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Thursday, August 16, 2012

Wm. F. KOCH-SURVIVAL FACTOR IN NEOPLASTIC AND VIRAL DISEASES (B)


CHAPTER 10


RECENT PHARMACEUTICAL STRIDES


Very recently, in the last few years, some highly substituted Benzoquinones have been introduced into medicine, as cytolytic agents in the treatment of cancer. The high substitution defeats any action, inherent to the quinone structure that might be curative. Such action depends upon high activation of the Carbonyl group, and upon the wealth of resonance hybrids that would be possible if the hydrogen atoms, held by the ethylene linkage were present, instead of displaced by complex groups that not only prevent electron migrations to the Carbonyl group, but prevent additions of free radicals to the carbon atoms of the ethylene groups. In certain instances, the benefit of Benzoquinone is due to its ability to absorb antagonistic free radicals, and the high substitutions annul this effect. The following well recognized reactions might be offered as a demonstration of this detoxicating quality, which is lost in the admitted non-curative commercial drugs.

 (Well-established free radical absorbing power of Benzoquinone...)

  



…yields the Quinhydrone, which is disproportionate to Hydroquinone and Benzoquinone. Thus, Benzoquinone inactivates free radicals and the therapeutic action is hindered, as clinical tests have proven. We therefore conclude, that the therapeutic activity of these Reagents is partly, at least, to be attributed to the free radicals they contained and which, were responsible for the oxidation and polymerizations in progress in these systems. There is nothing cytolytic about this structure.  It is constructive in action.

Pharmaceutical Substituted Quinones

As examples of these cytolytic agents that are admittedly unable to protect or to cure, the following of Schenley Laboratory may be taken as an example:

 

It carries toxic nitrogen, -2,5 -di-n propxy-3,6-bis-ethylenimine- 1 ,4 Benzoquinone.
And the following A-139 is of the same order:


Actinomycin is a natural nitrogen free antibiotic that has had some trial but without any curative results. Whatever they are, they might be a little better than that of the preceding or Bayer’s E39, which is built on the same order as Schenley’s and A-139In Actinomycin, Carbonyl activity is limited by the substituents, and by the failure to have even one hydrogen atom attached to an ethylene linkage. This again is for the benefit of the organism that produces it and not to serve as a therapeutic agent.

Certainly the analytical and synthetic work of the antibiotic chemist deserves the highest praise. The search for virtue in complexity of structure, however, has no basis aside from the needs of the organism that produces the antibiotic. These are not identical with the requirements of higher animals in the situations we have discussed. Rather the greatest simplicity possible wins the laurels here.

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CHAPTER 11


THE AZOMETHINE DOUBLE BOND


The azomethine condensation, like the free radical and the chain oxidation to which the latter is related, have not found much utility in past biochemistryexcept as we have employed them in our Postulate. If the criticism is offered that we are giving them too much speculation, the answer comes right back, that we are Postulating processes in matters that were not understood before, nor mastered until these Hypotheses were applied. The azomethine double bond is present in many vitally important molecules. Thiamine has it three times, adenine three times, flavine twice, pyridoxal once, cytochrome twice, porphyrin twice, cytosine twice, vitamin Bfour times, and it is found in many others and their derivatives. In view of its wide occurrence and great versatility it warrants thorough study. We have used it as a first step in the process of energy transfer and its block in reactions that belong to the high efficiency system oxidations. Recently, however, it is being written in the preliminary steps to certain hydrolytic reactions as where the Carbonyl group of pyridoxal phosphate condenses with an amine group to co-factor certain transaminations and the decarboxylations of amino acids. (Snell and Metzler, 1952). Here the azomethine double bond is hydrolyzed to reproduce an amine group and a Carbonyl group, whereas we use it in preparation for the oxidative destruction of the amine group and the restoration of Carbonyl. We regard it as a bridge for energy transfer and as an activator of dehydrogenations that lead to peroxide free radical formation and oxidative amine destruction. We also use it in preparation for the Amadori reaction as a first step in sugar oxidation. It impressed one as significant that guanidine and methyl guanidine contained it, and so we supposed it played a part in the oxidative cleavage that yielded urea, and in the synthetic reactions as where guanidine was built into guanine. So we noted the possibility that the parathyroid glands might have to do with the formation and destruction of this bond. Whether this supposition is correct or not, further investigation will open up a big field of information.

Glucose is more difficult to oxidize than fructose, and the consensus is now beginning to shift to the idea that all glucose is converted into fructose before it is burned. Let us assume that the functional mechanism where sugar is attached to be burned, presents an activated amine group as in creatine, adenine, etc., much the same way as it has the highly active FCG. This amine would condense with the Carbonyl group of fructose to form an azomethine double bond, which would undergo an Amadori rearrangement, placing the double bond between carbon atoms Cand C3. This would mobilize the hydrogen atom attached to Cand subject it to easy removal with production of a free radical that would add molecular oxygen to become a peroxide free radical. This would cause cleavage of the molecule into ketoglyceric acid and glyceric acid, with reversal of the Amadori reaction and regeneration of the functional mechanism’s amine group. If plenty of oxygen were at hand, there would be no interruption; simultaneous further dehydrogenations would produce more peroxide free radicals that would break the molecules down into carbon dioxide and water. If oxygen failed, the reduction chemistry in dominance would change the glyceric acids to lactic acid. These would remain until oxygen came along. This, of course, is not the fermentation process, and in the presence of oxygen no intermediaries would be trapped. Oxygen would be the electron acceptor right on the job. One finding regarding the effects of parathyroidectomy gave clues that led to a successful attack on the cancer and virus problems, with ramifications touching on the most pressing questions in the basic medicine of today. These orient us with regard to a Least Common Denominator in disease production.

The recent support to our Postulate offered by the structures and actions of antimitotic and antibiotic agents is strengthened by the phenomena and structure of the prosthetic group of Diamine Oxidase, as revealed by Zeller in 1951 (“The Enzymes” — edited by Sumner and Myrback — Vol. II, Part I, page 554 1951 Edition). Here Zeller shows that Diamine Oxidase removes one amine group from the toxic diamines by an oxidation process started with the dehydrogenating action of a proven Carbonyl group. The action is thus of the order of our Postulated FCG, and its range of action is similar, since it acts on loosely combining amines, but is inactivated by the firmly combining guanidines. Thus, it detoxicates putrescine, cadaverine, agmatin, etc. . . . but is inactivated by condensing with guanidine, just as the Postulated FCG is inactivated. This condensation blocks the oxidations and causes failure of function and then death, in line with our Postulate. For this reason, Diamine Oxidase is produced in greatest quantities in the placenta, the intestinal mucosa, and the liver. It is found in the blood of pregnant women, and, when its content falls, death of the fetus threatens. Its production in the intestinal wall protects the muscle and secreting glands of the mucous membrane from block in energy production for function. This is particularly necessary because the diamines are produced within the intestine by the decarboxylation of amino acids by bacteria, especially in an acid reacting (pH 3.5 6) colon. It is produced especially in the liver, too, to protect the tissues in general from toxic diamines entering the portal circulation. The action of the diamines is of the same order as those of virus, carcinogenic amines, guanidine, and other toxic amines of our Postulate. Their detoxication is likewise initiated clearly by the dehydrogenating action of the Carbonyl group, — oxidation. However, Zeller does not go far enough to identify free radical and peroxide free radical action, which would be the normal chemical sequel to dehydrogenation. He rather lets the enzyme conception carry the burden of explanation.

He also assumes the enzymatic activation of the two hydrogen atoms attached to the carbon atoms alpha and beta to an amine group, and that these are the hydrogen atoms that are removed by the enzymatic Carbonyl group. He assumes that a double bond is thus produced between these carbon atoms, and that this double bond is shifted to the amine group to form an imide group that is then hydrolyzed off as ammonia. Thus a Carbonyl group takes the place of the amine group, and the detoxication is accomplished. Prof. Zeller gives no thought to a condensation between the Carbonyl group of the enzyme and the amine group of the toxin to form an azomethine double bond. Nor does he refer to the oxidation, we have Postulated that replaces the amine group of the toxin with a Carbonyl group. However, the products of the reaction are ammonia and hydrogen peroxide, as would be expected from a hydrolysis in an enzyme system that operates in solution instead of on the grana surfaces, where oxidations would be expected, as in the case of the FCG system. This difference in position determines the reaction mechanism.

Diamine oxidase is inactivated by various guanidines and diguanidines, imidazole, such dyes as pyocyanine, methylene blue, streptomycin, pyridoxamine, by cyanide, and by the Carbonyl reagents, semi-carbazide, hydroxylamine, phenyl hydrazine, etc. The enzymatic Carbonyl group does form an azomethine bond with the latter, the Carbonyl Reagents, and with guanidine in agreement with our Postulate, so it can also form the same azomethine bond with the other amines except, as the direction of the reaction is determined enzymatically. Such enzymatic forces, however, are not able to prevent an inactivating condensation of the Carbonyl group with guanidine, phenylhydrazine, hydroxyla mine, etc., which take place outside the physiological range of control, just as they can inactivate the FCG. Both inhibited systems, that of the grana FCG, and of the enzymatic Diamine Oxidase Carbonyl group, require the oxidative rescue via a high O/R potential Survival Reagent, which indicates that they are both inhibited in the same way by a firm azomethine condensation. This will be demonstrated in the case histories.

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CHAPTER 12


GENERAL ASPECTS OF THE REAGENTS

   
The structure of the Survival Reagents is designed to carry out the chemical acts that are desired, and these are certain specific dehydrogenations to initiate oxidation progressions in pathogens integrated with the host cell’s functional mechanisms. The atomic groups of these functional mechanisms are their functional Carbonyl groups and supporting ethylenic linkages that activate them and with which they are conjugated. Two types of pathogen host cell unions were described, one via an azomethine condensation of the FCG and a tightly binding amine group, and the other via a free radical addition to one pole of the activating double bond. Anoxia or hypoxia was a deciding factor toward pathogenesis and molecular oxygen plus an adequate dehydrogenator were the essentials for the restoration of normal.

Necessarily the Reagents are highly reactive, with energy content reaching the “bursting point” so to speak. Nevertheless their chemistry is not crude mass action chemistry, but instead, catalytic in the sense that they initiate reactions that convert amounts of material far out of proportion to the amount of Reagent used. High dilutions are necessary for their best action. Activation also depends upon the high dilution, wide molecular and group dispersion, in addition to the activation of the specific groups that do the work. High dilution probably aids the electron migrations toward these groups that endow them with high activity. It is also characteristic that in nature the activating molecules or structures similar to the Reagents we offer, also work best in high dilution. This is true of Echinochrome A, Crocin and many other substances. (See Chapter XIV).

Highly reactive substances used in high dilution, require the greatest care in production and the higher the dilution, the greater is the care needed. Likewise in the management of any case that is treated, precautions against inactivation by contaminating influences or injuries from exposing the Reagent to strong light or even mild heat must be avoided. Contact of the Reagent with foreign substances may cause the expenditure of its energy, so that it is inactivated when it reaches the blood stream. Clean needles, syringes, and clean air are essential, and these must be FREE from even the slightest traces of contamination.

The physician’s eyes must be “wide open,” too, so he knows for sure that the regime that is selected for the patient to follow is entirely harmonious with its chemistry. This means the diet must be chosen scientifically, and not by guesswork, and other hygienic methods and measures must be helpful. Every patient is a complex of many factors in this complicated world, and the environment must be studied so the patient is protected from contrary influ ences both mental and chemical. The principle of the Therapy is simple, but its management is a job requiring expertness, intuition and patience plus a large measure of devotion.

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CHAPTER 13


CLEVAGE 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 dehydrogen ation 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.
  
  
The disadvantages of even the best quinone structures called for molecular set-up where crippling conditions were eliminated and so the chains of Carbonyl groups had to be developed. Among them, the following structures were compared with the straight chains of Carbonyl groups represented by the
Formula x, 

developed in various molecular weights.
  
The last mentioned structure offers great versatility because of different molecular weights that can be produced for fairly specific selection.

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CHAPTER 14


CATALYTIC DILUTIONS


The philosophy of the dominant therapy has been, up to now, to saturate the patient with as much destructive agent as possible, so as to destroy the enemy invader without too much injury to the patient. Quinine and Atabrine in Malaria, and the present-day antibiotics, are examples. So safe concentration is the logical procedure under this system. This is pharmacology. On the other hand, the physiological approach has different aims.  It is corrective, restorative and induces the changes it wants. Then, the question becomes what are the physiological ranges of concentration in which the Remedy shows best action by actual measurements and careful observation. The question not only is how dilute must the solution of the Reagent be, but also, how concentrated dare it be and still retain physiological activity. A look at the physiological natural reagents that carry activated Carbonyl groups will show how high nature dilutes them for best action.  As a starter, no better guide could be chosen. Here again, we see that our Postulate, of nearly half a century of application, is just recently receiving support from the physiological processes of Nature herself.

A dilution of one part of a Reagent to a trillion of water carries thousands of billions of molecules in each cubic centimeter. Since only one molecule is required to start a catalytic action that can grow with geometric progression, nature is not stingy when she supplies vitamin B12 in quantities so small that they can act normally in concentrations of 1 x 10-(9) or one part to a billion. Only three micrograms is an effective therapeutic dose. Only 0.01 millimicrograms gives definite growth response to bacteria. (U.S. Pharmacopeia Vitamin B12 Study Panel). Echinochrome A, is a naphthaquinone without one double bond carrying a free hydrogen atom. Its O/R potential is only 0.080 v. This is because the molecule has five hydroxyl substituents where hydrogen instead would have raised the potential 0.3 v. higher. Still, it is active in inducing motion in Sea Urchin eggs in dilutions of l:2x10-(9) (Fieser, 1944 Edition, page 753). Crocin belongs to the carotenoid family and presents two terminal Carbonyl groups conjugated with ethylene linkages, a chain of seven, with four methyl substituents. The Carbonyl groups are part of the terminal Carboxyl groups that have each been esterified with gentiobiose. It is active in the highest dilutions as demonstrated by Kuhn and Kuhn and Moewus — (1938-1940). Only one molecule is required to determine sex activity in the C. augamentos F. simplex and Chlarnydomonas genus of algae. Thus the dilutions may be higher than one part to a trillion of water, and Prof. Gilbert Smith, in 1947, reported the production of motility in certain plant sex cells by use of only one part of this reagent to 250,000,000,000 parts of water. Heparin is active in suspending blood coagulation in amounts so minute that there is no method to detect its presence (Fieser — p. 487 — 1944 Edition), and acetyl choline (Karrer — p. 239 — 1947 Edition), is able to renew suspended contractions in the intestinal muscle of the surviving guinea pigs in a dilution of one part to 1,000,000,000 parts of water. Since biological reactions are so much more refined than laboratory manipulations, one cannot judge physio logical activity by chemical detection or measurements. Likewise, clinical results are not to be predicted by the swing of a chemical balance. One thing must be observed, however, and that is when high dilutions are used, freedom from interfering reagents or measures are imperative, the work must be more careful and scientific, than when crude work is being done on a mass-action scale.

The chemistry of the free radical and mesomeric electron displacements will give biochemistry a different hue from the conceptions of the pharmacology laboratory that have controlled up to this time. The dosage and dilution are matters of expert decision, based on experience and enlightenment, not upon prejudice or superstition.

Following the 1955 and 1958 editions of this book, some eminent biochemists such as Szent Gyorgyi, have expressed opinions supportive to our basic philosophy with regard to the position of the free radical (lone electron) in carcinogenesis and other biochemical fields. This is indeed a gratifying advance over the dominant approach, and its correctness has already been established for decades as our text demonstrates.

See Appendix III, for further confirmation of the double bond and free radical phenomena concerned in pathogenesis and its correction.

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CHAPTER 15


TERMINATION OF THE MALIGNANT PHASE
RESTORATION OF THE FUNCTIONAL CARBONYL GROUP

We have already explained the two activated Carbonyl groups of our Postulate: One that initiates the oxidation progression and transfers the energy produced to carrier phosphate bonds. The other receives the energy from these bonds, and passes it on to the working mechanism of the cell, the contractile, the conductile, the secreting, or the mitotic fibrilla and units. They can both be blocked in their functions, by inactivation of their activating ethylenic linkages, or by a firm condensation with an amine group of some pathogen. When this takes place energy does not pass to the functional unit by the normal controlled route and only fermentation or Krebs Cycle energy is produced to pass directly into the working unit. Thus excessive contraction as the spasms of bronchial asthma, or excessive secretion as the secretion of hay fever, or excessive synapse closure as in some phase of insanity, a compulsion neurosis, etc., or impulse generation as of ticdoulereau, or excessive uncontrolled mitosis as of neoplasia will have to be the result in the tissue that is affected. The functional fault is demonstrated in the uncontrolled nature of the act, and all may be classified as allergies (Koch, Natural Immunity, 1934, and Cancer and Its Allied Diseases, 1929, where we attributed the abnormal energy transfer to a photosensitization process).

The correction is, of course, the restoration of the normal FCG activity in both capacities. That this can be accomplished no matter what the allergy happens to be is illustrated further in this section. Many more cases could be given in all categories, especially in the common allergies where the cure rate ran over 80% in the Court Testimony, but what is given is enough to illustrate.

The speed of the recovery is shown very well in the allergies of the respiratory system, and in the cure of the compulsion neurosis case, but it is also seen in the neoplastic category, too, as is illustrated immediately by biopsy tests or in the long run by the surgical tests outlined farther on. It is to be emphasized that the cure or correction of the disease in any instance is the restoration of the normal FCG function and the cleaning out of the debris and restoration of the normal structure and function, as the case requires. Then the normal being established, it can be broken down perhaps again when circumstances force this change. There may be some immunity or increased resistance due to a Carbonyl substitution for the ethylenic activation of the FCG, at any rate, though many cases stay well after being cured of cancer for several decades, there is no absolutely permanent and impregnable protection, and an understanding of the pathogenesis and what food diet means, is the best assurance of maintaining health after recovery.

There are some forms of primary cancer of the liver that are grossly pathognomonic. In such cases the expert surgeon can make a firm diagnosis without the biopsy, and he does so to protect his patient from embolism and hemorrhage incident thereto. This is not a matter of neglect, but of good judgment, and usually practiced. The type of greatest interest is that of diffuse distribution of myriads of small lesions over the surface and between the somewhat larger nodules that press up from underneath. The “feel” is also characteristic. In such cases there is deep jaundice because the smaller bile ducts are compressed or blocked by tumor tissue. The biopsy is characteristic also so that one can tell what the microscopic picture is from the gross features. In the diffuse type, the small surface nodules are much of the same size as if originating simultaneously, and thus speaking for a multiple origin of the carcinosis, a generalized equal distribution of the pathogen. As these nodules are smaller than many inside the liver, it is evident that the inner ones had an earlier start. Likewise, often, one lobe of the liver is more affected, especially the right lobe. Thus, in the beginning of the disease, the amount of pathogen is not so great that it makes an attack throughout all at one time. It is used up in one locality. However, at the terminal stage the myriads of small nodules equally and independently distributed speak for a swamping of the system with the carcinogen as if there were more toxins present than liver cells to combine with. Such a case will be described, and also a baby with a massive primary cancer of the liver proven by biopsy. This case is well described in the mother’s affidavit from which several points are reproduced. The series of photographs are also instructive. This information was sent us by Dr. M----, our collaborator, who had charge of the case, with his notes. The writer did not see this patient.

PRIMARY CANCER OF THE LIVER

CASE No. 14

Judy McW., three months old. “After a normal birth, Judy, before the age of six weeks, showed signs of illness. Her abdomen was enlarged, she was restless, and her face did not show the repose of a healthy baby. Her physician could not find anything wrong with her until his check-up and examination at the end of her eighth week. At that time the doctor found her abdomen hard and much distended. During the period from August 20, 1948, to August 27, 1948, a tentative diagnosis of cancer was made and X-Rays were given although the X-Ray technician stated it was hopeless to expect a recovery.”

“By the time Judy was three months old the attending physician and another surgeon made an exploratory operation on Judy’s abdomen at which time a biopsy was taken. The physicians reported to us that the biopsy showed a high degree of malignancy, which involved 85% of the child’s liver. They told us that there was nothing that could be done to save Judy’s life; that we should take her home and make her as comfortable as possible for the few days she could live.”

