SURVIVAL FACTOR
IN
NEOPLASTIC AND VIRAL DISEASES
An Introduction to Carbonyl and Free Radical Therapy
Copyright 1961
A Study of the Phenomena of the Free Radical, the Double Bond,
and its Alpha Placed Hydrogen Atom in the Pathogenesis and
Correction of Neo plastic, Viral and Bacterial Diseases
By
WILLIAM FREDERICK KOCH, Ph.D., M.D.
Detroit, Michigan, U.S.A. Rio de Janeiro, Brazil
Instructor, Histology and Embryology, University of Michigan, 1910-1914
Professor, Physiology, Detroit College of Medicine (Wayne State University), 1914-1919
Pathologist, Woman’s Hospital, Detroit, Active and Honorary, 1915-1919
Director Koch Cancer Clinic,
1919-1949
NATURAL IMMUNITY SERIES
Copyright by William F. Koch
Cancer and Its Allied Diseases, 1926, 1929
Natural Immunity, 1934, 1936
The Chemistry of Natural Immunity, 1939
The Survival Factor in Cancer and Viral Infections,
1955, 1958 Portuguese Edition 1960
TABLE OF CONTENTS
Chapter I—The Postulate
Chapter II—Virus and Cancer Cells
(a) Nature of Viruses
(b) Vaccine Problems
(c) Smallpox
Chapter III—Cancer
(a) Carcinogenesis
(b) Anoxia
(c) Warburg’s Irreversibility
(d) The Co-factor and Reversibility
Chapter IV—Proofs of Reversibility
(a) Official Test
(b) National Statistics
(c) Utility in General Practice
Chapter V—Animal Experiments
(a) Cure of C 57 Breast Carcinoma Transplants
(b) Cure of Sarcoma 37 Transplants
Chapter VI—Energy Production
(a) The FCG, Amine and Hypoxia Effects
(b) Pathogenic Integrations with the Host Cell
(c) Cleavage of the Integration, Recovery Process
Chapter VII—Clinical Proofs of High Efficiency and SSR Oxidations
(a) Acute Toxic States
(b) Chronic Toxic States
Chapter VIII—Atrophy, Anaplasia and Neoplasia
Chapter IX—Survival Factor Chemistry
(a) Antibiotic Problem
(b) Antimitotic Agents
(c) Quinones as Co-enzymes
Chapter X—Recent Pharmaceutical Strides
(a) Quinones as Cytolytics
Chapter XI—The Azornethine Double Bond
Chapter XII—General Aspects of the Reagents
Chapter XIII—Pathogenic Integration Cleavages
Chapter XIV—Catalytic Dilutions
Chapter XV—Termination of The Malignant Phase—Restoration of the
Functional Carbonyl Group. Illustrated by Case Reports in
Cancer, etc.
Chapter XVI—The Termination of the Malignant Phase. The Constitutional
Nature of Cancer and of the Survival Factor
Chapter XVII—Viral Infections
(a) Chronic Symbiotic Poliomyelitis Acute Lytic Poliomyelitis
(b) Epidemic Hepatitis
(c) Rabies
(d) Distemper in Dogs
(e) Hog Cholera
(f) Hoof and Mouth Disease (Aftosa)
Chapter XVIII—Tuberculosis
Chapter XIX—Pus Infections
Chapter XX—Fibrogenesis
Chapter XXI—Pathogenic Mechanism in Cancer and Connective Tissue Diseases
Chapter XXII—Sequelae to Infection
(a) Vascular Diseases
(b) Arteriosclerosis
(c) Coronary Disease
(d) Bright’s Disease
Chapter XXIII—Allergy
(a) Exfoliative Skin Changes
(b) Muscle and Secreting Cell Allergies
(c) Nervous System Allergies
Chapter XXIV—Percentages and Causes of Failure
Chapter XXV—Observations in Animal Diseases
Chapter XXVI—Diseases of the Articulations
(a) Osteoarthritis
(b) Rheumatoid Arthritis
(c) Acute Rheumatic Fever
Chapter XXVII—Case Management
(a) Elimination
(b) Repetition of Dose
(c) Crenation Test
(d) Diet, Medication, Hygienic Aids
(e) Food Preparation
(f) Food Quantity and Quality
Chapter XXVIII—Prevention of Cancer, Allergy and Infection
Appendix I- Sugar Oxidation
Appendix II- Diamine Oxidase Action
Importance of Divalent and Monovalent Cation Balance
Steric Advantage and Hindrance
Appendix III- Diabetes
Epilepsy
Late Report on Mrs. M. H., Case No. 49
Exercise and Rest
Appendix IV- Protective Action of Diformaldehyde Peroxide
Specific Effects of the Carcinogen, Viral and Chemical
Summary-
Supplement- Practical Application of the Former Chapters and Other
Essential Information
DEDICATION
This book is dedicated to the memories of two leaders in American Science and Industry, Dr. Willard H. Dow, and Dr. William J. Hale. Their humanitarian genius was great enough to build the vast Dow Chemical Company to its present pro portions and service, and also take interest in other humani tarian efforts, such as our own, which they investigated fully, evaluated carefully, and then supported effectively in our court battle.
