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INHIBITION OF FCG FUNCTION
Anoxia is necessary to the blocking of the activating function of the ethylenic linkage. Warburg’s Thesis (6) that anoxia is the cause of cancer, is supported here and one may add that it is necessary to certain types of viral integration with the host cell’s functional mechanisms to produce paralysis. When the FCG dehydrogenates a pathogen, viral or chemical, that enters its field during hypoxia, the free radical formed cannot add molecular oxygen to become a peroxide free radical and be combusted, so it adds to the attracting pole of a double bond with which it has contact. That must be the proximal pole of the ethylenic linkage that activated the FCG that removed the hydrogen atom. Addition here will block all electron migrations to the FCG and the oxidation initiating mechanism cannot function any more. The deprival of the functional mechanism (grana) of oxygen does away with them structurally and functionally as Warburg’s Thesis claims, however, we find that they are NOT eliminated from the cell. It is their identity that is lost and the change is clinically reversible by removing the pathogen. Warburg spoke only of cancer. We include cancer and extend the observation to all other diseases studied to date.
We will show that together, with the anoxia, a co-factor is required.In cancer, it is a carcinogen (viral or chemical) and clinically, a polymerized product of bacterial action in a hypoxic focus of fibrosis carrying a silent infection. The integration formed by the pathogen with the activating double bond of the FCG, or with the FCG by free radical addition or by firm condensation with an amine, respectively, is provided for by the activation of the position alpha to a double bond. This double bond is the electron withdrawer and the alpha activation also provides for the dehydrogenation of this position after integration of the pathogen takes place, so that cleavage of the pathogen from the FCG system with restoration of its Carbonyl group and of its activating double bond are had. The host cell is thus separated from the pathogen in good functional status, while the pathogen is no longer to be found. It undergoes a progressive oxidation favored by activation alpha to the terminal Carbonyl groups produced at each fragmentation. There are two means of securing this separation and they confirm our Thesis as to the nature of the pathologic integration. It will be seen also that one Corrective Reagent used is constructed on the same pattern and is essentially a highly activated Carbonyl group of a potential of one volt more or less according to the carrying structure which is built up to secure the greatest steric advantage for its particular attack, which is, of course, high potential dehydrogenation.
Reversal of the pathogenesis is closely followed by tissue reconstruction. Thus, when Ehrlich ascites cells are transplanted into the peritoneal cavity of mice, the liver and spleen reticuloendothelial cells immediately atrophy and both organs shrink. The neoplastic cells infiltrate and produce tumefaction with ascites. Treatment can be given at various periods after inoculation and the animals sacrificed for observation. It is then seen that, as the neoplastic invasions are removed and the peritoneum becomes absolutely clear and glistening, the spleen and liver and especially their Kupfer cells regenerate rapidly. If any traces of neoplastic invasions are found, they are undergoing nucleolysis, calcification, and coagulation as an early phase of digestion. Such changes are similar to what we observed in the biopsy material taken from skin squamous cell cancer during recovery. (Medical Record of New York, October 1920). The initiating factors are, of course, the activated Carbonyl group of the Reagent and the activated position alpha to an ethylenic linkage in the integrated pathogen tending to release its hydrogen atom unrestricted.
In reality, the ethylenic linkage is not an electron donor, but a weak withdrawer of electrons. When conjugated with a Carbonyl group, which is an active electron attractor, the ethylenic (pi) electrons are mobilized toward the Carbonyl group, and such substituents as CH 3, CH 2 CH 3, and C(CH 3 ) 3, which are active releasers of electrons will, when located at the opposite end of the double bond, supply their quota for attraction to the Carbonyl group of the FCG system. In addition, the Carbonyl group is negatively polarized with an oxygen atom rating 3.5 electronegative units and a carbon atom of 2.5 electronegative units. Only fluorine exceeds the electro-negativity of oxygen. Therefore, the Carbonyl group of the FCG system as conjugated with an ethylenic linkage serves as an active dehydrogenator of fuels and pathogens that enter its field, and the ethylenic linkage serves as the bridge for the electronic migrations toward the Carbonyl group. Where two or more Carbonyl group double bonds are conjugated in series, the orbital mechanics determine so heavy a concentration of electrons and electro-negativity at one of the groups that it becomes a most active dehydrogenator, and as in Triquinoyl, the strain becomes so great that one group even becomes expellable to form the more stable five member ring.
In addition, fuels and pathogens are especially equipped to mobilize their critical hydrogen atoms. In glycogen and the polysaccharides, the Carbonyl groups are inactivated and in the monosaccharides, the lactone structure makes the molecule inert. When the Carbonyl group is free, however, it attracts the electrons away from the hydroxyl group so that its hydrogen atom tends to be liberated unrestricted. This mobilization is seen when glucose or fructose is dissolved in heavy water. Here it is found that the hydrogen atoms trade places freely, and at random with the deuterium of the heavy water. Such mobility is surprising in view of the fact that the bond energy of the O-H group is one of the highest of the covalent bonds; namely, 110.2 Kilo-Calories and the bond length is one of the shortest; namely, 0.95 A units. Thus one sees the power of mesomeric induction to bring about reactivity without causing ionization. Pathogens and unsaturated fats also invite dehydrogenations in various degrees. Here we Postulate that a of an ethylenic methylene group positioned alpha to a double bond linkage offers two activated hydrogen atoms; one is important for the integration with the FCG system during the anoxia and the other invites its removal from the integrated pathogen by the Carbonyl group of the curative reagent continuously when oxygen is present. (This dehydrogenation can also be accomplished by an appropriate free radical). The activation of the pathogen’s hydrogen atoms is secured by withdrawing electrons from the alpha placed methylene group by the substituents placed at the other end of the double bond. Those that withdraw electrons are halogens, methoxyl, hydroxyl, aldehyde, Carbonyl, vinyl, phenyl, cyano, and sulfhydryl, but not by amino groups. Here one sees the possible place of iodine in activating the initiation of physiological oxidation. The withdrawal of electrons from the alpha positioned carbon atoms weakens the bond to hydrogen and facilitates dehydrogenation. The stage is thus set intrinsically for the oxidative reversal of the pathogenesis. The pathology actually provides for its correction. The philosophic implications deserve thought.
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