“Her life expectancy was placed at 21 days. We were told not to remove the bandage from her abdomen lest the stitches burst out. It was the doctor’s opinion that the incision in her abdomen would not heal.”

“Dr. Koch’s Therapy was given by Dr. N. T. M., of Cisco, Texas. The dose was injected into Judy’s hip on September 18, 1948. At this time and during the course of Judy’s recovery, Mr. N took a series of color pictures showing her progress. Previously he had taken two pictures at six weeks of age and before the diagnosis of cancer. The series of pictures gives a good idea of her case.

“At the time the injection was given, Judy’s abdomen was so much enlarged that she could hardly breathe due to upward pressure on her lungs. The circulation on the surface had greatly increased and she had a bluish cast from a diffusion of blood in and just under the skin. Veins under the skin of the abdomen were plainly visible. The abdomen was very firm, even hard. At the time the Koch Treatment was given, Dr. M. expressed no hope of securing a recovery as he thought the case was too far advanced.

“Within ten days after the Treatment Judy showed definite reactions which raised our hopes. Shortly, she began to pass large quantities of mucous with bowel movements. She also passed a large amount of water in the normal manner, sometimes requiring as many as twenty diaper changes per day. No medication was used after the injection of the Koch Treatment, and only minor changes were made in the baby’s diet, Apple juice was substituted for orange juice, and Judy liked it. After Treatment was given and until recovery was practically complete, only one doctor saw Judy that was a doctor residing at Azle, Texas, who removed the stitches from the healed incision about the middle of October 1948.

“Soon Judy began to gain weight and her abdomen rapidly reduced in size and became more soft and pliant so that she could breathe better. The hard growth receded toward the lower right side. By December 25, 1948, she had a healthy and normal appearance as the pictures mentioned before show, but some traces of the growth remained.

“Later, about May 12, 1949, I had her examined by a doctor in Paris, Texas. He could find nothing, after which he was told of the baby’s former illness and he could still find no trouble.

“On November 11, 1949, Judy and her mother appeared before a group of physicians and surgeons especially interested in cancer who met at the Blackstone Hotel in Fort Worth, Texas. While before this group, more than one doctor examined Judy and nothing was found wrong with her.

“On February 18, 1950, both parents and Judy attended a meeting of physicians at Tampa, Florida. Here Judy was again shown to the group of doctors. These were most friendly to the Koch Treatment. Judy is now past two years old. She has shown a normal growth and development, normal mental development, and absolutely no abnormalities that we are aware of. She is very active, mischievous, and friendly. She has had practically no illness after taking the Koch Treatment and recovering from cancer.” These statements by Judy’s parents are signed and notarized.

Dr. M---- sent a more technical account, which adds nothing to the facts given by the mother. This mother’s report should be studied. The observations are well made, and any physician who is experienced, can get a great deal of information out of them. The steady progress of the pretreatment period is plainly established. The manner of absorption of the neoplasm shows it was not of the diffuse type as the next case demonstrates, but was a massive cancer starting in the right lobe of the liver, and of very high (grade IV) malignancy no doubt. The block in the portal circulation was not due to destruction of the vein, but to simple pressure, and the quick relief had, shows also in the better bowel and kidney action as the massive growth underwent absorption. This case should be compared with Case No. 15, “Diffuse Type Primary Cancer of the Liver.”


No. 1.  Taken before the injection, September 18, 1948.


No. II. Taken at the time of the Treatment September 18, 1948.


No. III. Taken several weeks after Treatment.

No. IV. Taken a few weeks later.

No. V. Six months after Treatment.
 

No. VI. Taken a year later.


   No. VII. Taken a few years later.
         
No. VIII. Taken September 1960, twelve years after Treatment.

DIFFUSE TYPE PRIMARY CANCER OF THE LIVER

CASE No. 15       
Prof. R. S. L.

Mr. Geraldo A., early in March 1941, showed loss of appetite, progressive loss in weight and weakness. Dr. O. A. L. examined him and found a large tumor in the abdomen. The patient was conveyed to Rio de Janeiro and placed in the hospital of the Beneficiencia Portuguese where he was operated by Professors R. L. and J. M. G. and helped by the assistant physician. Laparotomy disclosed an extensive neoplasm of the liver that had infiltrated the colon extensively. So extensive were the infiltrations and so widely had it spread, the operators decided it was impossible to give any surgical aid. Further, the type of liver cancer was so definite it was not necessary to remove a biopsy to add to the information already provided by the laparotomy findings.

The writer examined the patient together with his surgeons and Prof. R. S. L. seven days later. The patient could not turn in bed, was vomiting black bile or blood continuously, could not eat, and was of a dark jaundice color, very thin, in fact so emaciated that one could feel the diffuse nodules over the whole liver surface as it bulged forward and extended down into the pelvis. His doctors said he might live a week or two but certainly not longer.

We gave him an injection of a Parabenzoquinone solution, 2cc. containing two micrograms in solution, on July 15, 1941. The patient, who up to that time had been showing only a light fever, had a severe chill three days later, and a fever of 39°C. On July 25th, he belched much gas, and had intense gastric pain for only a short time. The tumor steadily absorbed, and concomitantly his weight and strength returned. The jaundice faded and he gained 20 pounds in weight, was able to walk, and returned to his home in Barbacena where his health gradually returned. On October 3rd, he had another reaction with a chill and fever of 39°C., and a general oedema was shown. Everything yielded spontaneously, and the patient gaining then over 40 pounds had completely recovered and was back to work. The report in April 1953, and again in 1955 shows he is still in excellent health and cured.

CANCER OF THE STOMACH

CASE No. 16

Mr. Wesley R. had a past history of severe gastric ulcer from 35 years of age until he reached 50. When he was 69 he had a more serious stomach trouble — pain and vomiting, with rapid emaciation, and loss of strength. Pyloric obstruction became complete. Several physicians made examination and found a tumor at the pyloric region. Dr. Demling operated him on June 28, 1926. A gastroenterostomy was done and a part of the tumor removed.  The pathological report follows:


It is evident from this pathological report that the whole neoplasm was not removed and this is confirmed by the early recurrence of obstruction by the neoplasm.

Improvement was noted for only a few weeks and then the trouble recurred with more pain than ever and constant vomiting, rapid emaciation and cachexia. Dr. Harrison brought him to me on August 20, 1926. My examination revealed a large fixed tumor mass filling the epigastrium and extending below the level of the umbilicus. It was fixed to the liver, and bulged outward so as to be plainly visible and caused practically complete obstruction of the gastric outlet. The supraclavicular space on the left side showed a fixed lymphatic tumor as large as a walnut. There was considerable hemolysis. One dose of the serial systems of Carbonyl groups was given and recovery set in so that its effects were observed in a few weeks. The obstruction soon disappeared and he regained about twenty pounds to reach his normal weight in five months. Examination after the twenty-fourth week revealed no tumefaction. Radiographs show no tumefaction, but a stomach about one-third normal size, motility good. Only at the third, twelfth and twenty-fourth week periods were there reactions of note. Fever, tenderness in the stomach, loss of appetite, and a general achiness lasted about three days and then a much more pronounced improvement set in after each reaction. This improvement continued until full recovery was established. He has not had any stomach trouble since and enjoys vigorous health, works every day and walks to town in all sorts of weather as well as he did at fifty years of age. We heard from him last when he was 92 years of age and in good health, 23 years after Treatment. Certainly the restoration of the Survival chemistry was satisfactory in this case.

CANCER OF THE STOMACH


CASE No. 17 

Dr. W. Mantor

This was a case of cancer of the stomach equally far advanced as the former. His trouble started as indigestion in 1940. Radiographs revealed no pathology then. It soon changed to a progressive stomach complaint with constant pain and frequent vomiting, rapid loss of strength, and a weight loss from 150 to 120 pounds in less than a year. Several well-reputed clinics were tried in this year but the disease progressed. Radiographs made May 12, 1941, at the Tyler Clinic at Omaha gave a firm diagnosis of cancer of the stomach. At least two-thirds of the stomach wall was involved as the plates show. Exploratory operation at the Mayo Clinic within a week revealed massive involvement of the stomach wall, the pancreas, the glands about the aorta, and the liver. The supra clavicular glands of the left side were also involved. They gave a diagnosis of far advanced cancer, primary in the stomach, entirely inoperable, and hopeless, and sent him home.





On June 16 he was carried into Dr. Mantor’s office for Treatment. Dr. Mantor’s description includes the following, “extreme exhaustion, anemia, hemolysis, cachexia. No crenation of red blood cells in a one percent NaCl solution (all should crenate). Linear scar from exploratory operation, massive induration of the epigastrium, readily palpable and bulging forward so one could see it easily as he lay down. Since one year previously an X-ray of the stomach showed no pathology whatsoever, this neoplasm was very malignant and rapidly progressive and destructive.”

One injection of 2 cc. of the 12X dilution of the serial system of Carbonyl groups was given June 16, 1941. In a few days he started to feel better and soon took up the farm he had to leave because of the sickness. Nine weeks after the Treatment, examination could reveal no tumor mass whatever. He had gained weight, color improved, and was more active. By the 12th week, he could walk down the street rapidly without losing his breath and reported he was eating well and was feeling fine. By that time he had been working on his farm. There was no more cachexia. Dr. Mantor gave him a second injection on September 8, 1941, during his 12th week. He continued towards complete recovery. A third injection was given two years later, September 1943.

Radiograph III, taken on June 14, 1944, shows his stomach after complete recovery. He was still well in 1947 when we last heard.
  
Radiograph I, Taken at the Tyler Clinic before treatment.


Radiograph II.  Taken at the Tyler Clinic a few weeks after Treatment
showing marked improvement.


Radiograph III. Taken June 14, 1944, after recovery. 
These radiographs are court exhibits.

The Survival Chemistry of course is concerned with the oxidation of burnable substances for energy production. Fuels and disease producing toxins, which come within its O/R potential ranges, are destroyed. The energy is used for doing work in the performance of function, and for the growth and repair. One can estimate the thoroughness with which the FCG system is restored by the rate of tissue reconstruction after the most devastating of cancers. The following two cases will illustrate.
  
METASTATIC CANCER OF THE BOWEL

CASE No. 18 
Dr. F. Richards

Mr. J. K. was 42 years old when X-Ray studies and exploratory operation showed widely metastasizing cancer of the splenic flexure of the colon, which caused complete obstruction. A colostomy was made at the Henry Ford Hospital at Detroit. The neoplasm spread rapidly throughout the abdomen and per­forated the abdominal wall in several places as cauliflower growths with central fistulous openings that discharged feces and foul necrotic material. His general health deteriorated rapidly under the toxic strain, and the neoplasms grew proportionately rapidly under the same impulse. He had been a strong mus­cular man of 180 pounds swinging a heavy hammer all day when he took sick, and after the surgical aid he lost to 135 pounds, and kept on losing. The necrotic tissue in the abdominal wall had such a terrible odor it was necessary to slice away the most gangrenous part, and cauterize the borders to block the bleeding. The cauliflower fistulae took on greater speed thereafter. He was sent home to die, his case being entirely hopeless. On the way home he was examined at our clinic. Dr. Richards gave him an injection of the SSR Reagent on April 3, 1942. At this time the cauliflower growths were from 4 to 8 centimeters in diameter and equally high. During the following three weeks he did not show much improvement. Then he took a heavy reaction with such great congestion of the exposed cancer masses that another injection had to be given. The second Treatment was given at the beginning of the fourth week. Thereafter the bleeding quickly stopped and his whole condition rapidly improved. The cauliflower masses melted away and the abdomen was healed without leaving a visible scar. Palpation could reveal no more tumor masses after four more months. His bowels started to move normally through the rectum, and the colostomy stopped functioning. He gained weight to 113 pounds in June, and to 180 pounds in September when we sent him back to the Ford Hospital for repair of the colostomy, after he had returned to work a few weeks earlier.



This X-Ray was taken of Mr. J. K. on December 27, 1941 before Treatment.

His liver and other FCG’s that had been blocked by the carcinogen certainly went back to work for him, for he not only could digest food efficiently but was able to build up his tissue at the same time.  His gain is shown in part in the Ford Hospital records as noted by Dr. Bohr. For the month of July, the record notes that he gained from 113 pounds at the first of the month to 175 pounds at the end of the month, that is a gain of 62 pounds in a month, or just two pounds or one kilo per day. This gain, we must add, was made on our vegetable, fruits and cereal diet, without any meat or animal proteins. The Ford Hospital documents, that were part of the Official Court Record, are worth studying. Some are appended. This gain in good solid flesh and blood on a vegetarian diet is not just an incident in this case. It is our experience, and meat eaters who cannot curb their appetites for animal food, should give these facts some consideration.

The following significant statements are taken from the Henry Ford Hospital record, the interval history taken by Dr. Bohr on August 28, 1942. “Patient left hospital April 1 of this year with a diagnosis of fungating Cancer of Colon and a terminal prognosis. On the way home that day, he received one of Dr. Koch’s ‘Cancer Cure Shots.’ . . . On July 1 he weighed 113 pounds, but from that time on he began feeling stronger and gained weight. By the middle of July, his wound was completely healed. His weight was 175 pounds at the end of July and he has maintained this weight ever since.  He enters the hospital now, after being back to work for three weeks, for the first stage in a colostomy closure.”

This patient was examined at the Ford Hospital every year for many years and always found well. When last heard from he was still well. The radiographs show the obstruction of the bowel during the first weeks of his illness. The radiographs made after recovery are the same as any normal person’s. No adhesions or other sequelae are found, showing that the disease that existed formerly no longer exists.

What the Case Teaches:

Firstly, the Ford Hospital “General Memo” tells that they could not enter the abdomen to attempt a resection of the growth as it had infiltrated through out and invaded the abdominal wall throughout. When one considers the position of the splenic flexure of the colon, back against the posterior abdominal wall and diaphragm, the distance to the umbilicus is twelve or more inches and as it had finally ruptured through the belly wall in three different places as large cauliflower fistulous growths, the amount of involvement was about total. It is important to realize this and also that the amount of infection, throughout the whole neoplastic involvement, was tremendous. Fecal fistulas always heal with a great amount of scarring and distortion and epidermal change consequent thereto. But in this case there was no scar left, nor epidermal change left to mark the areas of neoplastic or infectious involvement. The abdomen wall healed right through the skin without leaving a mark. The abdomen looked as clear as any normal baby’s that had never been sick. Just as the bowel function was restored so the colostomy became obsolete. So too, the only sequelae to the neoplasm were completely restored structure and function.

To the regular physician this fact is not comprehensible, and indeed if the other patients to be demonstrated here did not do likewise, one would scarcely have the courage to make this report. There is an explanation, however, and the case is offered with others as a demonstration of this explanatory observation. It is this. The recoveries in these cases after the SSR is used are different from those that take place under the flux of regular ordinary healing. This is due to the fact that after the SSR does its work no toxin, either carcinogenic or from a disease’s germs, is integrated with the protective fibrosis or the cancer cells.Before the SSR was used the toxin content was tremendous, if the odor, cachexia and rapid tissue destruction mean anything. The state of integration as we explain here, and in the Appendix, actually invited oxidative destruction of the toxins of all types, so that the fibrosis and cancer cells became obsolete and were absorbed by the ordinary autolytic procedures, so that nothing was left to interfere with normal tissue reconstruction. So normal reconstruction was not prevented and the normal rectifying tendency had full sway. It is such an observation, so often repeated, that makes one think that the normal state of man was such that he did, at one time in his perfect state, really possess an FCG of the order of the SSR or even more efficient.

SARCOMA OF THE UTERUS


CASE No. 19

Mrs. McA., aged 43, was first seen on July 29, 1929. She was bedfast, emaciated, and exhausted. She had not rallied well from an abdominal exploration done by a very good surgeon two weeks previously to ascertain the cause of severe and frequent crises of vomiting and pain in the gall bladder region. The abdomen was found widely involved with neoplastic development from deep in the pelvis to the diaphragm, with the stomach, liver, and intervening structures heavily invaded. This was identified as the cause of the pain. A biopsy specimen was removed. The abdomen was closed as inoperable. The surgeon, Dr. Trimby, gave a biopsy report to us personally when he referred the patient. It showed a small round cell sarcoma of high-grade malignancy.
  
Our examination revealed a patient in bed, exhausted with weak pulse, sighing respiration, vascular shock, cyanosis, and an abdomen bulging with tumor masses, particularly on the lower left side. The liver and epigastric involvement could be readily palpated besides. The incision was not healed and appeared to be infiltrated with neoplastic extensions. This incision was made over the largest tumefaction within and it seemed that the neoplastic tissue underneath had invaded the abdominal wall. A photograph was taken and 2 micro micrograms of the Synthetic Survival Reagent were given.

She responded well up to the sixth week, gaining in strength and becoming rapidly free of the pain and vomiting attacks. However, at the beginning of the sixth week she started a reaction that continued to the middle of the ninth week.

It featured vomiting of a quite continuous nature whether she took food or not. No food was held. The pain feature that was so severe before Treatment was a minor matter, however. She lost weight and strength, and the dehydration was difficult to overcome. However, with the closing of the reaction at the middle of the ninth week she became very hungry and took on weight rapidly. For a few weeks she gained at the rate of five pounds a week, then at the rate of two pounds a week until she had reached 180 pounds. A slow gain followed to 200 pounds and then a slow loss to 180 pounds. Her health was fully established. All the tumefactions had disappeared before the end of the twelfth week after the Treatment.  She is still in perfect health, according to our last report.

  

Photograph II, Taken after neoplasms were absorbed.

Another way to estimate the restoration of FCG activity is in the cure of Leukemia. Here in the terminal phases, the exhaustion of the blood forming organs can be so complete that leukopenia instead of the former leukocytosis is observed. The FCG’s required for cell construction are blocked, no doubt, by the carcinogen and both the red cell count and the white cell count are not able to be restored until the FCG’s are liberated and can go back to work again. The following cases are illustrative. Here the bad effects of irradiation are to be observed as well as those of the natural carcinogen. One might compare the response in a natural case of acute lymphatic leukemia with other cases that have been irradiated, or have reached the point of exhaustion and impending death. These latter states are about the same, showing how irradiation works on the blood forming organs. It kills them, as does the natural pathogen. Red and white blood cell restoration demonstrates FCG restoration.
  

ACUTE LYMPHATIC LEUKEMIA IN A BOY


CASE No. 20 
Dr. A. Guzman

P. F., age 12 years, treated January 8, 1956, by Dr. Guzman. His family history denied leukemia. The onset in the boy was rather rapid after a period of ill health. The symptoms were classical with petechial hemorrhages under the skin and in the mouth, cough, symptoms of anemia with great weakness. The red cell count was 1,500,000, the white were 232,000, lymphocytes in very great predominance, large mononoclonals and immature forms. The physical examination showed a blanched out boy with hemorrhagic spots of various sizes under the skin generally, especially the legs, arms and body. The gums bled, and the breath was foul. The mediastinal dullness was increased mostly to the right. The spleen and lymph glands were only moderately enlarged. He had a cough, was very weak and showed fever.

The injection of the Synthetic Survival Reagent was given, 2cc. of the 10-(12) solution. He was put on a supportive vegetarian diet. The recovery was steady with periodic reactions of chills and fever, general achiness, etc., as characterizes the recoveries under this Treatment.

The results showed in an improvement after each reaction until in August 1956, he was completely well. There were no signs of the disease left. The hemorrhagic spots had disappeared and the mouth was clear, the breath clean. The spleen and lymph glands were no longer enlarged. The spleen could not be palpated, and he was strong, had gained a normal weight and nutrition, etc. His platelets count was then 350,000, the red cells 5,100,000, white cells 7,200, polymorphs 76%. The coagulation time was normal. The only reaction of a focal nature was a sore throat, and that in a boy is difficult to interpret. However, it might mean that this was the site of the pathogenic toxin or virus production. This is especially suspicious, since the mediastinal glands were enlarged and the mediastinal dullness returned to normal with the recovery.
  