ACKNOWLEDGEMENTS
Gratitude is due Professor Joseph Maisin, of Louvain University, for his many experiments in small animals with and without the writer from which conclusions of fact could be drawn.
Likewise gratitude is due Dr. Willard Dow, Dr. William Hale, Dr. Drake, Dr. Rubens and other Dow scientists for every help in every need, especially for their winning defense against United States Government attacks instigated by competitive drug interests.
The world’s leading surgical journal, the London Lancet, gave an editorial review of the present status of surgery in the treatment of cancer. It gave the same conclusions as did Sir James Paget a century ago, when he stated in his text on cancer that this is not a surgical disease, that the condition was profoundly constitutional, and that operated cases did not live as long on an average as those that were left untouched. From 1910 to 1950, the American Cancer Control Society created an energetic propaganda that 85% of breast cancer could be cured surgically or by irradiation, and that early diagnosis was a prime advantage. Now after the statistics are analyzed the Lancet quotes the world’s leading surgeons on the results of early operation with the same discouraging conclusions as Sir James Paget stated a hundred years ago. In the meantime life insurance statistics and others established the fact that operated cases, the early cases, lived less by two and a half months than the inoperable, far advanced cases that were not operated. Add to this two and a half months the year or so it took the early case to become inoperable and advanced, one sees that surgery done with all its courage, sacrifice and dexterity is not the attack that is required to win against this disease. The Lancet states, “The intensive campaigns to awaken the public to keep on the watch for tumors and report for the earliest possible diagnosis and treatment has met with good response, but the anticipated drop in the mortality rate did not follow.” “Despite a long and intensive educational program for the early detection and treatment of cancer, the death rate from cancer of the breast shows no downward trend.” In fact, “The comparative mortality index, which allows for changes in the age structure of the population, shows for men a rise of 6% in cancer mortality between 1938 and 1950.” “The size of the primary tumor is no guide to curability; two-thirds of patients reporting with tumors of the breast which were smaller than a hazel-nut already showed metastases,” and with regard to lung cancer, “If recent experience is typical, however, by the time definite abnormality appears in the radiograph, most cases of pulmonary cancer have progressed too far for successful resection.” “Survival rates after simple excision, radical mastectomy, and irradiation, are depressingly uniform.” “Our basic approach may be wrong; the attempt to treat cancer as a local disease rather than a general disease, may be as irrational as treating syphilis by excising the primary chancre.” “In most if not all lethal breast cancer, remote spread takes place by the blood stream before interference is practicable.” “The survival rates after different periods of delay before seeking medical advice often shows a curious paradox. Thus Swynnerton and Truelove reviewing 395 cases of gastric carcinoma, showed that the greater the delay and the longer the history of symptoms the greater was the survival rate.” Here we find in the Lancet of April 3, 1954, p. 714, with other statement so similar import, the conclusions of the world’s most advanced surgeons. A year later Dr. George Crile of the famous Crile Clinic in Cleveland gave thorough information to the profession and the public on this subject and was in exact agreement. Now comes the report of the 12th annual scientific meeting of the Detroit Institute of Cancer Research. The consensus was the same, Dr. Harden B. Jones, professor of medical physics at the University of California, gave the ultima tum, “The odds for or against the recovery from cancer are set long before the patient sees a physician.” and “There is no evidence that treatment by surgery or radiation, the only recognized methods of therapy affect the course of the really malignant forms of cancer.” and “Early treatment is a nice theory, but there is no evidence that it benefits the patient.” “Some drastic cancer therapies not only do not help but are harmful.” “The tumor easily could have a billion cells before it is large enough to be recognized as cancer. Some of these cells are already in the blood stream.”
