to another cleavage producing two more Carbonyl groups, etc. Thus, step by step, the virus would be burned off until the ethylene linkage to which it was added was reached, as at (c), and here a Carbonyl group would be made, thus activating the FCG in place of the ethylene linkage. This would prove an immunizing help as the Carbonyl group is a much better electron donor than the ethylene linkage, and thus a higher O/R potential would be gained by the FCG. Further, Carbonyl groups do not add free radicals as readily as do ethylene linkages, and the chances for integration with a pathogen during anoxia would be correspondingly reduced. The long lasting protection observed in our cured patients may thus be explained. The energy liberated in this combustion of the virus would pass on to the host cell and support its reconstruction. (See Appendix.)
The virus attached via an azomethine double bond by condensation of its amine group with the FCG could undergo the same stepwise oxidation with restoration of the original Carbonyl group of the FCG System, and leaving its ethylene linkage undisturbed as the donor of electrons to the FCG. However, alpha to the azomethine double bond a hydrogen atom could be removed and the oxidation at this point would burn off the amine group and restore the FCG. The virus would thus lose its pathogenic amine group and receive a Carbonyl group to change its whole attitude toward the world, as it was separated off as a whole. Likewise, the virus attached at the ethylene linkage could be burned off at the point of attachment and leave a similarly restored FCG activated by electrons from a Carbonyl group. The virus would also acquire a new Carbonyl group to change its behaviors. It is even possible that the acquiring of an active Carbonyl group would give it autonomous properties so it need no longer be parasitic to obtain its energy, but may be able to produce it itself.
Should the pathogen be a synthetic carcinogen or a polymerized toxin produced by some germ trapped in a scar where oxygen supply is low, the burning would start at the most active hydrogen atom exposed; that would be one that is alpha to a double bond located in the “K region”, as is now identified by cancerologists. At any rate, the pathogen is no longer to be found. It, therefore, is no longer a disturber of physiological processes. Normalcy is thus established.
Toxins attached to fibroblastic tissue where healing is going on and held in the scar as an integrate, no doubt, make the addition as a free radical or via an amine group, as described above. It is a clinical fact that scars disappear after the Survival Factor dehydrogenator starts to work on them. The toxin is thus burned out of the way and the fibrosis has no more incentive to exist. It becomes obsolete, and is absorbed. Extreme arterial sclerosis in very old people has been observed to disappear and senile dementia to clear up in a major way following one dose of the Survival Reagent. Under such circumstances, one is justified in assuming that the pathogen was burned out of the sclerotic tissue and the fibrosis could then be absorbed, without any reason for hindrance.
The ideal Therapeutic Reagent must possess an adequate O/R potential in a molecule free from steric hindrance, and of the simplest possible structure, so that one action and only one predominates. It is necessary to gain as broad a field of steric advantage as possible, since the steric qualities of the host cell’s functional mechanism- pathogen integrate changes, some with each different pathogen. Simplicity in structure is therefore an advantage. The Survival Reagent’s Carbonyl group, as so often stated, is activated by conjugation with the double bonds of an ethylene linkage, or of another Carbonyl group, or with the triple bonds of an acetylene linkage. The greater the number of ethylenic groups that carry free hydrogen atoms, the greater is the O/R potential of the Carbonyl group. Substitution of these hydrogen atoms must not be permitted. This is seen in the following quinone structures:
Anthraquinone with no quinone double bonds carrying hydrogen atoms and with two Carbonyl groups shows an O/R potential of 0.154 v. Alpha-naphthaquinone with one double bond carrying two hydrogen atoms and with two Carbonyls has an O/R potential of 0.484 v. Beta-Naphtha-quinone with one double bond carrying two hydrogen atoms, and the double bond of a Carbonyl group conjugated directly with another Carbonyl group of the quinone structure has an O/R potential of 0.576 v. Parabenzoquinone carries two ethylene linkages presenting four hydrogen atoms and two Carbonyl groups. It has an O/R potential of 0.7 15 v. Orthobenzoquinone with two sets of double bonds carrying four hydrogen atoms and two Carbonyl groups directly conjugated, offers an O/R potential of 0.792 v. Diphenoquinone with its four ethylene linkages presenting eight hydrogen atoms in two quinone groups united by a double bond, and offering two Carbonyl groups, shows an O/R potential of 0.954 v. As the dehydrogenating power increases with the O/R potential and likewise the energy content of the molecule, one will see to it that no substitutions are allowed unless the substituent offers a series of additional ethylene linkages in conjugation. Yet that may interpose some steric disadvantage. As the migration of electrons to the Carbonyl group make the ethylenic linkages more electrophilic, they will tend to add free radicals of toxins more readily and when hypoxia hinders peroxide free radical formation in the dehydrogenated toxin, this property of the ethylenic linkage is an advantage, as it will protect the Functional Carbonyl group’s activator unsaturated bonds from paralyzing additions. On the other hand, the quinone ethylenic linkages when present in excess, can add to and inactivate the free radicals produced in the pathogen that is undergoing destructive oxidation, and thus block further progress in its destruction, and also block the liberation of the host cell’s FCG. Too large a dose of quinone, especially of diphenoquinone, or its repetition when recovery is going on, competes with molecular oxygen and can block the recovery process or even reverse it. This is especially true when hypoxia reduces the opportunity to change the free radicals formed in the toxin into peroxide free radicals. On the other hand, some advantage may be had in protecting host cell unsaturated bonds from adding free radicals of the pathogen. The structure of the Reagent, therefore, must be understood for best use.
Another valuable consequence of not allowing the quinone structure to carry substituents of the hydrogen atoms, is that these substituents cut down the activity and formation of the resonance hybrid free radicals that have great value in starting oxidation chains, and continue the dehydrogenations after the Carbonyl group has accepted a hydrogen atom.