LYMPHATIC LEUKEMIA WITH TERMINAL EXHAUSTION

CASE No. 21                                                  
Dr. Julian Baldor

Teddy S., age 14 years, in February, 1949, when treated by Dr. Baldor. He was referred by Dr. C with the report, “Chronic leukemia (proved by bone marrow biopsy) with hemorrhagic diathesis.” The exhaustion of the blood forming organs was seen in the fall in the blood count of whites to only 15,000, while the hemoglobin was 40% and the red cell count 2,150,000. His first diagnosis of leukemia was made six months previously from the high lymphocyte count, the hemorrhages under the skin and the gums, the weakness, enlarged spleen and lymph glands, the fever, pains in his legs and arms and the anemia. He was given 57 blood transfusions. These pepped him up a little at the start, but soon were found to be less effective and finally to be of no help at all. In fact, they were wasted on him. It was then he was sent to Dr. Baldor for the Koch Treatment.

Dr. Baldor’s examination showed an exhausted bleached-out boy, suffering with pain and fright, depressed, unable to walk, with an offensive odor from the mouth, profuse gingival bleeding, and generalized hemorrhagic spots under the skin. The mediastinal dullness was definitely enlarged and so also were the lymph glands generally increased with tubular breathing in the right lung base, and moist rales over the entire field. The liver and spleen were enlarged and tender. He was put on fruit juices and intestinal lavage for two days and then given 2 cc. of the SSR serial system of Carbonyl groups. The fever at the time was 102°F.

In a week he was sent home with a normal temperature. The spleen and liver were reduced in size, but not yet normal, the bloody patches had changed from a dark purple to a greenish color, and no new ones had formed. They then turned to yellow and finally disappeared. Nine weeks later he returned to Dr. Baldor for a check-up. He was able to walk and had gained 12 pounds in weight. The blood picture was red cells, 3,350,000, hemoglobin 52%, and leukocytes 8,000. At the twelfth week, he gave a reaction showing slight pains in the extremities for a few days, and a little epistaxis. The blood count then showed 4,000,000 red cells, white cells 6,500, hemoglobin 72%. He had gained 25 pounds in weight, felt perfectly normal in all respects: feeling, behavior, and in his physical findings.

It was reported to Dr. Baldor in 1957 that Teddy S. at the age of 21 was examined for military service and classified 1-A. This was seven years after being treated for what normally is a 100% fatal disease, in its terminal stage. Upon knowledge of his full previous medical history, he was re-classified. Dr. Baldor reported at that time that Teddy S. had held the best of health since his recovery, is married and is the father of a robust healthy child.

It is to be noted that after being seen by Dr. Baldor he did not receive even one blood transfusion, but gained in all respects on a vegetarian diet. It might appeal to one that the extreme exhaustion is not only a matter of lack of nutritional elements to support cell function, but even more a lack of energy to perform the functions of work and nutrition. The impediment to the mechanisms concerned blocked all activities including the burning of all sorts of toxins absorbed from the bowel, the mouth, tonsils, etc. Then, with the liberation of the tissue’s FCG systems, every impediment was burned out of the way and was kept out of the way thereafter.

MYELOGENOUS LEUKEMIA WITH IRRADIATION LEUKOPENIA IN AN ADULT

CASE No. 22 

Dr. Julian Baldor

Mrs. J. W. L., age 47 years, came on December 7th, 1948. She gives a history of an acute process with chills, fever, nausea and perspiration, six months previously following an influenza attack. Examination showed enlarged liver, enlarged spleen and enlarged cervical glands. The breath was offensive and the gums were bleeding. Some dental abscesses were present. Her blood picture showed red cells, 3,160,000, hemoglobin 57% and white count, 14,800, ploys, 88%, lymphocytes 10%, monocytes 2%. Both myelocytes and premyelo cytes were present.

She had received two courses of X-Rays over the spleen and long bones, each of 600 R at an interval of 6 weeks. This did not improve her condition. The bleeding, weakness, fever and pains continued getting worse. Bone marrow slides showed definite abnormalities suggestive of Myelogenous Leukemia.

Because of the irradiation two doses of the SSR Reagent were given, one on December 13, 1948, and the other five days later. The improvement was prompt. The fever had left in five days. The enormous spleen that reached to the left iliac region, and the enlarged liver showed improvement and were less painful. The oral bleeding and infection likewise cleared up. The blood count March 15, 1949, showed red cells 3,850,000, hemoglobin 69% and leukocytes 8,500. Up to August 5, 1949, she gained ten pounds in weight. On June 16, 1949, the red cell count was 4,000,000, hemoglobin 72% and white cells 7,000. The chest signs improved slowly. By the end of 1950 her enormous spleen had receded to its normal position under the left ribs. The last blood count was taken May 1955 and showed red cells 4,150,000, hemoglobin 70% and leukocytes 3,500. She remains well.

This patient, like the others, was not given one blood transfusion after the SSR Treatment was started, and she improved on a strict vegetarian diet. Here the destructive effect of the X-Rays on the blood forming organs is easily seen, and the recovery of blood production could be better. The hemoglobin was only 70% when it should have been 80% or better and the white cell count could have been a thousand or two more. Thus the injury to the blood forming organs is not entirely corrected, and never will be, in line with our experience with the effects of irradiation. However, the gains made under this handicap when the FCG function is restored are well shown in this series of cases.

One should contrast these cases with the recovery from a slowly developing fatal form of bone sarcoma. Here it will appear that the rate of recovery is a function of the rate of development of the disease. It will be seen also that in the healing of the bone, the tissue is made much more dense and stronger than before the disease attacked it. Blood reconstruction is of this order, too.

ENDOTHELIAL SARCOMA OF THE BONE


CASE No. 23


Mr. Harold B. was age 41 in September 1934, when he appeared for Treatment. He first noticed trouble with the right arm when he threw a ball some weeks previously. His family physician took some X-Rays and noted the sarcomatous status and sent him to the University of Michigan Hospital for thorough attention. The pain in the arm was sufficient to prevent its use, and motion was limited because of a hard swelling over the scapula. The X-Ray studies, blood studies and biopsies of soft and bone tissues led to the final diagnosis of Endothelial Cell Sarcoma of the bone. To reach this diagnosis, Paget’s disease, all other bone tumors were definitely eliminated.   They gave him a hopeless prognosis since this type of sarcoma is always progressive and fatal, no matter how it is treated, but they offered to remove the whole shoulder girdle, if he wished. He refused and presented himself for our attention instead.


Our examination, made September 17, 1934, showed a lame right arm, a fist size mass over the spine of the scapula firmly fixed, and a walnut size mass closer to the dorsal spine and of the same texture as the other mass. Both were fixed to the underlying structures. There was some cachexia, but no tumor could be found in the abdomen or anywhere else. The X-Rays showed bone destruction extensively of the humerus and scapula, and neoplastic devel opment between the two. The progress of the disease was slow and steady. The etiological factors as well as the tumor products were poisoning him, following a downgraded course.



The Synthetic Survival Reagent (SSR) was given in a dose of 2 cc. of the 10-(12) solution. There was no immediate sharp reaction, that is, in the next few days. The major reactions were at the 24th and 36th weeks. But he continued to improve slowly from the start. It took a few months to be able to use the arm without pain. In a year the tumors were completely absorbed, and an X-Ray showed nearly complete recovery in the bone, with considerably more denseness in bone structure. He was able to return to work and made a full recovery. Our next chance to make a radiograph was when he appeared in Detroit to testify for us in the Federal Court. The X-Ray made then showed full recovery and is reproduced here. He has remained well. Our last report was received in 1950. Ewing’s estimate of this disease is as follows, page 361, 1942 edition, Text Book on Cancer:

“Angioendothelioma, multiple endothelioma, diffuse endothelioma, or endothelial myeloma, the entire group, is characterized by predilection for the bone shaft, a tendency to multiplicity, a cellular and vascular structure, marked osteolytic properties, failure to produce tumor bone, and a relatively slow but fatal course.”

Radiograph I.  showing condition before Treatment.


  
 Radiograph II, showing condition after full recovery.

This relatively slow course as seen both in the progress of the disease, its cure and in the recovery process in the leukemia cases just given should be contrasted with the cases of J. K. and Mrs. MacA.

The University of Michigan records selected from the court records give the details sufficiently for a working idea. This record, like those of the other cases cited is voluminous. All other details are available to anyone who desires them. The radiographs should be studied also. The fact that the tumor is not confined to the bone but has grown between the bones and out over the shoulder shows it is not Paget’s disease. One should note this in the radiographs.

RECURRENT METASTASIZED CANCER OF THE PALATE FOLLOWING SURGERY

CASE No. 24


Mr. A. J., age 60 years, was first seen by us on December 1, 1932. He gave a history of an attempt to remove one large and a few small growths from the hard and soft palates, by excision and touch-up cautery at the University of Michigan Hospital on October 15, 1931. The areas healed and all was well for a few months. Then the same type of growth reappeared over a wider area of the palate and enlargements formed in the neck and under the jaw. These were deeply fixed. The palate was well covered at the time of our examination. The large growth had returned with a dozen smaller ones around about it. The biopsy was squamous cell cancer.

We gave him the Survival Reagent injection and three days later he experienced a typical reaction. Generally a highly malignant cancer will give a recovery reaction twelve or twenty-four hours after the treatment is given and in the less malignant types as this one, the actions come as late as 72 or 84 hours after Treatment. But the symptoms are the same, namely a general achiness, chills and fever. All patients describe their reactions much alike, so we will give Mr. J’s description as an example. His Testimony stated, “About the third day I felt pretty badly. I became cold. I thought I was going to freeze. My wife put me in bed. We had the hot water bottles and about all the blankets we had to cover the bed with on me. It lasted possibly an hour. About three weeks from that time I had another cold spell, and for about six months, I believe, every three weeks, but they kept getting lighter.” The physical examination and careful questioning did not reveal any focus of infection, that contributed the toxin that excited the neoplastic change, as is so common in other cases. This case was probably a general viral infection.


After six months, no trace of any growth in the mouth, or in the neck, or under the jaw could be palpated. He remained well until a few years ago. It was reported he died of a stroke. He was then over 80 years old. There was no examination of the body to get the facts, however, only rumor.

In this case, as in so many that are biopsied or operated on, the recurrent growths are of a higher grade malignancy than when first touched with a knife, and that appears to be the case here, since the recurrence was rapid and the reactions so intense, though they came three days after the Treatment.

SARCOMA OF THE SPLEEN


CASE No. 25 
Dr. J. W. Kannel

B. G. was 6 years old when she was attacked with pain in the stomach and some fever. She had been experiencing an increasing difficulty in breathing for some weeks previously. Examination by Dr. J. W. Kannel revealed an enlarged spleen, enlarged axillary and inguinal lymph nodes, and a white cell count of 7,200. A few days later, June 23, 1943, the white cell count rose to 16,700, and on June 24th, it was 22,400. The aspect of the child was that of one very seriously sick. He immediately did an exploratory laparotomy, and found the spleen so greatly enlarged that it had compressed two-thirds of the left lung and had grown out against the intercostal muscles in ridges, so as to leave impressions of the ribs in between. The gross pathology was pathognomonic sarcoma of the spleen. It would have served as a good museum piece. It was besides, very hard and nodular, which is the case with spleen sarcoma. If it were an infection, it would have been soft and pliable. So the high white cell count was due to reticulo-endothelial disease, comparable to the high lymphocyte count in leukemia. Moreover, no abscess was found to account for the leukocytosis or the fever, which after all are characteristic of acute forms of cancer.  Dr. Kannel did not do a biopsy, as he felt there was too much risk of causing uncontrollable hemorrhage or embolism because of the vascular structure of the organ, and because the gross findings were absolutely diagnostic without microscopic aid.  Thus, his knowledge saved the patient from possible death resulting from embolism or hemorrhage.

On July 2, 1943, she was given 2 micro micrograms of the SSR and her recovery was gradual and steady until it was complete. The breathing became normal and so did the breath sounds. The projection of the spleen down into the abdomen 2 inches gradually subsided until it was of normal size. Her health became normal and so remains so far as we know. The last report was in 1956. One sees that the disease was corrected, and the straying tissues were normalized. The cause was removed right at its point of attack on the vital structure.

 

LYMPHOSARCOMA CASES


The call for lymphocytes to fight the toxins of chronic infection is standard experience. Though, the neoplastic hyperplasia no doubt had a protective purpose to start with (the reticulo-endothelial system always leads the combat against cancer) this type of hyperplasia does not accomplish any protection. It injures the patient just like the excessive production of poorly evolved thyroid secretion in Case No. I., the toxic nodular goitre case. No doubt the interference with function was a matter of Carbonyl group block, as it was in the goitre cases, and so if this is true, the use of the Survival Synthetic Carbonyl Remedy should restore the normal functional efficiency of protection and the normal mitotic process. A few cases of different types of lymphocytic cell lymphosarcoma are given to illustrate the disappearance of neoplastic mitosis and the restoration of protection. This is seen in the return of the regular health and disappearance of the pre-growth signs and symptoms similarly in lymphosarcoma, as in the other forms of cancer.

It is the consensus, that lymphosarcoma is a generalized disease and indeed most cases, when seen first by us, showed generalized tumefaction of all palpable lymph nodes, increased dullness of the mediastinum, and great enlargement of the mesenteric glands. However, there is a type that grows up rapidly in one region without showing great involvement of other areas. This is the type that is most rapidly fatal and may indeed kill in a few months, after the onset. Such a case is the following:
  

LYMPHOSARCOMA


CASE No. 26 
Dr. J. W. Kannel

Miss L. M., age 31, came under Dr. Kannel’s care in July 1925. Physical examination showed a tumor as large as a large orange involving the upper outer quadrant of the right breast and the axilla, which was completely and deeply involved. He removed most of the breast portion, but found the axillary development too deep to extirpate and left it in situs. The microscopic examina tion showed it to be a malignant lymphosarcoma. This tissue is not derived from the breast tissue itself, but seems to have its origin in lymphoid tissue. Characteristic of this type of lymphosarcoma, cachexia was developing rapidly, so Dr. Kannel prepared her for the Survival Reagent Treatment, and gave the injection on July 16,1925. The presence of cachexia shows the extremely toxic status of the patient, both from the pathogenic toxin and from the products of the neoplasm intended to be protective, but which were toxic as the thyroid secretion in Case I.

Following the Reagent, there was rapid absorption of the axillary and other extensions of the neoplasm, with a simultaneously quick recovery from the cachectic state. She remained well until 1931, when a lump appeared in the left breast the size of one’s thumb. It grew rapidly also, as a heavily infiltrating mass. It was removed by Dr. Kannel and diagnosed as a lymphosarcoma from the gross pathological features. She was given another dose of the same Reagent, recovered, and remained well thereafter, and on last examination in April, 1946, twenty-one years after Treatment, was still found well.

This experience plus the one that follows, shows that the cause of the neoplastic effort may return in the course of years, or maybe was removed by the Treatment sufficiently to reverse the neoplastic effort, and still a seed of the cause, — an old infection in an anoxic scar, might have still escaped complete removal. Later on the cause grew to pathogenic proportions, and started trouble again. This means that the Therapy should have been repeated a year or so after, or even three years after the first neoplasm was cured, to make sure the cause was fully removed. In this case, the infected scar was not identified. If it were it could have been removed and cultured, for further information. At any rate, the dose should have been repeated before any further trouble could start. The case shows that the second Treatment was just as effective as the first, and no resistance is built up to it.

LYMPHOSARCOMA, LYMPHOCYTE CELL TYPE

CASE No. 27

Mrs. M. S., 38 years old, came under my observation on October 27, 1944. She gave a history of a persistent crop of axillary boils that cleared up on an autogenous vaccine, but no other remedy or antibiotics helped. These appeared in April 1943, and persisted for nearly a year. During the latter part of this period the right side of her neck became stiff and painful. She could not stand a draft of air on it. Every diligent effort at treatment failed. Instead, swelling and stiffness developed and advanced deeply into the pharynx. In this bewildering condition, she stepped on a nail and sustained a severe infection of the foot. The condition in the neck became much worse then. A mass as big as an apple developed, involving the neck structures on the right side. Biopsy done October 14, 1944, and examined by several good pathologists confirmed the diagnosis of lymphocytic cell type lymphosarcoma.

Two weeks later my examination revealed a marked cachexia, and wide involvement of the palpable lymphatic system, axillary, groin and a large mass behind the umbilicus. It bulged, was hard and fixed, and could be observed on inspection.


The mass in the neck that was biopsied was 5x7 cms. in its diameters, and had infiltrated the surrounding structures even into the inside of the throat, and bulged greatly on the outside.

She received 2 cc. of the Synthetic Survival Reagent at 11 p.m. that night, and the recovery reactions started at 2 p.m. the next afternoon. Chills, fever and a general achiness as from the grippe accompanied by a relaxing of the stiffness in the neck were evident through the following three weeks. Her cachexia disappeared and her well being was being re-established. All of the neoplastic masses improved in the same way. By the end of the third week, the stiffness and swallowing difficulty was fully overcome. In three months, no more tumors could be palpated. However, her reactions were repeated at the regular periods of three months, that is the 24th, the 36th, the 72nd, the 84th, and 96th weeks and even later, and her health improved after each, in spite of the fact that her health had become much better than was normal for her, even as early as the twelfth week. Besides taking care of a large house and her family, she was able to work in a clothing shop, and carry on her social affairs. Following the absorption of the growths, there was no sudden reaction in the old site of the boils or the foot infection, as would be expected had they contributed the etiological agent. Instead, she showed a reaction in the tonsil area that presented the characteristics of a keloid. This came ten years after the cure of the lymphosarcoma. She was given a different remedy at this time, dipheno quinone, but its action was too slow. Within a year a pain in the dorsal spine developed as she had had for many years off and on since an automobile accident, some twenty years earlier. The radiographic studies by a well-respected expert gave a diagnosis of an old lesion of maybe thirty years’ standing. There was a history of suspected tuberculosis in early life, so, as a keloid is a response to tubercular toxins, and the old bone lesion that resembled a tubercular affair became evident as a reaction, our conclusion was that the lymphosarcoma was caused by the toxins of an old tuberculosis that had been suppressed.

The writer’s services were not available to her at the time, and she yielded to the persuasions of a radiologist, and took intensive X-Ray over the spine and the neck. In August 1959 she died.

In this case, a therapeutic fact was learned as in the former case of lympho sarcoma. Since lymphomas are primary protective in their intentions, one should give repeated doses every few years, a few times until there is no vestige of the exciting cause left in the system. Had this been done, this patient probably would have had no more trouble.

LYMPHOSARCOMA, LYMPHOCYTIC CELL TYPE

CASE No. 28



Mrs. G. G., age 40, at the time of Treatment with the Survival Reagent on May 17, 1937, came for our Treatment for a rapidly developing mass on the back of her neck, toward the right side. A biopsy had been made of an enlarging gland in that location three weeks previously, when it started to grow rapidly. The microscopic diagnosis was lymphocytic cell lymphosarcoma. At the time of our examination, the scar region had become tumorous and several smaller tumors had also developed in the area. The largest was the size of the ball of one’s thumb, or an English walnut, but was deeply infiltrated. She was ill and toxic, even in spite of the cleansing regime she had followed for a week before the Treatment was given. Two cc. of the 10-(12) concentration of the Survival Reagent was injected in the upper arm. At her visit four weeks later, the whole area had normalized. No vestige of any neoplasms could be found. Her normal health had also returned and she remained well until she was killed in an automobile accident seven years later. An autopsy established that there was no trace of any neoplasm to be found, so we can assume that she was cured even without a repetition of the dose. The exciting cause was not identified in this case and no one knows if or not some interesting manifestation would have showed up later, had she not had the accident.

 

CANCER OF THE BREAST


The resting breast is especially prone to take on malignant change. It has plenty of FCG structures, but they are inactive and not carrying on the oxidative functions of a working tissue. The circulation has no aid as occurs in muscle containing organs where contractions pump the blood along and move the lymph, thus aiding the metabolic exchanges and extending the equilibrium point of enzymatic reactions. A blow on the breast therefore produces a dangerous injury that can interrupt the circulation and create an anoxic area much easier than in a tissue with an active circulation. Blows need not be very hard to bring about the unfavorable change, and indeed after the tumor has developed, the trauma incident to vigorous physical examination by palpation may step up the malignancy of the lesion most dangerously. For this reason America’s great diagnostician, Cullen, recommends very clever means of inspection for demonstrating the malignant infiltrations, and thus avoids the need of adverse amount of palpation. Great pressure tugging on the growth, etc., are vigorously condemned. Cullen considers even the needle biopsy dangerous. Great care, then, is used in making the examination in breast cases. The various types are so characteristic that in most cases inspection alone should settle the diagnosis, when the growth is well established.