Unfortunately radiation does not answer the needs of the patient, but adds to the basic pathology. The convention of the American Roentgen Ray Society of September 1954, added to the report of the Roentgenologist of the University of Pennsylvania in 1925 when he stated that irradiation before and after surgery opened the vascular and lymph spaces and helped the spread of the disease instead of retarding it. His report was so unpopular that it was suppressed. But today the statistics are so disheartening that even the radiation therapists are bold in reporting that where deep therapy is poured into a neoplasm of one type, a more malignant form or a bone sarcoma is created underneath only too often. When one recalls that viruses are thousands of times more resistant to irradiation than tissue or cancer cells, the situation is logical.
Fifty years ago nothing was known about cancer except the diagnosis, which was about all there was to become expert in. The gross and microscopic pathology was so well learned that the resort to the biopsy was regarded as a sign of poor training (Ewing) (Warthin). Our professor of pathology insisted that we make 100% correct diagnoses and give the microscopic description from the gross findings alone. Every surgeon on the University staff did it regularly.
Today, however, high specialization makes the biopsy an essential for many. For many years ahead of my day, all that was known beyond diagnosis was that cancer was caused by “irritation.” But no one knew exactly what “irritation” meant, or how it operated to cause cancer. Further, there was no information to serve as a starter to investigate the problem. But still the walks through the hospital wards fervently cried for the solution. The surgeon was doing his untiring best and the radiologist hoped and hoped that his approach might some day prove fruitful. And yet no facts stepped forth to show how to even make a start nothing from within the cancer properties themselves.
So the writer decided it might be helpful to get the basic facts on any of the deepest injuries to the body chemistry that could be produced, observe their effects on every tissue quality possible, and then figure out how any of these changes might take part in the pathogenesis of cancer. The effects of complete parathyroidectomy were chosen for this purpose, largely because the great experts of that day on this very subject seemed to have overlooked the main factors in parathyroid insufficiency, and because a subject as important as that should be at least reasonably explored.
As the writer’s investigations progressed in accumulating more data it began to appear that he made the correct start. The findings were carefully evaluated, the conclusions drawn, and from these a Postulate was formulated and tested out in the broad field of disease. It was hoped that if the venture would be propitious, a century of ignorance would be hurdled, and a basis for investigating the cancer problem itself would be reached. A landing in barren territory simply called for a fresh start and another trial. However, the first attempt proved fortunate. Our Postulate had been drawn up with every effort at precision, and the conclusions were fruitful. Under the circumstances this was even more important than if our interpretations were correct or “true,” For the aim was to reach a position of utility.
The utility has two leading aspects. One lies in the proof that the four primary cell functions — contraction, secretion, conduction, and cell division —are provided with energy that is produced and received by each functional unit in accord with one and the same pattern, and when interrupted so as to produce disease, the fault is the same in pattern and subject to the same type of correction by one and the same atomic structure. The other phase of utility is the explanation of both viral and neoplastic parasitisms, the atomic bondings and electronic displacements that constitute the integration of the pathogen with the host cell, which not only accomplish the pathogenesis, but actually provide for and invite the oxidative cleavage that leaves the host cell in normal functional status, perfectly reconstructed, and the virus no longer to be found. The text demonstrates this as well as the fate of the neoplastic cell and the process by which it is disposed of. These matters are based on firm chemical laws, as the text will show.
So whether the cell contractile fibrillae as in asthma, or the secreting fibrillae as in hay fever, or the conductile fibrillae as in a compulsory neurosis, or some other phase of insanity, or the mitotic fibrillar system as in neoplasia, happens to be attacked, the basic pathology is the same and its correction is necessarily the same, too. This is the subject we will demonstrate in this text. We have no thought that our presentation is the best that could be made. However, since we have opened the door and uncovered the mysteries it enclosed, it is our chore to make the disclosure. This door stands open for endless investigation and for collaboration as well. It should be inviting for our proofs of the cure of the many forms of cancer offered in this text stand firm, firstly in their diagnoses made by America’s leading surgeons, with the patients housed in our proudest institutions where every facility for a firm diagnosis was at hand. Then, too, the clinical diagnoses were confirmed by our foremost pathologists. Secondly, the cures were demonstrated to be permanent with reconstruction of tissue so good function was restored, and accomplished by a definite process without leaving even a microscopic trace of cancer cells.
