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REVIEW OF CARCINOGENESIS AND ALLERGENESIS

As we have seen, the cause of cancer is a multiple affair in which anoxia and two pathogens are the principle actors, and the same pattern holds for the production of the allergies.

The only difference is that in cancer, the basic functional cell unit attacked is the mitotic mechanism for cell reproduction. We have classified cancer as an allergy of the cell’s mitotic mechanism decades ago (Natural Immunity, 1934, Christo­pher Publ. Co. Koch).

In the respiratory allergies, the secreting mechanism and contractile mechanism’s energy producing and receiving FCG’s, and their activating double bonds, are concerned.

In the neurological allergies, as epilepsy, compulsory neuroses, and fixed ideas, the conductile mechanism’s energy producing and receiving FCG systems, and their activating double bonds, are attacked.

The energy for excessive action of an allergy or neoplasia is not received from the normal sources of oxidation nor even glycolysis as Warburg sug­gested, for the FCG of energy production and acceptance is blocked by the pathogenic additions.

We conclude that the energy comes from the polymeriza­tion of one of the pathogens integrated with one terminal of the FCG activating double bond as a free radical addition.

In the case of cancer and any other allergy, the pathogen is a virus or a polymerizing toxin produced by bacteria trapped in the scar of an old infection where ischaemia protects it from oxida­tion. This pathogen is the sustaining toxin, which may be difficult to differentiate from a virus, or a bacteriophage living in symbiosis with the germ and paralyzing its activity, instead of causing its lysis. When it gains entrance into the blood stream and into the host cell, its critical double bond adds to the distal pole of the FCG activating double bond, which has become a free radical through addition of the free radical offered by the exciting or sensitizing pathogen to the proximal pole.

When it adds to the proximal pole of the FCG’s activat­ing double bond, the free radical formed at the other pole can co-polymerize with the sustaining pathogen, as just stated, whose energy liberated by polymerization forces, either an excessive uncontrolled mitosis (cancer), or a function, such as an allergy.

The smaller the molecule, the greater the content of double bonds, the more rapid the polymerization, and the greater the amount of energy produced, and hence, the more intense the pathogenic action, whether it is as an allergic affair, or as a neoplasm.

The initiating toxin could be one of the sulfydryl products of certain bacteria, trapped within occluded tonsilar crypts, the apical infection of teeth, or some occluded scarred sinus of long standing. Sulfydryl readily forms free radicals upon dehydrogenation by the FCG; and it also has the ability to add to the double bonds of ethylenic linkages conjugated with Carbonyl groups. It can therefore interfere with oxidations in several ways, for it can inactivate the quinone type co-enzymes as Co-enzyme Q-l0, which is an electron carrier or transfer agent. As when one closes a culture of such bacteria taken from a focus of infection, just mentioned, it soon shows the development of malodorous mercap­tans. In like manner, it may also add to the FCG’s activating system to initiate pathogenesis.

To show that the focal infection of long standing is a factor in carcino­genesis, a typical case history will suffice. This woman was then 56 years of age and her case history was included in the Testimony before the Federal Trade Commission in 1943, as a demonstration of the nature of the recovery process after the Koch Reagent was given. The uterus and most of the pelvis and lower abdomen were involved by ‘a biopsy proven’ cancer of the uterus; the right breast also presented a massive cancer of the simplex type, which extended into the axilla. There were numerous metastases to the skin, as well, when she received the Koch Reagent in 1938. Recovery was in evidence within three weeks and continued with reactions at the twelfth and twenty-fourth weeks, and by the end of the twenty-fourth week, the absorption of all growths was complete; but an acute, violent, inflammation of the tonsil and lymphatics on the right side of the neck, set in at this time. She could neither swallow nor speak for about a week, then it quickly subsided and she felt very well in all respects. When describing her symptoms, she stated that she had the very same thing happen some 20 years earlier, and her health was never as good afterwards. During that attack, she could not speak or swallow, otherwise, both symptomatologies were identical, except that this recent attack left rapidly, leaving her in exceptionally good health.

Here we have an example of the reversal of the pathogenesis as the essence of the recoveryprocess.The first symptom in the initiation of the disease was the last symptom to be brought to light and its causative pathology cleared away at the wind-up of the correction process.

The interpretation is what we have offered since 1926; During the recovery the de-polymerization of the sustaining pathogen was going on and finally when the growth was gone, the monomeric form of the toxin only was present to produce the same symptoms, as it did when the germ (and its virus) infected the tonsilar area and produced the original inflammation and its subsequent cicatrization.

Both inflammatory reactions to the monomeric form of the toxin were identical, except that the recovery reaction induced by the corrective Reagent burned away completely the infection with its toxins, once adsorbed in the protective scar tissue. These were also burned away, so that the scar tissue became obsolete and was absorbed like the neoplasms, themselves. The correction was therefore complete for no scar tissue was needed after the toxin was burned away.

The completion of the recovery from diabetes with its gangrene conforms to the same pattern.Here the block to FCG’s function of energy production and acceptance left the islet cells unable to produce insulin and the evolution of the pathology that followed included bacterial infection of the ischaemic bones, which then under­went necrosis. The recovery process removed the basis for this infection and the infection left so the bones could be restored in minute detail. The radiographs demonstrate this. The pathogenesis patterns, as outlined here, need not be rigid and must conform to the attending circumstances. They are in har­mony with the clinical experience and the established facts of physiology and chemistry, and therefore, are a guide to successful Treatment, which after all, was the goal of 50 years of investigation.

Healing without infection or scar tissue also permits the parenchyma to be redeveloped, so that the injured and defective organs are reconstructed to their normal architecture and function.Thus, the uterus can bear children normally, the stomach can do its normal digestive work, and the bowel can again function, as it was intended to do. Likewise, the bone is restored to do its supportive skeletal work with increased strength and structural density. The complete text should be consulted for more examples.

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