To return the breast cancer cell to a normal functional status when it is not at work because of the normal lactogenic stimuli seems a little paradoxical. However, the restoration of the FCG does not necessarily mean it has to produce milk, but only that its impediment that blocks its dehydrogenating power is removed. When the energy producing and energy receiving Carbonyl groups are freed and able to function normally, no energy is shunted vicariously into the mitotic mechanisms to produce neoplasia.

In breast cases, the great problem is early diagnosis to give the surgeon a chance, but as the vast majority of cases are well metastasized before the lump is discovered, its early total removal by simple resection is the logical procedure to give the patient every possible chance, and then correct the Survival chemistry and teach the victim how to live.

When the breast case is under the Koch Treatment, the affected area must be kept warm. Internal cancer has a better chance to recover because of the natural normal temperature that is sustained. Breast cancer must be well covered, and must also be protected from strong sunlight, perfumes and powders women usually use. Then the examinations must be made with care, as the fine blood vessels that grow up into the coagulated and digesting mass are indeed very delicate and are easily injured. Hemorrhage at the point of vascular rupture complicates the situation, as the circulation is cut off and an excellent medium for infection is created. The continuance of the digestive process is blocked also, and one has a bad situation that may limit the recovery process at this point of injury, and indeed may prove to be the starting point for a reversal of the recovery. The patient’s responsibility for protecting the breast is a matter that must be emphasized. Of course, the physicians of experience will know what type of patient needs this advice most and will illustrate the need of care by his own manner of examination with care.

CARCINOMA SIMPLEX

CASE No. 29      

Prof. R. S. L.

Miss C. F., age 50 years, Brazilian, referred by Prof. A. P. on November 17, 1941, was suffering with a painful tumor of the right breast for six months. It was considered inoperable, and 12 applications of deep X-Ray therapy were given. It continued to grow and become more painful. The nipple was already retracted, and the skin hard and infiltrated, and the whole mass was fixed to the chest wall, making it immovable to touch or by change of position, as on stooping or leaning to the side. It had become the size of a large fist. Two micrograms of Parabenzoquinone were given on November 17, 1941, intramuscularly. She recovered gradually. But six months later the dose was repeated. One year after Treatment, no tumor could be found and she was considered clinically cured.

SCIRRHUS CANCER OF BREAST


CASE No. 30 
Prof. R. S. L

Mrs. M. S. was 42 years of age and married. She found a lump in the breast in 1938, when living in Lisbon, Portugal. It was removed surgically and diagnosed cancer microscopically. Recurrence was well advanced in 1941, as a large tumor in the same location had developed as early as April, but she was not Treated until on October 14, 1941. She was given two micro grams of Benzoquinone solution intramuscularly. Examination seven months later showed that the tumor had entirely disappeared, leaving a scar isolated and no larger than a grape. Her general condition was excellent.

In the writer’s experience, the hard-calcified residues of digestion of the tumor may be removed for microscopic study. They are found to be composed of calcareous material and some dense fibrous connective tissue without epithelial structure. Right after the malignant status is corrected and calcification starts, they become subjects for removal as vascular in-growth, which may be compared with a blood clot or the casein in milk, undergoes calcification as the first step in its digestion. This is shown in Plate No. I. Then after the digestion and absorption have become complete, stones of the type described in this case may still remain. We have never seen them go malignant again, but their absorption is very slow. Whether they give any protection against cancer is not established, though we thought for a long time that they did.

METASTATIC CANCER OF THE BREAST


CASE No. 31


Miss H. P., age 32, Canadian, was treated with the Serial System of Carbonyl groups with free radical terminals in 1927. She had been operated and the microscopic study showed a grade IV malignancy of the carcinoma simplex type. It had infiltrated the axilla and quickly showed renewed activity there and it had also metastasized to the lungs and over to the right supraclavicular space as a good sized (half egg) fixed tumor. The dyspnoea and chest signs showed heavy involvement of the mediastinum and cough was incessant.

Six months after the Treatment, there were no more symptoms or signs of the disease left. The supraclavicular space was clear, and the chest examination indicated the metastases had been absorbed. The photographs made at the time of Treatment and after recovery. In 1955 we heard from her again, that she is in perfect health and no signs of recurrence have appeared.


CASE No. 32 


Miss G., age 45 in December 1930, when first Treated. These are interest ing cases because they are exceedingly slow to recover and often requiring a year or two to be free of the growth. The most intriguing feature in such cases is that the toxin that causes cancer is fibrogenic, that is, it stimulates fibrosis as we explain later on, and when the fibroblastic response peters out, neoplasia is due to start. The protection offered by fibrogenesis probably is due to the integration of the pathogen with the fibroblastic tissue and its neutralization in that way, so that when fibrogenesis fails, the toxin must add to some other cell structure and this seems to be the mitotic mechanism. In this connection, it is significant that neoplasms came later on in such cases. The photographs tell the story in this case. The second picture was taken after the absorption was complete. It is 30 years since her Treatment was given, and she has not developed any cancer as yet. The photographs were part of the evidence in the U. S. Federal Court.

Photograph I, before Treatment.

Photograph II, after Treatment. The recovery was complete, no vestige of the growth can be found.

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CHAPTER 16


THE TERMINATION OF THE MALIGNANT PHASE,

THE CONSTITUTIONAL NATURE OF CANCER

AND OF THE SURVIVAL FACTOR



We have considerable data on the speed with which the malignant state turns to normal, or is corrected, and the cancer cells are digested and disappear. The biopsy photo in Plate I, shows the calcification and organization of a squamous cell cancer of the skin within a month after Treatment. However, complete microscopic disappearance may take place in less than two weeks as is revealed in the report of Dr. E., a prominent internist, whose daughter was found to have a Grade III squamous cell cancer of the cervix uteri that was deemed inoperable from its state of advancement. She was given a dose of the SSR on June 2, 1957. On June 14th, the examination showed that all of the evidences of the disease had disappeared. There were no extensions into the adnexia and the cervix appeared normal and showed a normal texture. A series of biopsies were then taken from different parts of the cervix to see if any cancer cells could be found on serial sectioning. Every biopsy proved negative. She has remained free of any sign or symptom to date. This is the second case of cancer cured in this physician’s family, both cancers confirmed by biopsy, and the cure fully established.

Twelve days is a short period when one thinks of the long time it takes for a cancer to reach recognizable features, and when one thinks of the years of the pre-growth toxic period that is characteristic. However, we have often observed that the last expression of the recovery process is an acute inflammation of some old focus of infection, as the tonsil on the same side as the breast under our Treatment for cancer. After the growth disappears from the axilla and the breast, the tonsil or a scar located where an infection once existed, lights up with an acute inflammation much like the inflammation that existed there years ago, long before the breast growth came. In about a week, the sore throat or other inflammation normalizes and then the tonsil that was deeply scarred or calcified and fixed becomes loose and pliable. We take this event to mean that the infection that gave rise to the carcinogen was still present in a partly asphyxiated state, elaborating its toxins which polymerized until they reached a carcinogenic structure, and then during the recovery process, a stepwise oxidation of the polymer tore it down through the various stages by which it had been poisoning the patient until it could produce cancer. Now, however, it had reached the monomeric form as produced by the captive germ, and while it was being burned out of the way with its imprisoning scar, this inflammation was going on. This event is the cleaning out of the pathogen of the very inception of the disease. It must be also recalled that each act of the correction process is going on independently in the different cells and regions concerned, and these may occur in parts of the body that are far apart. This is not only because the metastases are spread all about, but because of the distance of the “primary” lesion, the focus of infection that was able to brew the carcinogen because of its hypoxia. One would have to say then that the case is not constitutionally cured until this primary focus was eliminated. However, locally at the site of the cancer growths, wherever they occur, the cure may be complete as shown by the biopsies taken, as in the case just mentioned, even in less than two weeks and is confirmable in five years, as in the case of Mrs. M. W., Case No. 11, by radical biopsy procedures.

However, getting the pathogen out of the way does not mean that some day another may not come along and start trouble again, that is, a new cancer develops or some other fatal condition comes about as in Case No. 11, five years after being cured.

The speed of recovery has an additional significance. It is the last feature of the disease that regularly disappears first, in the reversal of the disease process and this is the malignant change. But as each region that plays a part in the disease is also undergoing recovery at the hands of the SSR independently, the events in the last tumors to come have no direct influence on the events of the first rumors, or of the primary lesion, the scar where the pathogen is brewed.To test out this proposition, we waited for some cases to show the need of getting rid of the necrotic material because of its toxicity and bad odor. The cases shown in the photographs demonstrate that after the SSR starts its work and the absorption of the corrected cells is well under way, manipulation which would regularly stimulate an untreated cancer to metastasize and grow faster and kill quicker, has no such effect. So the recovery process continues on in the extensions, as well as in the primary growth and even in the focus of infection that gave rise to the carcinogen. Both of these patients were permanently cured. The breast case visited in Detroit ten years later and was examined as thoroughly as possible physically. She was found completely well so far as one could tell. In the other case, the melanotic extensions of the growth continued to be absorbed and disappear, while the non-malignant pigmented moles remained unaltered. The independent correction course in each affected cell is thus demonstrated. The time element also speaks for the correctness of polymerization process we assign to the pathogen.

In considering the constitutional nature of cancer and of its correction, one must recall that when cancer is induced by applying chemical carcinogens, the lesion does not show malignancy until the applied pathogen is no longer detectable in the cells undergoing malignant change. It cannot even be detected by spectography, according to Peacock. Neither can it be detected in the blood stream or in the other tissues of the body. It is our opinion, that it is integrated with the cancer cell under the alteration we assign to it. Hence, it would show an entirely different spectrographic character, if it showed any at all, when combined with the cell grana.

The situation should be compared with the clinical fact that while the recovery from cancer is progressing ideally, no trace of the injected SSR can be identified in the bloodstream or other tissues than those where the curative process is going on.


Miss N. after the growth started undergoing digestion after the Carbonyl catalysts were given,
and before crude removal was done.
   

Miss N. after complete recovery.

Mr. L. after Treatment when the growths were undergoing digestion
just before crude removal.   


And here it is identified only by the curative change and not by any spectrographic or other tests. To illustrate a case under Treatment by Dr. Treiger is cited. This patient, age 38 years, developed a carcinoma simplex of the left breast. It was considered inoperable by the referring surgeon as the whole breast was involved including the axillary glands, and the chest wall was invaded so as to cause pleural pain. The nipple was completely retracted and the skin invaded so as to show the “pig-skin” appearance, indicating the high-grade malignancy, mucinous Grade III adenocarcinoma, on biopsy. Seven weeks after one injection of the SSR, and after several strong reactions, the tumor had reduced to the size of a small egg or big plum, was loose, the axilla was clear, the skin normal and the nipple out in normal fashion. There was no more pain and her health had returned very satisfactorily. One would think that she held an excess of the synthetic Survival Factor Reagent circulating in her blood, just as one would think that the progress of the cancer growth depended upon new pathogen attacking non-malignant cells. But this is not the case. It is likely that the pathogen-malignant-cell-integrate is estab lished at the start and is a localized affair, and the reproductions carry the pathogen with the new generations of cells forward as metastases. The initial foci may be multiple, however, and the virus may multiply within the cancer cells and infect normal cells nearby when the parent host cell disintegrates in its death. In the untreated case the death of each cancer cell would then supply virus for the infection of many other cells and cause them to go malignant. One occasionally sees an “independent” adenocarcinoma of gastric mucosa origin spring up in a case of squamous cell cancer of the cervix, and both cancers recover under the same Treatment.

The case mentioned show that there are no excess molecules of the SSR in the bloodstream seven weeks after the Treatment is given. The family of this patient all came down with mumps at the same time. She did also and it ran the regular course of eight days. Had there been excess SSR in the blood, it would not have developed, or would have cured up in hours, as mumps regularly does if treated early. The recovery from the cancer, however, went on uninterrupted. We consider this situation important to the management of the case and to the understanding of the recovery process. Whatever SSR was left in the system after the recovery is well under way is in the diseased tissue, and the infectious lesion that gave rise to the toxin that started the trouble, where it mediates the burning of the toxin polymer down through the initial monomeric form until no more is left as a chain process. That is what the clinical data shows. The constitutional quality rests in the fact that the lesion that sends the pathogen into the blood stream is generally at some distance from the injured area of anoxia or hypoxia where the pathogen has the chance to integrate with the cells injured by the anoxia, and in the early, widely spreading metastases. The rest of the body and particularly the reticulo endothelial system may be injured by the pathogen, in many ways for years, as it is polymerizing.

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CHAPTER 17


VIRAL INFECTIONS



It will be recalled that within a minute and a half after a virus has penetrated the host cell, the integration is so firmly set that no amount of vaccine, immune serum, or antitoxin can dislodge the virus and rescue the host cell. It is doomed. On the other hand, it is our chore to show that any time after the virus has penetrated and integrated with the host cell, so long as the latter is still alive, it is possible to accomplish the separation in a way that leaves the host cell in good functional status, while the virus is no longer to be found. In fact, the atomic bondings that constitute the integration, according to our Postulate, actually invite and provide for the oxidative separation.

To prove this the best field of observation is the paralytic viral diseases. When a nerve cell is integrated with a virus its functional mechanism is paralyzed, and it has to die. This will be soon if the integration is lytic, but death can be postponed if the integration is symbiotic. However, as soon as the integration has taken place, function is stopped. Therefore, after paralysis is demonstrated, its restoration means two things.  1) It means that the virus is no longer integrated with the cell.  2) It means the destructive changes leading toward the death of the cell and which supported the viral vegetation, have been repaired.  It also means, since the integration prevents host cell function and vital activities, that the energy required for the reconstruction came from some other source than its grana and enzyme activities. The only other source of energy during the integration must be the oxidation of the virus. So while it is possible to burn off the virus at its point of attachment, in line with our Postulate, it is indicated that the oxidation of the virus is stepwise, starting in the last units laid down during its vegetation, and ending up at the point of attachment. Thus the whole energy taken from the host cell to accomplish the vegetation is returned for host cell reconstruction. This will appear especially in the cure of rabies, because the time relations are so clean cut.

We chose a variety of paralytic viral infections that are 100% fatal to the host cell, and three of them, 100% fatal to the host as well. Thus the data presented should be substantial proof of the correctness and certainly of the utility of our Postulate. Somatic cell infection by virus as the 100% fatal hog cholera, and the picturesque epidemic hepatitis are also used.

ANTERIOR POLIOMYELITIS


Infantile Paralysis (Polio)

In the cases to be presented there are the two types, the lytic and the symbiotic. However, no case is purely of one type, they are mixed with one form or other predominating. Why a virus makes a lytic type destruction in one case and a symbiotic type of integration in another, or why a virus having made a symbiotic type integration suddenly goes lyric, is not explained so far as I know. However, since the same virus type is concerned in any epidemic, the variant is probably the patient or some change in the patient’s host cell. The effect of the symbiotic integration is paralysis and atrophy of dependent nerves and muscles so that the invalidism cannot be distinguished as to whether a symbiosis exists or if the nerve cells are dead and not restorable. We will show that the symbiotic type can cause extensive paralysis and atrophy for many years, and still both the host cell and the virus are still alive and so firmly integrated that neither shows any sign of life. To all intents and purposes they are dead. Yet the virus can be oxidized off and the energy evolved during the process will still support the host cell reconstruction so it can function again. Naturally in any case where a symbiotic integration has existed for 20 years, and produced extensive paralysis and atrophy, some of the host nerve cells have had a chance to die, and the restoration will not be 100%, but we can show a good 90% or 95% restoration of function and muscle reconstruction which means host nerve cell reconstruction after 20 years of invalidism of this kind. To solve the puzzle as to why the integration is lytic in one case and symbiotic in the other, the situation in the host cell can be postulated or assumed, but since no practical aid is had by this type of discussion, it is best to defer it for future experimentation.

Each case to be presented shows a determinative pretreatment control period showing that the virus actually has integrated with the host cell and has started the latter’s destruction to support its own vegetation. It will be seen that the time required for restoration is proportional to the time required for the amount of destruction done. So in all of the cases nerve cell destruction was started, and in all, the reversal of the pathogenesis was accomplished. The time ratio is not the same as in the rabies cases or distemper cases cured by the same Reagent. Thus a difference in species of host cell or of the virus is a factor to be studied.

RECOVERY FROM CHRONIC SYMBIOTIC TYPE PARALYSIS AND ATROPHY ESTABLISHED THREE YEARS

CASE No. 33 

Dr. Julian Baldor

Myrna R., age 10, presented an atrophy of three years’ standing with complete paralysis of the left leg from the waist to the toes. The leg was too weak and atrophied to wear a brace. There was also a contracture of one toe of the paralyzed foot. The calf measured four inches (10 cm.). The rest of the body was normal. She had been at Warm Springs Foundation in Georgia but they decided they could not help her and sent her home without improvement.

The Synthetic Reagent (SSR) was injected February 11, 1944. Following this Treatment there were two reactions with pain spreading from the head, down the back to involve the left leg. These came the third and sixth weeks. Following each, there was noticeable improvement. The muscles began to regenerate and motion began to be restored. By the end of the twelfth week she could walk with the leg very well and play with other children. The muscle reconstruction was practically complete, for one could not tell by observation which was the affected leg. She later took up toe dancing. The third and sixth week reactions are characteristic of recovery from chronic infection.

The history in this case showed a sudden overwhelming infection with instantaneous full paralysis of the whole leg. This is characteristic of the symbiotic type of infection, and is borne out by the recovery reactions that came the third and sixth weeks. The following case showed the same characteristics.

Therefore, where the paralysis is sudden and complete in the affected area, one may suspect the symbiotic type of integration and also a hope of securing improvement years after the acute stage has passed.

RECOVERY FROM CHRONIC POLIOMYELITIS WITH PARALYSIS AND ATROPHY ESTABLISHED OVER TWENTY YEARS

CASE No. 34 

Dr. Wendell Hendricks

Mrs. V. N., age 23, was first observed April 5, 1943. She was carried into the office by her husband as she was not able to walk because of poliomyelitis since the age of one and one-half years. All efforts were made with braces, casts, operations to fix the joints and shorten tendons, but to no avail. Both legs were atrophied and paralyzed completely, from the waist to the toes. The right leg was 4 cms. shorter than the left. The circumference of the calf of the right leg was 4 inches (10 cms). The left calf was 10 inches in circumference, but equally useless. She stayed in bed most of the time or was in a wheel chair, but with the aid of crutches and steel braces from hips to toes she could swing herself about inside the house and stand as per 3 point suspension. During the last two years of the invalidism the contraction of the fibrous tissue where muscles should be, caused the legs to cramp up stiffly so the braces were not comfortable and she did without them, staying in bed most of the time or swing ing about with the crutches and sitting in the wheel chair. She never had voluntary control of any of the muscles, and never walked. There were several operations aimed at stiffening the legs but they gave no help. She had continuous migraines, besides. Such was the pretreatment control period, paralysis atrophy and finally the contractures the ultimate result of the paralysis and atrophy. There were some vestiges of muscle fibers present even though in the atrophied state and paralyzed for want of nerve impulses. No one knew at the time of our Treatment, if or not the nerve cell bodies in the cord were dead or blocked and also atrophied, by the integration with the virus. The results of Treatment proved that the latter situation prevailed. On April 7, the Synthetic Reagent (SSR) was given and by June 8, that is in about nine weeks, there was motion and visible development of muscles in the right leg. She could also stand by herself without help.

On August 13, 1943, she had a reaction of chills, fever, and headache. Following this reaction complete control of both legs developed steadily. There was much muscle restoration. She walked about unaided without crutches or braces. The improvement continued in all respects. She could do her housework and adopted a baby. On June 12, 1944, she had another reaction with pain in her right foot and thigh and some fever. The migraine still persisted so another injection of the SSR was given on June 23, and again November 14, 1944. At that time the migraine was still present at times, however, the right leg grew so as to be only one-half inch shorter than the left. The circumference of the calf of the right leg was then 10 inches, or 25 cm., and the left calf, 11½ inches, or 28 cm. She was able to run up and down stairs and walk about or drive her automobile like any other person. She clerks in a store, is on her feet all day and requires no aid whatever. The migraine disappeared in 1944, and her health seems fully restored. This case illustrates the principles of our working Hypothesis throughout.