It will be seen that whether the correction happens to be in far advanced cancer of the vital organs, widely metastasized, and the patient in extremis, or the correction happens to be in the terminal phase of rabies, hog cholera, or some other 100% fatal viral disease, the reversal of the pathogenesis follows the same definite order. This physiological aspect of the correction, we will attempt to show, depends upon well proven laws in chemistry that are basic to tissue cell energy production and energy use, and primarily basic to all vital processes. Thus a Least Common Denominator in pathogenesis and its correction has been reached. It serves as a key to the interpretation of disease production and also to its correction in the whole field we have investigated so far.
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Chapter 2
VIRUS AND CANCER CELLS
Cancer cells and viruses are both parasites; that is they have to depend upon sources of energy and material that belong to other usages to conduct their characteristic activities. The virus cannot produce the energy it needs for its vital processes, so it gives signs of life only so long as it is integrated with a living source of energy and food which it diverts to its own ends. The cell it preys upon, the Host Cell, is killed thereby. The cancer cell is not able to perform the functions it was created to do for itself or any of the other cells of the body to which it belongs and is responsible. It has lost its capacity to conduct oxidations, and also the mechanisms that use the energy of oxidation for useful work. Instead a low-grade process, wasteful fermentation, is used to produce energy. This energy is transferred to the mitotic mechanism, where it forces cell division, as it has no functional mechanism to use it where its production is normally controlled by the demand for the function. The mitotic mechanism thus becomes parasitic upon the rest of the cell and the body as a whole.
Viruses may cause normal cells to go neoplastic; maybe all cancers require them. Several hundred synthetic substances are known to cause cancer. It has not yet been decided if or not viruses play a part here, too, but many cancerolo gists think so. It will be seen how the synthetic carcinogen may prepare the way for the virus to integrate with the mitotic mechanism and complete the neoplastic change.
The institution of parasitism within a cell, be it viral or neoplastic, is a complex affair that depends upon a disposing cause besides the particular virtues of the pathogen to show its specific action. Of these anoxia or hypoxia is a leading factor. With plenty of oxygen available as normal structure determines, there would be no pathology if the oxidation catalysis were adequate, and logically enough, it happens that an adequate oxidation catalysis prevents oxygen deficiency in any tissue. This fact will become apparent as we go along. So the key to the correction will be seen to be the restoration or provision of an adequate oxidation catalysis. The initiating act in the oxidation process, namely, dehydrogenation is a main subject of this book. Then there is the subject of the environmental factors that have contributed to the block in the oxidation catalysis. These are discussed also in the hope that a good working picture of the matter is at hand.
NATURE OF VIRUSES
The electronic microscope and bacteriophage studies have yielded rich information on this score. Their sizes vary from 8 millimicra, the size of a protein molecule, to 175 millimicra, the size of the smallest bacteria. Each type has its own shape and these vary from rod to spherule in form. The essential structure is a protein capsule within which lies a nucleoprotein mass.
They are specifically cytotropic obligative parasites and always pathogenic. The protein capsule has specific antigenic powers that yield specific immunological responses, and serological reactions. The latter, for example, serve the differential diagnosis of non-paralytic Polio from La Grippe and other viral infections. This is the part that is convertible into a vaccine used to excite immunological reactions in the patient. There is no immunological response to the nucleoprotein part though this is the part that causes the pathol ogy. The protein capsule protects the inner part and carries it to the cell where it attaches to its outer surface and injects the nucleoprotein content into its victim. An acquired immunity inactivates the capsule and prevents the attachment to and hence the penetration of the host cell. As soon as the material is injected, it breaks up into a myriad of similar units of nucleoprotein as by a de-polymerization process, and each particle unites chemically with a nucleoprotein particle of the host cell, and thus integrates or becomes one with it as by a co-polymerization act. The host cell particles with which they integrate are the “grana” that perform the vital functions of the cell and produce the necessary energy thereto by oxidation. As the virus shunts this energy into itself and uses it with host cell material for its vegetation, the host cell grana break down and are used up to form the viral colony, which is soon a mass of provirus ready to mature and break forth from the dead host cell as infectious parasites.