The recovery reactions noted in this case are similar to those observed during the recovery from cancer and tuberculosis and others with seriously damaged tissues. In this case, they took place where the state of paralyzing symbiosis was established over twenty years.

ADVANCED BULBAR POLIOMYELITIS WITH RESPIRATORY PARALYSIS

CASE No. 35 

D. H. Arnott, M.D.

John K., a boy of 16, was in the acute stage of Landry’s ascending type of paralysis. It started in the right leg and within a week involved the other leg, the arms, torso, neck, swallowing muscles, and respiratory muscles; and oculomotor nerves were paralyzed on the right side also and he was unconscious when he was first seen at a cottage near Port Huron, Michigan, during the polio epidemic in August, 1934. He was cyanotic and appeared to be dead except for a faint heartbeat. There were no respiratory excursions nor signs of breathing that could be distinguished. The abdomen was blown up. The abdominal muscles were relaxed in a flaccid paralysis. Later, we learned that the bowel and urinary bladder were also paralyzed. The (SSR) was given and within a few minutes there was some respiratory movement, the flaccid abdominal muscles contracted some and the cyanosis started to leave. Within twelve hours, he could move his arms and respiration was well established. The neck, eye, and swallowing paralysis had left and speech returned. The left leg showed improvement also and some of the back muscles demonstrated a return of tonicity. So far as we could learn, the pathogenesis was reversed in the order in which it developed. Two accidental matters intercepted a fine recovery. The cook brought him a hot cup of tea the next morning. Within an hour a reversal of the recovery set inwith great rapidity, and it took several days for him to regain his status before the tea was taken. After a week of improvement, he was taken in an ambulance some eighty miles. The trip was too much for him, for after being removed from the ambulance he had a general convulsion in which all of his muscles took part. This showed that the nerve cells had regained their function. Yet it proved disastrous, for they seemed to be burned out and the relapse took twelve weeks for function to return to the affected muscles. Satisfactory restoration of muscle development and control required about two years. He is well now except for some 30 percent atrophy of his right transversalis muscle, and the quadraceps extensor of the right leg shows a 50 percent atrophy. This does not impede walking, but it weakens his ability to climb stairs.

It is evident from this case that the recovery results will be determined by the care received, as well as by the length of time the disease is established. It also shows that the Oxidation Catalysis reverses the disease process immediately, but that the recovery process can be upset by being thrown out of balance by physical and chemical means. Yet once it has started it will reassert itself and partly at least overcome the impeding factor. Thus the recovery process behaves like a chain reaction.

One observes the dominance of the lytic type of integration of the virus with the host cell here in the steady spread of the disease, in the face of exhaustion of Nissle substance consequent to exposure and intense effort fighting a storm on Lake Huron, in a small sailboat. The nerve cells were all open to infection directly and as fast as virus was produced it found a host in each successive layer of motor nerve cells. Here the culture predominated over the virus production and each cell took a minimum of infective agent, in contrast to the symbiotic type, where the infected cells were each flooded with an abundance of virus all at once, and the hydrolytic, as well as the oxidative glycolysis systems were excluded from material energy production.
  

ACUTE BULBAR POLIOMYELITIS


CASE No. 36 

Dr. Julian Baldor

Patient: Sandra F., aged 9 years, female, student, admitted
September 19, 1951, 7:30 p.m.

Exposure: Brother seven years old, died of acute bulbar poliomyelitis proven by autopsy (two days before), September 17, 1951, State Board of Health Certificate No. 3920. He presented the same symptomatology as Sandra, and died shortly after reaching the state in which Sandra was when she received the Treatment by the oxidation catalysts.

Personal History: Measles, Chicken Pox, at five years of age.

Present Ailment: Temperature 102°F. for the past four days, with nausea, severe occipital headaches, and extreme difficulty in breathing. She was required to raise her shoulders at each attempt to breathe, to get some chest motion.

This suggests a diaphragmatic paralysis was present as well as the intercostal muscle paralysis. Abdominal excursions not palpable.

Physical Examination: Both patellar reflexes were practically abolished, although extremely weak motion was still elicitable. B.P. 100/75. Because of the respiratory failure, no further time was given to the physical examination, and the Synthetic Reagent was injected immediately in a dilution of one to a trillion, of water, two cubic centimeters by volume, into the gluteal muscles.

Progress: Twelve hours later a reaction occurred in a negative phase with more intensive headaches and nausea. The temperature remained the same. There was no change in leg function, voluntary or reflex.

Seventy-two hours later she went into a semi-coma which lasted three days. In this period, the temperature and respiration became normal and she also emerged from the stupor with normal cerebral functions. However, there was paralysis of the muscles of the back and of the left arm and both legs, which cleared up within one week, except that some weakness remained in the legs and left arm. This difficulty became nearly well within three months so that a slight drag in the left leg remained, which did not hinder her walking without the aid of braces, etc. Speech, vision, hearing, and alertness tests, showed 100 per cent recovery. Memory and other cerebral functions were found to be normal.

During the past two years the weakness of the left leg has not changed very much for the better but persists as a slight in-coordination, according to Dr. Baldor.

Remarks: A residual, very slight atrophy and corresponding slight flaccid paralysis of the right rectus anterior with very slight atrophy in muscles of left hand are still retained in spite of a third dose given in July, 1952. This shows that the injury is spinal and more or less permanent. In checking accounts in this case, the full cerebral recovery plus the timely cure of the respiratory paralysis without the use of an “iron lung,” and the retention of the minor spinal injury in such a virulent case of bulbar paralysis, speak well for the method of treatment. Had the patient had time for a thorough intestinal lavage and the elimination of interfering drugs like aspirin, even the spinal injury may have been avoided.

POLIO WITH PARALYSIS


CASE No. 37 
Dr. George Franklin Smith

This case is given since differentiation between anterior poliomyelitis and encephalitis is not always easy in babies without waiting for the symptoms to develop further defects. The Treatment was given to avoid further injury and possible death, and the recovery shows that the choice was good practice no matter which diagnosis was applicable. The fact that the paralysis became flaccid without voluntary motion or reflexes point to anterior poliomyelitis of the most dangerous type, where integration with the nerve cell functional material was well established, and sequelae would be expected to be extensive had not the treatment been given as early as possible.

Robert L. was eight months of age when affected with this paralysis.

When Dr. Smith first saw Robert L., the baby was having mild convulsions, that is his eyes were twitching and maybe some little part of the muscles of the face were also twitching mildly. He was limp and he had been vomiting just before Dr. Smith arrived. His temperature was 99°. His mother told Dr. Smith that he had been having convulsions one right after another, that he would draw his right hand up to his shoulder.

Dr. Smith recognized the case as being that of Infantile Paralysis. The following day there was paralysis of the right arm and leg. He continued to have the convulsions. His foot began to draw, and his eye turned toward the side of his head so that you could not see the iris. It was two days before the Carbonyl Catalysts could be given. At that time there was complete paralysis of the right side of the body. He was perfectly limp. There was no motion or reflexes in either the right arm or leg.

Dr. Smith gave him two-thirds of one Treatment (1½ cc.) of the SSR. The following day there was some improvement, and the improvement continued until the child was perfectly well. There was no muscle impairment as a sequel.
  

SUBACUTE POLIO WITH PARALYSIS


CASE No. 38 

Michael R., M.D.

The I. child, age 10, came to the office on September 10, 1941. The patient complained that for three days he had a headache and pain in the legs. His pulse was 90, temperature 98.6°, and the urine examination showed no pathology. The next day the symptoms of Infantile Paralysis were more evident; the Kernig sign was positive, he had a tenderness along the spine, he had neck stiffness, he could not lift his legs and the fingers of his hand were so weak that he could not turn on the radio. He had to lift himself with the elbows.

The Health Commissioner was called in the next day and he confirmed the diagnosis of Infantile Paralysis.

The Benzoquinone arrived on Sept. 13 and 2 micrograms were injected intramuscularly. The next morning the patient said that he felt some better, but his symptoms were about the same. A second injection was given on September 14th. About two days later he had less pain, he could bend his legs better and he had less neck stiffness. By September 20th, he had less lameness and he felt well.

On September 22nd, his temperature was 99.4°, and a third injection was given. Two days later the adductors, that is the muscles that bring the legs together, were less lame. He could bring his legs together. On October 8th his temperature was normal and from that day on he did not have any more symptoms. The Health Commissioner was called on October 15th and he was shown how the boy could walk through the room. He had no more symptoms. In 1943 he was active playing basketball and football. This case shows that benzoquinone offers inferior survival reagent qualities.

ACUTE ANTERIOR POLIOMYELITIS WITH PARALYSIS

 

CASE No. 39 

Dr. Wendell Hendricks

The following case is typical of many we have treated and illustrates the early reversal of the disease process following the administration of the oxidation initiators, the SSR.

Loman A., age 10 years, came down with the prodromal symptoms of headache, pains in his back and legs, stiffness of the neck and back muscles, vomiting, and fever of 104 degrees on February 3, 1944. The condition did not abate but became steadily worse through the night and the next morning. Our examination found the symptoms mentioned and flaccid paralysis of both legs from the waist to the toes. There were no knee jerks, or other reflexes to be induced in the legs or feet. The spinal fluid was taken and found to be 4 cms. on the manometer. We waited one-half hour so as to give plenty of time to see if the withdrawal of the few cc’s of spinal fluid would alter the symptoms. He continued to get worse, the fever mounted to 104½ degrees and his pains increased. The pulse was 128. We then gave the SSR solution. Recovery started to make itself evident within two hours in a reduction of pain and headache and the vomiting ceased. Seven hours after the injection he could move his legs. His neck was limber and his temperature normal. He ate a light supper. The next morning he got up and walked to the bathroom unaided. His recovery was complete in a day or so and no sign of return has been observed. However, during the third week following the Treatment he had a reaction of chills and fever that lasted three hours, after which he felt very well. There was no development of atrophy whatsoever. The third week reaction is of interest. It showed that a destructive or symbiotic integration was established.

The rapid establishment of widespread paralysis indicates the symbiotic type, but as the back muscles were becoming involved a lytic type extension was also probable.

POLIOMYELITIS


Acute Polio with Extensive Progressing Paralysis
The Case of Walter N.

CASE No. 40

This child was two and a half years old when carried into our office September 19, 1931. Both legs were paralyzed from the waist down and there was foot drop. He had fever and suffered pain. No reflexes could be elicited from the legs. The paralysis was of the flaccid type and progressing. The spine was rigid. He had been vomiting. One dose of the Synthetic Reagent was given subcutaneously. He was held by his father about an hour longer, while being observed; then he slid off his father’s lap and stood on the floor, making a few steps, but was quickly raised from the floor and prevented from further action. The paralysis had existed from eighteen to twenty-four hours previous to the Treatment, so the release was rapid. The Testimony of the mother has been paraphrased and is given for your consideration.

“I took my son, Walter, to Dr. Koch when he was two and one-half years old. He had been playing the night before but during the night he did not sleep, and cried; and when he got up he could not walk. I did not take his temperature, but felt his forehead and thought that he had a temperature. His leg was still sore, so the next day we took him to Dr. Koch’s office. My husband had to carry him because he could not stand.

“Dr. Koch gave him an injection in the leg. We were in the office about an hour and soon after he had the shot, he wanted to get off my husband’s lap on to the floor. He could stand a little, but we carried him to the car and kept him in bed that day. The next day he was up and playing. That was the summer of 1931.” The recovery was complete and has remained.
  
ATROPHIC ANTERIOR POLIOMYELITIS COMPLICATED BY ANTIVARIOLIC VACCINATION

CASE No. 41 
Dr. J. Treiger

Miss P., age 7, seen first by Dr. Treiger March 8, 1957. Her weight was 20 kilos. She had had measles, varicela, whooping cough, and at 3 years of age a nasal diphtheria, following which she has always been underweight in spite of a good appetite and sleep. Examination showed slight dyspnoea and constant cough with a hypertrophied left tonsil, much flatulence, fearful, crying at nothing, without appetite, very thin and weak, with paralysis and muscle atrophy of the right leg. The history showed that she received smallpox vaccine in March, 1957, and had a very strong general and local reaction. Her ill health continued with the added disadvantage of the paralyses and atrophies of Anterior Poliomyelitis which struck her in May, 1957. She caught colds very easily and every contusion produced a swelling that became purulent with ease. Good homeopathic prescribing helped her sustain herself at this status but something more fundamental had to be removed. From March, 1957, to March, 1958, she gained only one kilo in body weight. So, before the polio struck her, she was practically a metabolic invalid. The vaccination mark, however, developed a large mushrooming keloid raised high above the surrounding skin. The atrophies prevented her from raising the right foot when she was lying on her abdomen on the table, and from bending the right knee when standing. The right leg gave no support when standing as the knee and the ankle were both wobbly and without strength or control. The foot hung loosely from the ankle joint. She needed braces to support both.

On April 15, 1958, she received 2 millimicrograms of the SSR from Dr. Treiger, intramuscularly. The results were: four weeks later she had gained two kilos, and had better muscle tone. In two more weeks, she gained two more kilos. In the middle of the twelfth week, after Treatment, she had a characteristic reaction (July 7th). There was pain in the right leg, general achiness and fever, and itching of the keloid. Three weeks later another reaction occurred with fever of 108°F., much coughing with the elimination of clear mucous. This lasted only two days, but in these three weeks the keloid reduced remarkably. One year later, in August 1959, she weighed 29 kilos, and showed another reaction with pain in the leg and the return of an itchy rash on the eyelid, plus a general itching that she had six years earlier. In this period, the keloid reduced so as to be at the same level as the skin and so it had shrunk.  At the time of Treatment, it was 10 to 12 mms. in diameter, and raised 6 to 8 mms. above the level of the skin. How deep it went is not known, but its present depth is not great as it is flexible. Still, there is maybe 20% to be absorbed to become an ordinary scar. Her appearance is healthy, she is vigorous and has a stable nervous system, and she walks without any bracing apparatus with a practically normal gait. She can now raise the right foot when lying on her abdomen, and can raise and bend the right knee when standing. The right leg supports her when standing and the ankle has regained fair function useful in walking without braces and with ordinary shoes. The circumference measurements showed an increase in the right thigh from 28½ to 34½ centimeters while the left thigh stayed at 38½ cms. and the right calf gained from 19 to 20½ cms. and the left stayed at 25 cms., between April, 1958 and Nov. 16, 1959. It would be interesting to decide, if or not the smallpox vaccination gave the polio infection. Since the keloid reacts concomitantly with the Polio reactions this might be suspected. However the eczematous rash also reacts at the same time and points to a fungus infection received at an earlier date. The keloid is not yet fully absorbed and the atrophies are not yet fully corrected. More reaction is still expected. These will solve the etiological position of the vaccination. On Nov. 4, 1960, the right calf measured 22½ cms.

EPIDEMIC HEPATITIS


It will be seen in this group of Infectious Hepatitis cases that the virus host cell integrations follow the same pattern as in Anterior Poliomyelitis and the time relations of the recovery process measure up similarly to those of the recovery from paralytic polio, rabies, and dog distemper. Both the acute lytic and the chronic symbiotic types are observed, indeed the virus appears to exist in some cases as if integrated with foci of long suppressed infection, either in symbiosis with some germ or with the scar tissue that imprisons it. The relation of the vaccination scar to polio and to cancer, as revealed in their recoveries, might be compared with the fecal contaminated scar of the fourth case given here. In all such stored viral infection, a drop in the resistance of the patient allows the symbiosis to go rapidly lytic with rapid multiplication, and then the burst through as a general infection that attacks the most susceptible tissue dominantly.

The examples offered here present the four types of classification. The second case represents both the protracted type with remissions and relapses, and also the fulminating type when the infection suddenly fulminated and quickly went into the terminal phase with wild delirium, hallucinations and then a state bordering on coma, when the Survival Reagent was given and quickly reversed the pathogenesis. The first case represents the common type with jaundice and sickness that hangs on regularly for a month or two before it starts to yield, but here the reversal was evident in hours, and was completed in a week or two. Interesting is the thyroid disturbance, like the brain disturbance in the second case, showing that the virus can integrate with more tissues than the liver cells. The third case directs attention to the rate of recovery of function by the liver cells, as do the others, though they were more complicated. This is regularly about 48 hours in the acute lytic type of integration. In this time the bilirubin drops to a near normal, as from nearly 6 mgms. percent to less than 0.5 mgms. percent, while the bile absorbed into the skin and other structures takes longer to be liberated and eliminated. The patient, however, is well with good liver function, and no toxicity whatsoever. The following cases are reported by Dr. Treiger. The last one was observed by the writer.

INFECTIOUS HEPATITIS

 

CASE No. 42


M. C. S., a girl of 12½ years, 41 kilos, student, with a good school record, appeared Nov. 12, 1959, and gave the following findings. She was changing color from the healthy hue to a greenish yellow, great urgency to move the bowels after eating, slight pain in the muscles, pain in the bowels with marked nausea, that was violent in the days preceding school examinations, which were at hand then. The pulse was 120 per minute, temperature 37.6°C. and a sub icteric tone of the sclera. When examined, complained of pain over the liver and epigastrium, with an accentuated tympanism, and terrific itching. There was excessive sweating of the hands and feet, and together with the tachycardia the thyroid gland appeared to be attacked. An epidemic was running at the time in her school.

Blood analysis on 11/16/59: Bilirubin, 1.43 mgms.% instead of 0.2% to 0.4%; Van den Bergh, positive, but weak and delayed; Hemogram normal; Crenation test, only 20% crenated, 80% remained round.

Treatment: 2 micrograms of Benzoquinone solution was given on November 16, 1959, with homeopathic doses of iodine and chelidonium. Improvement showed the next day, was very good in 48 hours, and continued until on the tenth day, when she was practically well. The pulse had dropped from 120 to 86 per minute, the jaundice had faded away, no more pain or itching, and no nausea or sweating. The blood showed Bilirubin 0.41 mgms.% which is normal, the Van der Bergh was negative, the Crenation test was 90% normal.

She took her exams without any nervousness and with good results between Nov. 25 and Dec. 12. The correction was permanent.
  
INFECTIOUS HEPATITIS PROTRACTED SYMBIOTIC TYPE WITH SUDDEN LYTIC CHANGE FULMINATING TO TERMINAL STATUS

CASE No. 43 

Dr. J. Treiger

S. M. L., age 31 years, gave a history of pyelitis in early childhood, frequent colds and in April, 1958, a broken leg, weight 45 kilos., when she consulted Dr. Treiger on 5/4/59. She had a fever of 38.8°C., complained of grippiness, muscular pains, tonsilitis, worse on the right side, halitosis, dirty tongue and facial neuralgia on the right side. This attack came after a season at the seashore on a heavy crab and shrimp diet. She was given homeopathic medica tion without result and she continued to get worse. On May 8, 1959, the fever was gone, but she was prostrated with nausea, repugnance to all food, feeling like a drunkard, and a terrible taste on her tongue. The muscular pains were gone, but there was a severe pain over the gallbladder. On May 11, 1959, the blood picture was: Bilirubin 5.95 mgms.%; Van den Berg strongly positive, immediately, three plus; Cefalin-Cholesterol (Hanger) three plus; Thimol turbidity 7.5 units; Thimol Flocculation (MacLaglan), positive three plus. That night she was much worse, again with a high temperature of 39.5°C, extremely agitated, afraid of dying and of being alone, hallucinations and delirium She had received a new homeopathic prescription that did not work. Dr. Treiger gave her two millimicrograms SSR when the agitation gave place to a new phase of prostration bordering on coma. However, the nausea did not develop though it had been strong and constant. After 48 hours the improvement was evident with lowering of the temperature and the return of appetite and bowel functions. She steadily improved and on June 17, 1959, the blood showed Bilirubin, 1.02 mgms.%; Van den Bergh, delayed and weakly positive; Cefalin-Cholesterol negative; Thimol turbidity 5.5 units; and Thimol flocculation, negative.

July 10th, during the ninth week after the Treatment she had a reaction with violent nausea and dizziness. She was given another dose of the SSR. The improvement was observable in three hours. Two weeks later the blood test showed a normal Bilirubin 0.41 mgms.%, and all other tests negative.

During the 12-15 week reaction period she showed an intestinal upset and this cleared up quickly aided by Ipecac and Terrarnycin. In the 27th week reaction period there was a transient light pain in the left lobe of the liver that cleared up quickly, but there were no other symptoms. The correction was complete. No doubt the intestinal tract was the first to become infected and was therefore the last to become normal, in line with the characteristic behavior of the recovery process after the FCG is rescued and restored to action.
  
AN ACUTE LYTIC TYPE CASE OF EPIDEMIC HEPATITIS

CASE No. 44 

Dr. J. Treiger

J. H. C., age 13 years, student, appeared with a history of having drunk water that was under suspicion of being filthy 15 days previously. He had abdominal pain that was helped by intestinal lavage. The urine was loaded with bile. There was deep jaundice and profound drowsiness. His state was subfebrile, and the blood examination on February 5, 1959, showed Bilirubin 5.83 mgms.% (Malory and Evilin). The Van den Bergh was immediately directly positive, the cefalin-Cholesterol positive, the Thimol Turbidity 5 units, and the Thimol Flocculation positive. Two millimicrograms of the SSR were given on February 5th. On February 7th the jaundice had faded considerably and he felt very much better, no more pain or other disturbance. The bile stained tissues had not completely unloaded until three weeks later when the Bilirubin test was almost to normal, namely 0.86 mgms.% and the Van den Bergh and other tests were normal. On March 10th he was fully recovered and back to school. Here again we see the restoration of liver cell function, which means the rupture of the viral host cell integration, and the restoration of the host cell to functional structure, required 48 hours. In rabies it required 72 to 84 hours, and in polio the restoration was proportional to the time the paralysis had lasted, and the host cell injury had been going on. Thus, this disease supports our postulate very well. While this virus is not killed by chlorine oxidation, it is destroyed by induced oxidation after it is integrated with the host cell.
  
CHRONIC INFECTIOUS HEPATITIS WITH MALNUTRITION

CASE No. 45

John S., age 28, when appearing for diagnosis and treatment, height 6 feet 3½ inches, weight 137 pounds, on August 4, 1957. When he took sick in 1952, he was in the air force. He had been in good health until an attack of appendicitis called for an operation. This resulted in severe peritonitis, and the use of 70 injections of antibiotics, mostly of streptomycin that favors virus infection so markedly. Ever since this attack, he was an invalid steadily getting worse, losing weight and strength, becoming more and more anemic with less ability to digest his food until he had lost his appetite completely. The use of digestive ferments medication failed to help. Moreover, the liver did not metabolize what little he was able to digest. This deterioration progressed until August 4, 1957, when he appeared for observation.

Examination showed slight jaundice, profound anemia, enlarged tender liver, loss of elasticity of the skin, great weakness, and gastro-intestinal failure with its consequences. There was severe prolonged headache at times and difficulty to perform his obligations. The operation scar was hard and extensive.

Two cubic centimeters of the SSR solution containing two millimicrograms of Reagent were given on August 4, 1957. There was no sharp turn for the better as usually follows, but he did not continue to get worse, and a slight improvement could be reported on the 14th week. This trend gained a little momentum up to the 36th week when a sharp reaction took place, with acute inflammation of his enlarged liver and the abdominal wall scar, severe jaundice, high fever, abdominal pain, vomiting and increased headache. This lasted only a week and cleared up spontaneously with fair rapidity when one considers his greatly depleted condition. The blood examinations were interpreted by his physicians as indicating Infectious Hepatitis. But as the course of the disease was so different from the regular course and the improvement so rapid, we interpret it as a reaction to a chronic infectious hepatitis in which the virus was integrated with the fibrotic tissue of the extensive abdominal scars as well as his liver tissue. The oxidation of the toxic virus factor off from the liver cells gave rise to the inflammatory changes, and jaundice, but as soon as the liver cells were free, they were able to function again, and normal status returned.

He gained a good digestion, strength and weight so that when seen in December 1959, he was perfectly well, the liver was normal, the scars soft and pliable, and with good vigor, and ambition to work.

RABIES


In April 1955, the Fleury type live rabies vaccine made from street dog virus, was injected into 650 thoroughbred Zebo cows at the Fazenda Indiana, near Rio de Janeiro. The vaccine was prepared by the Health Department of Rio, and given by expert veterinarians. Six hundred cows showed no adverse effects, neither intoxication nor rabies infection. However, 23 younger animals did come down with virulent rabies. They all progressed in their symptoma tology, and died in from 3 to 5 days in the classical course. The brains showed negri bodies, and the mouse inoculations were positive for rabies.

The writer arrived on May 19, 1955, while, some of the animals were still alive but showing the disease in well advanced stages. Only one calf was in the early stage of deglutory paralysis, but she had to be given saline transfusions to combat the dehydration consequent to impeded swallowing. Two cases were under heavy hexamethylene tetramine treatment, and were not offered to us until they were in the terminal stage, and were not fit for statistical observation— only for experimentation, because of the saturation with the drug, which is an inhibitor to the Survival Remedy. Six cows were in the terminal stage, about the fourth day, with typical torticollis, convulsions, deglutory paralysis, and were either paralyzed so as not to be able to walk, or if able to stand, would fall if pushed and not be able to get tip again. Six were moderately advanced, and could stagger about, showed torticollis, and short convulsions, but could not swallow. They were in the third day or at the end of the second day in some instances. So there were thirteen cases treated for statistical observations, including the calf, Iberia, that had only beginning deglutory paralysis for a day or so. In the entire symptom course was the same as in those that died, and started with deglutory paralysis. There were seven other cases used as testimonials — collateral controls, but as the opportunity was a rare one we used them for experimental observations in a way that did not prevent them from going the regular course to death as the cows that died before them. We had learned in dogs that the quinone structure does not affect rabies favorably, so we treated some of these with diphenoquinone one part to a million, and some we treated with high dilutions, that is, a billionth of a microgram of the serial system of Carbonyl groups, used in a dose of ten micrograms in the treated cases. Of the thirteen treated cases, eleven made complete recoveries, and two died.

All treated cases required 72 to 84 hours for restoration of controlled movements including deglutition. Its paralysis was the first symptom to come and the last to clear up. Animals treated during the fourth day of their down ward course, were then widely paralyzed and had gone through a heavy convul sion period. They lay paralyzed for four days longer, before they showed restoration of function. An interesting case will illustrate. The government veter inarian who took charge of this epidemic had no faith in the cure of rabies, which was always 100% fatal, and as fast as any diseased animal showed it was following the classical course of the disease, he took it away for sacrifice, to save it useless suffering and to have better autopsy material. Our Treated animals were allowed to follow along without interference except one cow that was treated at the end of the third day or the beginning of the fourth day, when it was already badly dehydrated. It lay paralyzed for four more days when the Government veterinarian ordered it dragged to the truck to be taken away, but on reaching the truck when they tried to hoist it in, it kicked up a fuss and tried to run away. The Fazenda veterinarian was passing by and as he saw the cow show coordinated movements he ordered a halt and led it to water, where it drank greedily. He then let it loose in the pasture to eat its way back to health. Here we see that at the end of the quiet period, which is as long as the symptomatology period the reconstruction is complete. In other words the type of integration is such that it affords a reciprocity between the virus and the host cell. During viral vegetation the energy and material passes over to the viral colony, but during the viral oxidation a stepwise burning of the virus returns the energy to the host cell that was taken from it, and the food that diffuses into the cell supports its reconstruction. This explanation is the only one we can think of since a full reversal of the process takes place even after the host cell is at the point of full destruction and the viral colony ready to burst forth as myriads of mature parasites. This is especially significant since so long as the host cell and virus are integrated, the former cannot carry on constructive or functional processes, but must yield to complete dissolution. So the oxidative destruction of the’ virus supplies the energy for grana reconstruction so that the grana can then control enzymatic activities for function. One should contrast this evidence with the fact that a minute and a half after a virus penetrates a host cell the integration is complete and no amount of vaccine or serological effort is able to cause the separation and rescue it. It is doomed. Serological aids are merely substitutional. The SSR rescues and restores the host cell and burns up the pathogen.

DISTEMPER IN DOGS


(Cinamose)

The hospital of the Army’s veterinary service for small animals, Col. Columbo and his staff with Dr. Adelberto Carneiro, and Dr. Cantuaria Guimaraes, arranged for the treatment of dog distemper as brought in from the street, and homes. For the first 17 cases treated we had to guess at the dosage and get it regulated for a systematic treatment of this disease. These cases were lost, and although they are included with all treated cases in the statistics, they bring the cure rate down from 90-95% to 80%. The detailed report is published in Veterinaria, the official journal of the University Veterinary Department of Brazil. Columbo and Carneiro, Veterinaria Ano IV, Num. 1, p. 21, 1950.

In private practice in the nervous form of distemper the recovery percent ran 80% or over, but only small groups of dogs were treated. Many of these animals were paralyzed for several weeks, even longer than a month with involvement of the respiratory and cardiac centers beginning to show. Thus the chances to live as long to accomplish the restitution, as the nervous system was involved were certainly reduced. However, the time required for restoration of the affected cells, like in those of rabies, is about equal to that which accommodated the destructive process. We have the documentation of some private veterinarians, and professors in the University, on a short series of cases, where 80% of well-established distemper of the nervous system were cured. However, a case of polio in a dog that acted just like distemper of the nervous system was the subject of the Official Testimony before the Federal Trade Commission in 1946 by Dr. B. J. Myers, of Oklahoma City, a veterinarian who attended the dog through its recovery. It was a valuable Pekinese that had been playing with a little girl neighbor when she came down with paralytic polio myelitis during a severe epidemic. The paralysis started in the hind legs and tail and then affected the front legs and body, in the course of a week the neck and “bark” were paralyzed and death threatened from respiratory failure when the SSR was administered. It took a week to ten days to undo the paralytic degeneration. First starting with the “bark” and neck and reversing the paralysis until last of all the hind legs and tail regained their functions. Cinamose does not attack human beings but polio does attack humans and other animals. So far as the symptoms were concerned it could have been either disease that affected the dog, but because of the polio epidemic that was raging at the time and the contact the dog had with the sick child, the diagnosis of polio was made. No serological tests were perfected at the time to make a differentiation. The case is of value in that it shows the identical nature of the attack of a virus of different types on the same functional mechanism even in different animal species. The similarity of the pathogenesis and of the correc tive process regardless of species is demonstrated. Also, that the recovery course is not a matter of imagination, but a definite procedure, without psychotherapy.

HOG CHOLERA


Hog cholera attacks the whole body generally including the intestinal and respira tory tracts, the skin and vascular system, and the nervous system. At the end of the disease, just before death, the whole body is involved. However, in a small percentage of cases the nervous system infection dominates the symptomatology very early. There is ophosthotonus, torticollis, and convulsions. The animal behaves as if it had rabies. So far as this writer has seen this type, there was no attempt to swallow, as the head could not be bent to reach the trough. Less than 20% show this type of infection in Cuba, and in Brazil it is even more rare. The disease is 100% fatal in three to five days after symptoms begin.

The following report is taken from an official record at the Veterinary Department of the Cuban Army under Fidel Castro:

A. “On May 15, 1959, Dr. Rodriques, Director of the Veterinary Center of the Estado Major of the Army, in Ciudad Liberdade, facilitated and arranged for the treatment of animals involved in an epidemic of Hog Cholera at Quartel 10, of San Antonio, that had already caused the deaths of 15 vaccinated pigs. The remaining pigs of the colony comprised a total of 74 infected pigs, 35 small and 39 large.

B. “Prominent Symptoms: Among the prominent symptoms that established the diagnosis were:

1. The deaths of the 15 pigs before our arrival.

2. All the pigs that were still alive showed,
a. Prostration,
b. Respiratory difficulty, strenuous in type, characteristic of bronchi ogenic pulmonary lesions,
c. Hemorrhagic plaques, small and large in the skin of the abdomen of all animals, extending in some cases under the neck and jaw.
d. Excretion of solid and liquid material with rectal congestion in some cases.
e. Teats inflamed and hemorrhagic, very severe in one case,
f. Nervous manifestations with torticollis, very severe in one case.
g. Fevers running between 39,5* and 41°C. in various animals, the small animals with 40°C. The sickest animals showed a drop in temperature to 39.5°C. characteristic of the advanced stage.

C. “Pathology: The conditions of the material was the poorest as a result of the observed facts and changes. The animals had already carried the incubation period of 10 days with a prognosis of 100% fatality, according the virological standards, for after the virus is integrated with the host cell, no serological measure can set the host cell free and rescue it.

D. Treatment and Material Used: The 74 animals were treated in two sessions, the first on May 16, 1959, and the second on May 19, 1959. The first group to be treated was 10 small pigs and 12 large pigs. The second group treated was 25 small pigs and 27 large pigs.

“A solution of diphenoquinone, freshly prepared, containing 1 micro gram per cubic centimeter, was used. Small pigs were given from one to two cc. of the solution, and the larger pigs received from five to ten cubic centimeters by injection.

E. “Results:
“First Group. This group was observed on May 23, 1959:
a. No deaths,
b. Temperatures normal in checked pigs with the exception of pigs No. 3 and No. 4; on these the injection was then repeated,
c. The red hemorrhagic spots on the abdominal zone had disappeared in all animals. The congestion of the cornea had also left,
d. The rectal areas appeared normal,
e. The respiration was normal in all animals,
f. The female’s teats that were formerly inflamed and hemorrhagic were normal in all animals,
g. One male of the group segregated as the most debilitated, attempted one week after treatment to accomplish reproductive relations with the females, successfully.

“Second Group. This group was observed on May 23, 1959, five days after Treatment. The following results were observed:
a. No deaths,
b. Normal temperatures in all that were checked,
c. The red hemorrhage areas had disappeared,
d. The rectal areas were normal,
e. The respirations were normal in all animals,
f. The teats of the females appeared normal.

“This group was examined again May 26, 1959, one week after Treatment when Group No. 1 was also examined. All pigs were found normal and attested to by the officials in control of the test.”

In Brazil, the epidemics were small. At the Ministry of Agriculture Maracana Station, where cresol was used liberally, and the pigs were exposed to other inhibitants, the results were 100% failure in a group of seven pigs. But at the Deodora Station where no interference was met, the results were 60% cures that is two cures out of three treated. These pigs were all in extremis, at the time of Treatment. That is, unable to stand or eat, symptomatol ogy typical. In another epidemic at a private farm 5 far advanced large pigs were treated with diphenoquinone, each receiving ten micrograms each at two different sessions 3 days apart; of the five only one could walk. They all recovered in 5 or 6 days, and were able to eat again, completely clear of chest and skin changes. In another epidemic at Santa Cruz seventeen of eighteen pigs in the herd had just died of Swine Pest. One still was alive and sick, it did not eat or drink, but could walk. The skin and chest symptoms were charac teristic. It recovered also.

At the same time at a neighbor’s farm several herds were affected. One group of four pigs equally advanced at about the third day, except a very small “runt” that was near death. It had not taken water or food all this time and died within a few hours after being treated. The others all recovered. Another neighbor’s farm had four pigs with symptoms in the second to third day of the disease. We treated the three that were worse, and held the other as a control. The third day later these were found cured and eating, having fully normalized. The control pig was quite advanced and not able to live more than another day, perhaps. We treated it, and two pigs in another neighbor’s farm that was characteristically affected. They all recovered within a week when the next visit was made. Thus in the Santa Cruz group there were nine treated, including the far advanced “runt”, and eight recovered and the “runt” died. This is a fair percentage and gives an idea of how the infection gets around. In another epidemic of ten pigs we used a different atomic arrangement, — the serial system of Carbonyl groups. The results were 100% failure. This serial system of carbonyl groups gave 80% cures in rabies, and the quinone structure gave 100% failure. Thus there are two different 100% fatal viral diseases, each of which takes the same time to kill, that do not respond to the same Carbonyl group when activated by different sources of electrons. The steric advantage and hindrance are different in each integrate evidently.
  

HOOF AND MOUTH DISEASE

(Aftosa)

There are three types of Aftosa virus, and their virulency varies. There is the deadly cardiotropic type that can wipe out a herd in short order. Some of the infected animals drop dead from heart failure before they can develop any lesions in the mouth or on the hoofs. It was such an epidemic that started at the Agriculture College, Institute Quinze de Novembro on October 14, 1949. There were 59 head of cattle and 200 pigs. The professor in charge was afraid this virus would wipe out his herds, as five cows had already died a few hours after the epidemic had started. Others were lying on the ground unable to get up. They appeared doomed. Others showed lesions in the mouth and feet but were able to walk. We treated all 54 animals that were still alive, of these seven were newborn, 15 were calves, 17 were young bulls, and 15 were cows. Thus two-thirds were most favorable hosts for the destruc tive action of the virus.

Results:
Two cows and one calf died of the disease. All others recovered and no new infections developed. Of the 200 pigs, 35 were adults, and 165 were young. 167 were well-established cases of Aftosa, while 33 were symptom free. All were treated. Four pigs died of the infection giving a cure percentage of 98% and as no new cases developed, a prevention percentage of 100%.

The following year Aftosa again struck the Institute. The cows we treated did not conic down with the disease except a few showed mild symptoms for a short time. The new cows brought into the herd took sick and died before we could be notified to come. A year later the treated cows were still immune, and again a year later we had the same report.

At the Rural University, the government’s Agriculture School, an epidemic broke out that was reported by Dr. Adelberto da Silva Carneiro, in Veterinaria No. I, page 75. The virus was found to be type C. There were 68 cows in the herd. This virus was endemic and was active every year at the same time. It never killed over 10% of the cows, so it was not too fatal. However, the affected cows lost their milk production, and that was the big point of worry. Practically all of the cows showed symptoms including the drying up of the milk secretion. But a few were symptom free. All were treated. There were no deaths. Twenty-four hours after the treatment was given, the dried-up mammary glands started producing milk at the normal rate. Thus there was 100% cure, 100% prevention and 100% restoration of function. Only one cow needed a second injection, and then cleared tip normally.

CONTROLLED AFTOSA EXPERIMENT


At the Rubino Institute at Montevideo, Uruguay, a controlled experiment was arranged in which 30 calves, all bulls, of the same size, age and “texture,” were inoculated with a standard cardiotropic virus that killed 80% in from 4 to 9 days. The other 20% became chronic heart cases that died somewhat later. But the virus was 100% fatal in the dose used. The experts prepared a vaccine from this virus, and protected 10 of the cows therewith at an optimum interval before inoculation with the virus. Ten cows were held untreated as controls, and ten were given the SSR reagent. Since we were promised plenty of leeway and material for a good period of experimentation, we gave these cows the usual human dose used in cancer, that is a concentration of 10-(12), that is one part to a trillion of water. They were treated three days after the inoculation. The cows we treated and the untreated controls were held together in a small room with a bare cement floor in the coldest month of the year, July. They were grouped together with their noses all touching and the untreated cows were smearing the treated animals with their dripping infected saliva. The vaccinated controls were held in a warm barn with plenty of straw and given medical aid, transfusions and all the care possible for success.

Results, On the fourth day we had one death, and the vaccine-protected animals had four deaths. The rest of the control animals were very sick with myocarditis, but our animals, the nine still alive were not, and they recovered fully. Since the control animals that had not yet died were getting ready to do so as the myocarditis progressed, the director of the institute asked us to treat them since they did not have cremation facilities for so many animals, and the law required cremation. We treated the rest this time as well as our test cases with the one to a million dilution, and the results were rapid. All of our cows recovered and so did our treated controls. The cure percentage on the one to a trillion dilution was not over 90%, but the cure percentage of the one to a million dilution was 100%. The experiments were stopped because of political pressures that will not be discussed here. Another volume is devoted to curiosities. In Aftosa we see one virus type that paralyzes function of heart muscle and another that paralyzes milk production, both cured by the same reagent as cured the nerve cell paralysis in rabies, cinamose and poliomyelitis. The structure of the virus-host-cell integrate must be atomically of the same order then, in them all, since the end results of action of one reagent is the same — functional restoration of the host cell and disappearance of the virus.