It is the consensus among experts that once the nucleoprotein of the virus has penetrated, integration with the host cell is complete within a minute and a half and no amount of vaccine, antitoxin, or other serological effort can separate the virus and rescue the host cell. It is doomed. On the other hand, we will show how the bondings we Postulate as forming the integration actually invite oxidative cleavage in a way that leaves the host cell in good functional status while the virus is no longer to be found. In this process, the energy taken from the host cell to serve viral vegetation is returned to it to support its reconstruc tion, while the virus undergoes a stepwise oxidation. This explanation is based on the repeatedly observed fact in the cure of rabies, that when the Reagent is given to promote the oxidative destruction of the virus, in an animal that has only maybe 12 to 24 hours to live, a period of 72 to 84 hours are required for the paralyzed victim to be free of paralysis and the affected nerves to be func tioning normally. We have proved this restoration not only in terminal rabies, but also in paralytic dog distemper, paralytic hog cholera, and paralytic Anterior Poliomyelitis. The same chemical corrective measure was used in all and fit the pathology in all. This is taken to mean that the state of integration of the host cell and the virus presents the same atomic bondings in all instances. The same corrective attack was employed in the sensory nerve atrophies with loss of function and in neoplastic disease with success, so it is concluded, that the state of integration of the host cell and the pathogen is of the same order in all, and a Least Common Denominator in pathogenesis and its correction has been established in a broad field.
Though the atomic bondings that constitute the integrations are of the same order, the states of integration vary.
A. —Squamous cell carcinoma of the neck biopsy before Treatment. (150X)
PLATE I
Thus in “Polio” an acute lytic type causes the death of the host cell in hours or days as a rule, while a prolonged symbiotic type may cause extensive paralysis and atrophy that invalids the patient for many years or until death. And yet the host cell is not dead, but as its energy producing mechanism is paralyzed by the integration with the virus, it cannot function any more than a dead cell and the results appear the same. We have found by trial, however, that such cases can be freed of their offending virus and the host nerve cell returns to normal in function and so the atrophied muscles again get impulses to contract and rebuild themselves. Cases that were extensively paralyzed and atrophied for three years have required three months to be restored to 95% or more of normal in function and muscle reconstruction, while a case extensively paralyzed and atrophied for over twenty years has required two years to be restored to 95% of normal, functionally and structurally. Since nerve cells do not reproduce, the cleavage of the integra tion is proven by these tests.
Since the lytic type of infection only takes days or only hours to kill the host cell, the quicker the patient is treated the better the chance to have living cells freed from their viruses, and get complete recoveries. The case records illustrate these situations.
PLATE I
B. — Taken from the same tumor several weeks after Treatment, showing the calcified coagulated hyali nized debris, into which angioblastic tissue is growing with an area of liquification preceding each in-growing bud of angioblastic tissue.
In neoplasia the integration of the virus or synthetic pathogen or bacterial toxin with the host cell is originally with the functional grana energy producing mechanism, until the latter is destroyed in building up the virus and nuclear material integrated with it and undergoing mitosis. This is the only mechanism left to accept energy produced by an uncontrolled process of fermentation, and so neoplasia is the expected result. The details will be discussed later, where it will be seen that the Carbonyl groups that institute energy production and storage as ATP, and creatine phosphoric acid, are like those that mediate the transfer of this energy to the working mechanism and both are paralyzed by condensation with firmly binding amines, of virus or other carcinogens. The virus bound in the atrophic muscle of “Polio” we picture as similarly integrated. The integrations may exist long periods before actual destruction of the paralyzed functional mechanism is accomplished and, during this period, liberation of the cell from the pathogen can restore it to normal. For a period the pathogenesis is reversible therefore in viral infections and the same holds for cancer. This situation is exemplified in the microphotographs (A) and (B). (B) shows the destruction of the cancer cell after the pathogen is removed and the cell residues can function no longer. They then undergo calcification and digestion like a blood clot. Plate I(Medical Record of New York, Koch, October 30, 1920).