SYPHILIS


CASE No. 46

This subject will be amply aired in the completed text; we here just give a case in photographs, to touch on the subject. This boy was sent into the hospital at Louvain University, Belgium, in 1934, with a diagnosis of cancer of the skull since he did not respond to anti-syphilitic treatment though given expertly and with vigor. We found on biopsy and serological tests that he had syphilis. However, the neoplastic taint was not ruled out thereby, and his resistance to anti-syphilitic treatment may be due to a neoplastic agent that may have been present. He was given a dose of the carbonyl catalysts and at that time his photograph showed as in No. I. Six months after Treatment, he was serologically cured and the photograph shows good healing of the area. The necrosis had gone into the middle layer of the bone, and the healing involved bone reconstruction as well as skin healing. One year later the fibrosis shown in the second photograph was replaced by perfectly normal tissue and could not be detected.

==========================

CHAPTER 18

 

TUBERCULOSIS


Several bacterial infections will be given a little attention to show that the bacterial toxin integrates with the host cell according to the same pattern as the virus or carcinogen. This is our conclusion since the same Reagent causes the destruction of the toxin with liberation of the host cell. In tuberculosis, staphylococcus, streptococcus and corynebacterium infections, the walling off process is often extensive. Here the fibroblastic tissue evidently integrates with or co-polymerizes with the toxin since after the high efficiency Carbonyl groups are admitted to the field, the toxic fraction is burned off and the fibrous tissue has no more function, as there is nothing to protect against. The fibrosis disappears. It will be seen that the shaggy walls of the tubercular cavities first become smooth, and the cavity enlarges as the wall and debris are removed, then nothing more is to be seen of it as it becomes replaced with efficient breathing lung tissue. In the dairy cattle, the extensive fibrosis of the udders is seen to disappear completely in over 80% of the cows after only one Treatment, as part of the recovery process. Besides, the hemolysins of the Staph Aureus likewise disappear and none of the bacteria are toxic any longer. So wherever the toxins are, freely circulating, integrated with the tissue cell, or as part of the germ, they appear to invite dehydrogenation by the activated Carbonyl group, and in the presence of molecular oxygen they are burned away. The fibrosis is then replaced by functioning tissue as milk production increases to normal or better, and respiratory efficiency is restored.

As bacteria mutate against the best of antibiotics, all infections including tuberculosis become surgical diseases again. The old fashioned drainage is required and lobectomies or pulmonectomies in such cases as are favorable. It will be observed, too, that cases of lung infection that are not good surgical material as the bilateral cavitations and those with heavy walls that involve the mediastinum may respond favorably under the therapy described here, and thus give the surgeon the aid he needs until the case becomes a good surgical risk. Many factors enter into the management of such cases and the expert will have to make the decision as to procedure. It is observed in cases with large cavities, that while the patient’s health is improving, the heavy toxic symptoms as fever, sweating, flush and weakness are disappearing, and the germs are thrown out in great numbers until the healing is complete. These bacilli are often seen to be phagocytized, and undergoing fragmentation and dissolution in the phagocytes, instead of the phagocyte being destroyed. We conclude that after the toxic fraction is burned off of the germ substance, it is readily digested, like tissue debris.

Prolonged bed rest is not needed in the care of these patients, even though far advanced. In fact, as soon as the fever disappeared, which is rather early, they are expected to move about as they please and rest enough so as not to get tired. Long before the cavities have disappeared they do light work, and it helps them physically and mentally.


Mr. S. M. came to our Clinic on October 20, 1938, for Treatment by Dr. G. Warnshuis.   His case history revealed that his father had died of intestinal obstruction.   His previous illnesses were pleurisy in the left chest, which was followed by pneumonia in 1935.  In September 1938, he began feeling badly, had cough raised sputum and had night sweats. We had his sputum examined by the Public Health Laboratory.  It was reported positive for tuberculosis. Our own sputum examination was confirmatory. His weight was 153½ pounds, normal weight being 182 pounds.

Radiograph I was taken at the Herman Kiefer Hospital on September 16, 1938. Radiograph II was taken at the time he came to our Clinic. A definite increase in the extension of the large cavity and tuberculosis infiltration is seen in this short time. His condition also retrograded constitutionally and with regard to the cough, night sweats, fever, etc.

He received 2 micro-micrograms of the Synthetic Survival Reagent. At that time he spent several weeks at our rest home, but was not put on the strict bed rest so rigidly enforced for patients in his condition. He was then sent home and kept on a vegetarian diet. He was allowed to be up and about, but told not to exert himself so that he got tired whatsoever. He kept a record of his temperature and other symptoms. He did his own cooking, shop ping and drove his car from his country home, about 40 miles away, to our clinic every two weeks for a checkup. His improvement was slow at first, but steady. In a year he could do a little work. Radiograph III was taken on July 8, 1939. It shows healing of the large cavity during the recovery process.

On July 19, 1939, Mr. S. M. was examined by Dr. Douglas. He states in his letter of July 21, 1939, that “there has been some clinical improvement since last September,” but that it was his opinion, “that this man is totally and permanently disabled because of pulmonary tuberculosis.” Thus we see that in spite of Mr. S. M.’s condition when he came to us, he did make some definite improvement during this nine-month period. Dr. Douglas still considered Mr. S. M. “totally and permanently disabled,” and by this he meant, “… that the chances of recovery to the degree that this patient might be able to work are so poor that it is proper to say that he is totally and permanently disabled.”


July 21, 1939
Dr. Peter Ivkovich
14128 East Jefferson
Detroit, Michigan

Dear Dr. Ivkovich:

In re: Stanley M----:

Stanley M---- was examined here on July 19th and I have procured the films from Dr. West for comparison.

This man has a far advanced pulmonary tuberculosis and while there has been some clinical improvement since last September, still there is evidence of quite extensive disease of both lungs and sputum tests run last month in the laboratory here showed the sputum to be strongly positive for tubercle bacilli. With a disease of this extent existing for this length of time it would be in my opinion that this man is totally and permanently disabled because of pulmonary tuberculosis.

Very truly yours, Bruce H. Douglas, M.D.
Tuberculosis Controller.

BHD
M

Mr. S. M. continued under our care. In February 1940, we had an X-Ray taken at St. Francis Hospital. At that time there was no evidence of a tuberculous process in either lung. The report of the Roentgenologist is reproduced here.


SAINT FRANCIS HOSPITAL
HAMTRAMCK, MICHIGAN

X-RAY ROOM PERMANENT RECORD

Patient’s name: Stanley M---- Age: 45 Date 2-2-40
X-Ray ordered by:       Dr. Wm. Koch X-Ray No.: 17339
Region: Chest Address: 269 River Road.
A flat roentgenogram was made of the chest.

Diaphragm: The leaves are smoothly rounded and normal in position. The costophrenic and cardiophrenic angles are clear.

Heart:   Is normal in size, shape and position.

Right lung: There is some increase in the lung markings toward the base. The lung field is otherwise clear.

Left lung: Here also there is some mottling at the base. The upper portion of the lung field is clear.

Conclusions: The findings are those of a low-grade respiratory infection. There is no evidence of a tuberculous process in either lung at this time. The patient should be re-examined in from two to four weeks.

S. FORD, M.D.
Roentgenologist.
  

A summary of his progress, as seen in the radiographs, is given by Dr. Hague, a noted expert.


DR. OMER GRENVILLE HAGUE

“The radiograph of September 16, 1938, is that of a male chest with the bony cage and ribs and collarbones and heart cavity in the middle and diaphragm down there. There are some infiltration shadows in parenchyma, or the active portion of the lung in these areas, in the fourth, fifth, and sixth and seventh interspaces anteriorly and a large cavitation shadow in the mid-lung zone.  I am measuring the left lung. That cavity measures 2½ inches by 3¼ inches, a little better than 3¼ inches. The outside measurement of the capsule of the cavity. By a little better than 3¼ inches I mean about 1/8 of an inch more. The reason I am not saying that with certitude is that the upper border of that cavity is very, very thin and very, very faint, but we can see that line that it follows and I would say it would be 3¼ inches at least. That is being very conservative. There is a small fluid level at the bottom of that cavity. There are, also, some heavy hilar shadows, and some thickening of the peri-bronchial trunks; that is, the lymphatics that follow the bronchi and smaller bronchioles. Those shadows indicate repeated infections that have resulted in inflammation and the inflammation has gone on to scarring.

The film dated July 8th, 1939, appears to be a film of the same chest; the ribs strip with the previous film. The lung tissues on both sides show soft infiltrated shadows throughout the lower two-thirds of both lungs. There is an interlobar line, indicating a thickening of the pleura between the middle and lower lobes, on the right side. There is a shadow in this area. It is smaller than the cavity on the left side previously referred to. It is in the same inter-space level, so that I conclude it is related to the previous cavity. It measures 1½ inches by 1 inch. The wall of this cavity is less distinct. That is why it is a little harder to see. The shadows in the lung are of a soft consistency, which would suggest an activity of disease in the lung structure itself.

In the film dated September 16, 1938, the linear markings are fairly well fibrosed, hard. In the film dated July 8th, 1939, we see them softened and in an active state of inflammatory change. In the film dated June 18, 1940, this inflammatory reaction has disappeared and the outline of the cavity is very, very faint, practically disappeared. It would be very hard to measure it accurately. It would be about 1 inch by an inch and a quarter. The general appearance of this chest is much better than in the films taken September 16th, 1938, and July 8th, 1939.

Cavities almost of any size are a poor prognosis type of tuberculosis cases. The tendency usually is for individuals that have cavitation, that they get more cavitations rather than less. Cavities usually tend to get large and unless they are treated successfully by a pneumothorax, or some other compression therapy, and are held down for a long time, they usually get worse and the patient’s outlook is serious.

The cavity in the film dated September 16th, 1938, I think is about as large a one as I have ever seen and I would say that patient’s condition would not be a good risk at all.

The two succeeding pictures dated July 8th, 1939, and July 18th, 1940, show that there has been an extensive constitutional change taking place; that is, the soft tissue of the lung has undergone a remarkable exudative change; that is, there is a softening of the structure all through and in an instance like this that patient would have more cough and more sputum and it might be in the healing phase following this type of chest. For instance, the tubercle from this cavity may have been coughed up and spread out throughout the whole lung and that might be a cause for the infection from here to become broad spread in that chest almost like a tuberculous pneumonic condition and then in this view, this pneumonic process has disappeared and the shadows in the lung are back to what you would expect of an individual of this age and following conditions of a tuberculous recovery.

Radiograph I, taken at Herman Keifer Hospital, September 16, 1938.


Radiograph II, taken at our Clinic on October 20, 1938 and showing extension of the tubercular process.


The prognosis on the first film dated September 16th, 1938, would indicate a very serious situation.

The prognosis on the third film dated June 18th, 1940, without knowing anything about the other two, would be very good.”

In the Spring of 1942, Mr. S. M. went to work for Fisher Body, a division of General Motors Corporation. He did hard manual labor, worked long hours and overtime as well. During his employment he was given examinations and X-Rays were taken. They established his good health and he was permitted to continue to work. His sputum has been negative since his recovery. He has continued working and testified in the Federal Court Trial in 1946.

Radiograph III, taken on July 8, 1939, about nine months after Treatment and showing healing of the cavity and the lung tissue undergoing reconstruction.



EXTENSIVE MILIARY TUBERCULOSIS

With Tubercular Meningitis and Tubercular Nephritis and Splenitis

CASE No. 48

The rapid advance of the disease in Miss N. A., age 14, when treated by the writer in July 1922, was reversed from the terminal stage by one injection. She had been in the Detroit Tuberculosis Sanitarium from the end of January until April. The radiographic findings of January 30, 1922, were:

“Both diaphragm leaves are clear. The trachea shows no compression or deviation. The heart shadow is normally placed. Increased deposit at the hilum on both sides. Some accentuation of the linear markings throughout the right lung field. No definite evidence of a parenchymal lesion in the right lung field. There is extensive parenchymal infiltration throughout the left lung field, with greatest changes in the upper half. Several small annular shadows at the apex and at the level of the first and second ribs anteriorly. We believe these represent small cavity formations. Diagnosis: Advanced parenchymal tuberculosis confined to the left lung field.”

It will be noted that the lesions are located subclavicularly as in the most rapidly disseminating type. Six months later I examined her. She was emaciated, bedfast, comatose, with frequent projectile vomiting for three weeks, cyanotic, with rapid shallow respiration, very rapid, thready, practically uncountable pulse, with the head drawn back in continuous opisthotonus. The fever was 105.5°F. The heart was drawn over into the right side of the chest; the left chest was empty of viscera so far as could be determined, but contained fluid that splashed on shaking her. This lung had spontaneously ruptured.

The right lung showed huge cavitations and consolidations, and the splenic area presented a hard, fixed tumefaction as large as her head. It could not be determined then if this was kidney, spleen or both involved in the tuberculosis process. She was also near death with a tubercular meningitis. Two micro-micrograms of the Synthetic Survival Reagent were given intramuscularly. The recovery process was slow at first, but this was to be expected considering the condition she was in at the time I examined her. It was some months before she got out of bed. A year later the heart was still on the right side of the chest, but the left chest was not empty anymore, it was full of apparently a fluid and fibrotic tissue. At the time she was walking about, her heart rate was still exceedingly rapid and weak, though it had dropped from around 150 to 130 per minute. Her temperature was normal. After that she gradually got better and the heart went gradually over into the left chest where it belonged. The heart rate slowed down.

An X-Ray taken July 24, 1944, shows that the left chest, which was so badly involved, is not exactly normal yet in all these twenty-two years because there is less lung tissue there. That is because part of the chest is replaced by the structures of the mediastinum. The lung tissue shows markings in chests that one would interpret as healed tuberculosis. These marks are very, very small, about a millimeter or two in diameter, dense, fibrous, showing calcifica tion. It shows that the healing process has been very complete, and the scar tissue present from the large lesions healed and are very, very minute.

In this case we have a recovery with reconstruction in both lungs. The other pathological conditions cleared up during the recovery process. Her weight has increased to 145 pounds. She is married and has given birth to twins, pretty husky children. She has remained well to date (January, 1957).

The large mass in the splenic area disappeared completely, but the first improvement was noted in the nervous system, the disappearance of the opisthotonus and comatose state. This showed the SSR had taken effect, but still it was doubted that so much lung destruction could ever be repaired. Time showed that the advantage given here by the SSR not only permitted full lung reconstruction and return of the abdominal lesion to normal, but a general excellent health was gained that proved resistant to the usual infections. Her twins showed a remarkable immunity to the usual school children infections that none other exhibited, indicating a possible gene change.

FAR ADVANCED TUBERCULAR PNEUMONIA

Or Acute Military Invasion, in Extremus at Time of Treatment


CASE No.49


Another case of pulmonary tuberculosis in extremus at the time of Treat ment with a dose of SSR is that of Mrs. M. B. and is of the type that has always advanced to fatality, namely originating in subclavicular lesions in both lungs. At the time of our Treatment April 2, 1934, her condition was too critical to permit a thorough differentiation as to whether she was dying of an acute tubercular pneumonia, or of an acute widespread military tuberculosis. She was “sunk in bed,” fever hovering about 104°F., rapid, thready pulse, cyanosis, with flush from the fever, yet the skin showed yellow hemolytic color after compressing the flushed capillaries. The breathing was very shallow and rapid, and very little but bloody sputum was raised. The physical findings scarcely revealed the cavity, only rales and solidification. No radiograph was taken at the time. A 2 cc. injection of the SSR, 10-(12), was given immediately. She had progressed to this stage from an early subclavicular and apical involve ment thought to be a “cold” in August 1931, when she entered the Herman Kiefer Hospital of Detroit. The condition advanced to that shown in their film of April 23, 1932, Radiograph I. She remained in the two Detroit Public Tuberculosis Hospitals up to late in March 1934, when she was brought to our Clinic. Films of January 18, 1934, and March 8, 1934, show the advance of the disease under their care with the development of the large, shaggy cavity with slight fluid level behind the right clavicle. The latter film being reproduced here, Radiograph II. The experts offered to perform a Thoracoplasty operation upon her at that time. She left because she did not want this operation. She felt too sick for such a drastic operation, with her high fever and exhaustion. Her sister brought her to our Clinic on March 31, 1934. The sputum was loaded with tubercle bacilli. The films show the advance of the disease in both lungs and the infiltrative development of the cavity wall.

This report shows the condition of Mary B. when she entered the hospital.


Radiograph I, made in April 1932, shows advance of disease from August 1931, in the hospital.


The films show the advance of the disease in both lungs and the infiltrative development of the cavity wall. We took no radio graphs until six months later when she was up and about and doing light work. Radiograph III, September 24, 1934, shows a smooth wall cavity. At this time there were no tubercle bacilli found in the sputum at daily tests for two weeks. 
 
Radiograph No. II., shows advance of disease in hospital up to March 8, 1934, with cavitations.

This cavity represents the area where the infection had taken place, and where lung tissue was again healing in after the disease tissue was removed, and the completed process is shown in Radiograph IV, September 12, 1942.

She left the city after leaving our clinic and within a year went to work, at which she has remained ever since besides being married and living a normal life. Frequent sputum tests showed no more germs of tuberculosis and her gain in weight and perfect health mark her cure as complete. Physical findings are normal. Her X-Ray report at the time of entering the Herman Kiefer Hospital is reproduced in Photostat, from the Court Documentations. Reports in June 1960 show persisting recovery, good health, and working regularly. (See Appendix).


Radiograph No. III, shows the cleaning out of the tubercular infection and a sterile cavity undergoing healing.  This radiograph was taken on September 24, 1934, about 5 ½ months after Treatment.


Radiograph IV, showing the cured state in 1942, eight years after Treatment.

 

ADVANCED TUBERCULOSIS

With Cavitations in Both Lungs

CASE No. 50


This is a case of bilateral cavitation with subclavicular lesions and two large thin walled apical cavitations on the right side. She steadily deteriorated under the best sanitarium care in Cleveland, Ohio (Sunny Acres), and in Detroit, Michigan, from 1931, when her thyroid gland was removed at the Crile Clinic of Cleveland, until September 2nd, 1934, when she received Treatment in our Clinic at Detroit.


Miss C. P. was examined at Herman Kiefer Hospital, Detroit, Michigan, in March 1932. A Photostat of the hospital X-Ray report is reproduced here. This is done because the radiograph does not show all of the lesions well.

Radiograph I shows the extent of the disease on February 24, 1934, about six months before she came to us for Treatment. Phrenectomy and pneumo thorax had been unsuccessful in curing this patient. At the time we first saw her, the prognosis was serious. Bloody sputum loaded with tubercle bacilli was expelled up to the time of our examinations in September 1934. We found the upper half of both lungs invaded and a highly toxic state that resulted in unusual muscular weakness. On September 2, 1934, she was given 2 cc’s of the serially arranged SSR Carbonyl groups. This toxic state quickly left so that two weeks later she went to work instead of being confined to bed rest. She received a second Treatment on November 24, 1935. Since then she has had three more Treatments over the years, one in 1937, 1939, and 1942. She has been working, is married and in good health, according to our last report. Radiograph II, taken March 22, 1943, shows the cured state, with minimum of scar tissue and return of normal lung parenchyma.

This case shows how the basic toxic state that caused hyperthyroidism requiring thyroidectomy, also removed her resistance against tuberculosis infection, and caused other disturbances resulting in muscular weakness. This latter effect persisted until the time of receiving the Carbonyl Therapy, and then very quickly disappearedIt was no doubt due to suprarenal cortex inhibition. Her statement on her weakened condition includes this: “When I first visited Dr. Koch, I was very short of breath and was able to walk a short distance only,” and “I felt better almost immediately after the Treatment, and went back to work fourteen days later, September 16th.”

The testimony of Dr. Hague on this patient’s X-Rays has been paraphrased and reproduced here.

After examination of the X-Rays from Sunny Acres Sanitarium, Dr. Hague stated in regard to the X-Ray taken 8/6/32 that: “This is a radiograph of a thorax of a female patient, showing the chest cavities with a tuberculous process in the upper half of both lungs, of an advanced degree, with cavitations in the left apex, about three of them contiguous with one another, so I shall measure them all together. They measure two inches by one inch.

“There are also some shadows in the opposite side that suggest smaller cavitations behind the second rib anteriorly on the right side. This area of whiteness is an extensive tuberculosis process in the upper lobe of the right lung. A similar condition exists on the left side, but it doesn’t show so much density as on the right, because there is a cavitation process which has taken away some of the fibrosis and that has been spat out as sputum.”

“The descending bronchi are thickened because of repeated drainage from the upper areas of infection that have passed down into the lower trunks on both sides — lower bronchial trunks on both sides.”

X-Ray film dated 11/5/32: “This film shows the same patient with an aggravation of the disease, in which there is a shadow in the first interspace anteriorly, suggesting cavitation; and an enlargement of the shadows on the left side, indicating enlargement of the previous cavities. And, I believe an angular shadow that is on the left side in the previous film now shows more clearly that it is becoming a cavity, too. So that you now have an area of potential multiple cavitations measuring three inches by two inches. I would say that this patient is worse on this (11/5/32) film than on that one (8/6/32).

“X-Ray film dated 2/11/33: “The tuberculosis process in the right lung has increased. The cavitation is large; measures an inch and a quarter outside measurements in both diameters. The total area of cavitation in the left upper lung is slightly more, but there is a concurrent factor of a pneumothorax in which there is air in the base and up over the upper lobe of that lung.”

X-Ray film dated 5/17/33: “The only significant change in these two sets of film is that there is a little better compression over the apex of this lung, and one fairly strong adhesion band at a level of the third rib anteriorly is holding lung structure from complete collapse in that area.”

X-Ray film dated 8/16/33: “The same conditions exist in this film, with the exception that the outline of cavity in the right upper lobe, measuring two by one inches, is more clearly seen. There are still adhesions on the left side.”

X-Ray film dated 11/29/33: “I would say the left lung doesn’t show any significant change from the left lung in the immediately preceding, but the changes in the right upper lobe indicate the cavitation a little more sharply outlined, and a little heavier in cavitation wall thickening, which would suggest to me that there is more activity (the tuberculous process would be more active, creating more inflammation), and the response to the inflammation is characterized by a deposit of fibrous tissue surrounding that cavity.”

X-Ray film dated 2/24/34: “This is a little lighter film. The right apical cavity is clearly seen. The fibrous tissue surrounding it is a little less in density, but it is still present.”

X-Ray film dated 5/26/34 was then shown to Dr. Hague and he stated his opinion as to the general picture of the pathological condition of this patient at the time of this picture. “The three last views show no appreciable improve ment under pneumothorax therapy. The diseased area of the left lung, with its cavitations, has not completely collapsed, because there are adhesions remaining, and the cavitation in the right apex with the associated fibrosis still exists, and I would say that that is a very serious case of active tuberculosis.”

Where the patient is still showing positive sputum, the prognosis is serious. (It should be noted that this last X-Ray (5/26/34) was taken over 3 months before the author treated the patient.)

Dr. Hague was shown an X-Ray taken about seven and one-half years after the patient was first treated in Dr. Koch’s Clinic. He stated that the X-Ray taken February 19, 1942 “indicates a very marked improvement of this patient. The pneumothorax previously seen has now disappeared, the gas has been absorbed, and the lung has re-expanded to fill the chest cavity. The areas of former large cavities in this side, in the left upper first and second interspaces, have practically gone, and the annular shadow on the right side in the first interspace also is gone, but there still remains a mild fibrosis in the first and second interspace at the site of the previous infection. There are fairly heavy hilar shadows in the left upper mediastinal area which have come from the inflammatory reaction of the large area of cavitation previously seen.”

The last film that had been taken, on March 22, 1943, is reproduced here and is Radiograph II. Dr. Hague stated: “That it does not show very much change from the one immediately preceding (2/19/42). I would say it is about stationary.”

To the question: “Assuming at the time of the last two films that the general health of the patient was good, and there was no sputum or no blood, what would you say as regards improvement or recovery process in these films?” Dr. Hague answered: “Well, having seen all the cavitations of the left side and the large one on the right — these two show a remarkable removal of disease process. It would be considered an excellent recovery if it were in the ordinary course of observation in a sanitarium. We would consider that a cure, under sanitarium conditions.”

 
Radiograph No. I, taken February 24, 1934, about six months before Treatment, showing cavitations in the right apex.
  
Radiograph No. II, taken March 22, 1943, showing recovery.  It was taken for Court purposes.

TUBERCULOSIS OF LUMBAR SPINE


CASE No. 51


J. A., age four, came to us with a diagnosis of tuberculosis of the spine in August 1924. He had been diagnosed by Detroit’s leading Orthopedist, Dr. La F----, Sr., who advised an Ablee Splint operation. He was supported by a brace that limited motion and reduced the pain only partially.

The family history showed his older sister had far advanced pulmonary tuberculosis.

For about a year he had increasing pain in the lower back and legs, found it difficult to get up after falling and would cry out with pain when he relaxed in bed on going to sleep. We fitted him with a brace, too. It did not limit his motion too much, but it did aid him during his sleep.

Examination showed a typical tuberculosis kyphosis in the lower lumbar spine. The two lower vertebrae showed a sharp angulation that protruded with collapse of the bodies of the vertebrae. There was considerable swelling of the soft tissues and muscle spasm about the region, which limited motion.

We gave him 1 micro-microgram of the SSR serial system of Carbonyl groups. There was a steady improvement so that he could discard the brace entirely in November 1925. The kyphosis gradually disappeared and the pain and limitation of motion disappeared with it. Within a year the spine was straight.

The radiographs made by the Orthopedist, at the time, showed the collapse of the bodies of the fourth and fifth lumbars and the angulated deformity. The radiographs taken after he was cured more than eighteen years showed the two vertebrae fused in perfect alignment so as to form one vertebra. In the upper thoracic spine an area or rarefication the size of a large pea was to be seen. This showed in the healed spine as an area of dense bone where the disease was cured before it could do any damage. The radiographs showing the healed state were submitted as exhibits to the Federal Trade Commission, but we did not receive them when the exhibits were returned and thus we are unable to reproduce them here. In April 1957, two radiographs were taken of the lower spine; one an anterior-posterior view and the other a lateral view. The perfect alignment in all directions is seen. The spine is found now to be one vertebra short.

In high school he participated in sports and received a letter in track. He attended the University of Michigan. Since his graduation, he has continued to live an active life and earn his own living. In April 1957, he reported that he is in excellent health and that his back never bothers him.

Normally, tuberculosis of the thoracic vertebrae usually results in severe deformity under conventional methods of treatment, i.e., by holding the patient in a rigid shell for many years. Where there is present a metastatic lesion as in this case, the chances of survival are only slight.
  
Radiograph I, was taken in April 1957, of Mr. J. A. and shows the anterior-posterior view of the lower spine.

Radiograph II was taken in April 1957, of Mr. J. A. and shows the lateral view of the lower spine.
  
Extensive discussion is due this disease since it supports our working hypothesis so nicely. After the dilute dose of the Reagent, the most virulent tubercle bacilli, even as found in exceedingly destructive skin tuberculosis in Brazil seem to lose their pathogenicity, and the most resistant and progressive lesions have healed with complete cure, just as we have seen in leprosy. The disappearance of the fibrosis with its captured germs and the replacement with angioblastic tissue and then with normal lung parenchyma, the increase in strength and general health of the patient, even while tubercle bacilli are thrown out during recovery has been our observation for nearly 40 years. It suggests the curing of the germ as well as the patient, and implies that the germ was pathogenic only because it was sick itself — defective in its own Oxidation Catalysis.

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Chapter 19

 

PUS INFECTIONS


The etiological position of chronic infection in the causation of cancer requires that any treatment that will cure cancer must very efficiently cure infection. We will show by a few of the many cases cured how fulminating Staphylococcus Septicemia of the most virulent kind, that failed to yield to the other methods at hand, did reverse and become cured after a dose of one of the Reagents reported here. Since these cases are decisive more need not be given.


ACUTE FULMINATING STAPHYLOCOCCUS AUREUS PYEMIA
With Double Pneumonia and Pyelonephritis Complicating Osteomyelitis in a Boy

CASE No. 52 
Dr. L. Andrews

N. R., age 5 years, took sick with 105* fever and pain in the left tibia. This was opened at the Victoria Hospital and yielded 300 cc. of pus, which proved to be a pure culture of the Staphylococcus Aureus. In a few days the symptoms pointed to infection of both kidneys and the urine showed the same organism in large amounts. Lobar pneumonia in both lungs appeared immediately and the blood culture showed a pure rich infection of the same organism. He rapidly and steadily declined and soon it was difficult to get him to take food and water. The fever remaining high, led to progressive weakness and a sort of mummification in spite of all of the best hospital care. His brother was immunized with a vaccine made from a pure culture of the Staphylococcus Aureus. Then the brother’s blood serum was given to the patient. He had nine blood transfusions while in the hospital between July 13 and August 2, 1940. Neither this nor other measures as sulfathiazole made any impression on the advance of the disease. The patient was given up as hopeless and taken home on August 2, 1940, and present treatment was continued for a few more days, but with no improvement. He refused all food and even water.

On August 9, 1940, he was given an injection of the serially arranged Carbonyl groups. In twenty-four hours the patient was better. In forty-eight hours, the patient was taking food. He was hungry and ate in quantity for the first time of his own choice since he took sick. He made a rapid improvement from that hour on. By September 10, 1940, the urine and blood were cleared and the lungs had considerably improved. The X-Ray of the tibia bone showed a “moth eaten” appearance. On September 12, 1940, Dr. Andrews operated on the leg to clean out the dead bone and any infection that was present. It was packed with iodoform gauze. A second injection was given after the operation.

By November 4, 1940, the effects of the pneumonia had practically disappeared. The patient was discharged. The child is strong and vigorous. He made a complete recovery.
  
SUBACUTE STAPHYLOCOCCUS AUREUS
INFECTION OF THE PROSTATE GLAND
With Septicemia Following the Incision and Drainage of a Boil

CASE No. 53 
Dr. J. M. K----

The boy, aged 18 years, while at camp in July 1940, developed symptoms of appendicitis and was operated on because of the diagnosis but the appendix was found to be normal. Soon afterward the pains concentrated in the kidney region and the urine showed the infection to be the Staphylococcus Aureus which was also found to be the cause of a superficial boil that was incised a month previously and after which all his troubles began. The pain, however, soon showed the major location of the infection to be the prostate gland. Sulpha drugs were used with other of the best hospital care that was guided by ample laboratory data. But they gave no help. The condition steadily became worse with high fever, and steady loss of strength and nutrition. Since incision for drainage of the prostate has uniformly turned out fatal, this course was eliminated and when hope was abandoned, Dr. K---- phoned the writer for an Ampoule. It arrived in Los Angeles, by airmail, and was given without delay. Here again an infection that was steadily winning for months quickly reversed after receiving the SSR injection, 2 millimicrograms.

The change may be reported from Dr. K---’s testimony, which has been paraphrased and reproduced here. It shows the intense interest of a father finding favorable facts. “The Treatment was administered. The next day, from my observation the boy was better. He was definitely improved. There was a definite change. The change was one such as you see at a sick bed. I watched him from the next day on. The boy improved. He had an appetite then. He complained less, was less nervous and had less pain. His general condition was definitely improving until the seventh day after Treatment when the abscess broke (as Dr. Koch advised it would). The pus discharged through the penis. The pus was cultured and it showed Staphylococcus Aureus. On the day it broke he had quite some pain and after this he was, to all appearances, well. I kept him in bed and kept him under close observation, but he was perfectly all right. His temperature was normal. He commenced to eat better. Of course, he showed the effects of the sickness, but he had no more of the septic condition. The fever never came back. This was followed, of course, by a definite and lasting and complete recovery.”

In these cases, two things are to be recalled. The advancing infection poisoned the nutrition, food could not be taken, nor even water, and the fevers persisted and mounted until they became chronic when the protective reactivity broke down and the mummifying process set in. The hopeless prognosis was then evident, too, and the sulpha drugs gave no help, but seemed to injure the patient as did the toxins of the infection, it should be recalled that the activated amine groups plays a part in both poisons. The infection steadily went forward also. Then after the Carbonyl Catalyst Treatment, the change was for the better. The appearances changed. Appetite returned, the fever stopped, the resistance showed up by sequestration of the infection and its discharge as in the prostate case. Examination of the discharged pus showed it to be the same Staphylococcus both before and after Treatment. But after the Treatment the infection became suddenly harmless and was quickly thrown out. This is the experience with cows with infectious mastitis, as reported by the Ministry of Agriculture of British Columbia in five years of observation in cattle infections. In a few days, the gangrenous infections that laid the cows low subsides and the cows then are up and about, even as the germ count increases, the wounds heal.

This is an important observation as is also the disappearance of the fibrosis of the chronic mastitis infections in the dairy cattle. Evidently a change has taken place in the germ as well as in the patient. The metabolisms of both have become normal and no toxins are produced. Thus the physiological approach, which does not aim to injure or kill the germ, makes it no longer pathogenic and the patient burns his accumulated poisons out of the way so he is again hungry, even after weeks and months of inability, to take food as he should.

The metabolic fault in the tissues during chronic infection is well represented in bronchiectasis, for here not only is there an excavation of the lung substance starting in a bronchus, but the bronchial walls carry the infection forward so that lobectomy is the only hopeful procedure, from the orthodox standpoint. The following case, like the others in our experience, shows the normalization of the tissues resulting in the cure of the disease locally and systemically, for this patient showed a terrific allergy to her bronchial infection through a most severe asthma. The correction of the fault made it impossible for the infection and its sequel the asthma to find soil, and the cure was therefore consequential to the restoration of an efficient Oxidation Catalysis.
  

ADVANCED BRONCHIECTASIS

With Asthma


CASE No. 54 
Dr. Wendell Hendricks

On January 26, 1944, Mrs. P., a woman of 31 years of age, was helped into Dr. Hendricks’ office. She weighed 82 pounds and was in a severe state of asthma and coughing. The condition had persisted for many days and prevented sleep and correct nutrition, and brought her to the point of collapse. She raised enormous amounts of pus-laden sputum for many years, but the asthma had persisted only for the past three years. A severe sinus infection was probably the initiatory factor. Her pulse was 130 beats per minute and temperature 100 degrees. The blood pressure was 100/80. It was necessary to be propped up in bed to secure any sleep. The red blood count was 4,000,000, the hemoglobin 80%.

Radiograph No. I, taken at time of Treatment.

One dose SSR was given on January 28, 1944. Three weeks later she exhibited a reaction with chills and high fever. Following this reaction the asthma ceased, the blood pressure rose to 112/80, she gained 10 pounds in weight, and the fever dropped to 99.2°. By the 12th week the temperature was normal (98°) pulse 72, and the blood pressure 110/80.


Radiograph No. II, taken August 4, 1944, showing recovery.

In another month the blood pressure was 120/80, and she gained to 93 pounds, but real marked relief from the cough and the excessive sputum did not come until the 24th week had passed. During the 27th week she was given a second injection. She made a complete recovery. There were no more symptoms of the disease, no more pus to be expelled and no more asthma. She slept normally and lived normally again, tending to her card parties and home duties as usual, and lived a brisk life thereafter. We believe that only through the proper restoration of the oxidation mechanism and its catalyst, can tissue vitality be restored and a permanent recovery obtained. X-Ray films, taken before and after Treatment are submitted in demonstration.

Occasionally during the observation visits she was given a lavage of the nasal sinuses to aid their elimination. Colon lavage was part of the general care, together with vitamins and the vegetarian diet upon which we insist in all of the cases under Treatment. No honest physician or expert in this dire disease will claim that an occasional nasal lavage would cure a deeply established bronchiectasis when indeed they admit the only cure is removal of the lung or the lobe that is affected. Even such cases relapse, it is found, as the fundamental tissue weakness still remains. Only the proper restoration of the oxidation catalysis can restore the tissue vitality.

ANTIBIOTIC RESISTANT GONORRHEA


The response of the antibiotic resistant gonococcus infection to the Carbonyl Therapy depends partly on the general health of the patient, and partly on the chronicity of the case when one is comparing the time required to make a full recovery. One may compare the progress of the two young men of nearly the same age each with about the same involvement, and both anti biotic resistant. One had the infection two years and the other four years. The former was in fair health giving a test of the red blood cells of 100% no crenation. The other was very depleted and showed a very poor crenation of his red cells in a one percent salt solution.

Case 54 A, was a boy of 22 years of age. He sustained his infection two years earlier and had received all the antibiotics on the list without stopping the specific infection. This germ had acquired immunity to antibiotics before it infected him. The urethral discharge of gonococci continued. The urine sediment was also positive to Gram-negative “coffee bean” intracellular diplococci, on January 15, 1960, when he received two micrograms of Benzoquinone (2 cc. of the 6x homeopathic solution) intramuscularly. His prostate was seriously involved so that it interfered with the passage of urine and feces. Two weeks later there was still the same secretion of pus and gonococci. But the crenation test of the blood had improved to 90% crenation two weeks later and only a few extra-cellular diplococci could be found in the urinary sediment. Two weeks later the urinary sediment gave only a few gram-negative diplococci. But they were pleomorphic and extracellular. No intracellular “coffee-beans” were found. Ten days later and ever since until now, there were no symptoms either prostatic or urethral, and the urinary sediment was free of gram-negative diplococci. Only a few leukocytes could be found. Thus he made a full recovery on one dose of 2 cc. of the 6x homeopathic solution of Benzoquinone given intramuscularly, though the germ in this case was persistently resistant to all the best known antibiotics right from the very start.

Case 54 B, was 25 years old when he became infected in March 1956. Besides the urethral involvement there was a venereal papyloma and a prepuce lesion, but the blood tested negative to the lues. He received 1,600,000 units of Penicillin. There was a slight improvement and then an acute recurrence with prostatic involvement that interfered with both the passage of feces and urine. On October 23, 1959when he received his dose of 2 micrograms of Benzoquinone the urethral discharge showed the typical “coffee bean”. Gram-negative intracellular diplococci of gonorrhea. There was a reaction with aggravation 84 hours later (this is typical of the recovery process). There was some pain on passing urine, but the pus discharge had become only slight, and in a few days he felt much better in many ways. The feces passed easier with less prostatic interference. But on February 19, 1960, there was abundant secretion, though he had gained 7 kilos in body weight as he was overcoming his great depletion of ill health. This was the beginning of his 18th week after the Treatment and is a usual reaction week in a chronic infection. But it was not a reaction that won recovery. The Benzoquinone was not adequate. On March 16, the dose of SSR was given. A reaction followed in two days with headache and burning in the stomach. The secretion started to diminish the day following the Treatment, and then disappeared. On May 30, he was free of every symptom and of gonococci in the urinary sediment. He had gained 10 kilos, and the urethra and prostate were normal. The urinary sediment showed only a few extra-cellular pleomorphic diplococci. He was found cured again on June15and has remained well ever since. It took six months for his health to reach the good level where he could react with a full cure. The SSR gave an immediate response while the Benzoquinone was helpful to his general health and improved the infection considerably but did not produce a cure. For this the more highly efficient Carbonyl groups of the SSR were needed and then the response was immediate and complete.

In both cases it is seen that the resistance gained by the germ to the toxic amine group of the antibiotic did not influence the response to the oxidation initiating Carbonyl group. Indeed, resistance to the injury is along the same line as welcoming improvement in the vital chemistry. Evidently the germ was made non-parasitic and non-pathogenic for surely it was not injured by an agent that gave its oxidations a boost. And the patient was improved in his whole vital chemistry at the same time. Thus both patient and germ were not injured, but benefited. These observations, like so many others, show that the physiological attack on infection has a rational basis, while the pharmacological attack, which rests on a destructive principle, may invite failure. The data at hand again emphasize the paradox of trying to correct by way of destruction. Here success is had within certain limitations or excluded entirely where nature has full sway. The constructive philosophy, on the other hand, is not hedged in by limitations and nature aids the corrective process from every side and angle. It appears here also that the sicker the patient, the sicker the germ and the longer it takes to establish the correction. The correction of the fault in the patient and in the germ run parallel—“hand in hand.” Both faults are of the same order, as they respond to the same Reagent.
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