VACCINE PROBLEMS
From what was stated so far it is seen that vaccines for a specific virus do not immunize against the nucleoprotein that is the actual pathogen, especially after it has penetrated and integrated with the host cell, so to talk about curing cancer with vaccines or immune sera is a waste of time. Even the prevention of viral infection by vaccines is meeting the strongest statistical opposition since large-scale smallpox and Salk vaccinations have been recorded. In line with what is known about vaccine structure, statistics appear logical when they show that paralytic “Polio” is increased both in incidence and fatality by use of the vaccine. One may compare various regions of different climatic conditions for the data. In all of these the Salk Vaccine was enthusiastically applied, in greater number each year, and the incidence increase was tremendous each year, whereas, if the vaccine were effective there should have been at least a little statistical improvement. In Montreal, generally cool, they reported on August 27, 1959, 521 cases with 27 deaths, just while the “Polio” season was getting well under way, as compared with less than one hundred in 1958. In Ottawa, generally cool, 455 cases with 41 deaths were reported on August 22, 1959, as compared with 64 cases with 7 deaths in 1958. In all of Canada, even before the epidemic started to decline, there were 7 times more paralytic cases in 1959 than in 1958, with a greater death rate. In Detroit, much warmer, where vaccination was thorough, the number of cases in 1958 was 697, against 226 in 1957. In the District of Columbia, still warmer, the Health Department reported 7 times as many cases in 1958 as in 1957. In New Jersey, in 1958, the Health Department reported twice as great an incidence as in 1957. The United States Public Health Service reported an increase of 15½% of paralytic cases in 1958 over those in 1957 (49% against 33.5%). In Hawaii (tropical) there were 65 victims including 32 paralytic cases in 1958; half of these paralyzed cases (16) had received three Salk shots, in an island where 60% had been vaccinated. In 1957 only 25 and 8/10ths % were paralytic instead of 49 and 9/l0ths% in 1958. If the vaccine were effective there should have been a 60% decrease in the incidence in the whole island of the paralytic infections, instead of an increase of nearly 100%.
Nationwide statistics issued January 4, 1960, by the United States Public Health Service, show that for the year 1959, up to December 26th (51 weeks), the increase in the incidence of Polio rose 85% over that of the same period of 1958. There were 8,531 cases listed for 1959, of which 5,661 were paralytic, as compared to 5,987 in 1958, of which 3,090 were paralytic. We just showed the great increase in 1958 over the incidence of the total and the paralytic cases of 1957. Where compulsory vaccination was practiced as in North Carolina and Tennessee, Bealle’s investigations report a 400% increase in paralytic and non-paralytic Polio during 1959 over 1958. So it seems that the more vaccine that is used the more the actual infection that comes about. The statistical analysis teaches much about the nature of the virus.
Of course, this is comprehensible when one considers that the virus breaks up into its component units on penetrating the host cell, as if by a de-polymerization process, and it grows by acquiring new units to add to each, as by a co-polymerization process. Some investigators compare the viral structure to a deck of cards. The complete deck or complete virus with all its units is the parent pathogenic killer type. The vaccines may be regarded as incomplete decks, with not all the units required to make up the full killer type. Now, if a person carried vaccine units of, let us say, half or less than the killer type requires and another vaccination or infection by a crippled non-fatal virus comes along that presents the units missing in the protective infection or vaccination of a previous period either one of which alone can not produce the disease, the units all added up could constitute the complete killer type, and it has been shown that they are “shuffled” in at random to make up the full virus, vaccination may add to the incidence of serious or fatal infection, and the more the vaccination the more the chance for building fatal viruses.
This happened in the writer’s early practice (1920). Two cases were vaccinated against smallpox from the same vaccine lot. One had no effect. The other came down with a rapidly fatal smallpox. There was no epidemic at hand in Detroit at the time, so it was concluded that the fatal case’s inoculation carried units required by a previous silent infection to make it fatal.
SMALLPOX
Statistics on vaccination against Smallpox in the Philippines when the United States took over are instructive. Reports run thus: In 1918, the Army forced the vaccination of 3,285,376 natives when no epidemic was brewing, only the sporadic cases of the usual mild nature. Of the vaccinated persons, 47,369 came down with smallpox, and of these 16,477 died. In 1919 the experiment was doubled. 7,670,252 natives were vaccinated. Of these 65,180 cases came down with Smallpox, and 44,408 died. One sees here that the fatality rate increased in the twice-vaccinated cases. In the first experiment, one-third died, and in the second, two-thirds of the infected ones died. This speaks for the retention of viral units from the previous vaccinations, and indicates that, in the vaccine the shuffling in of units varies in different specimens of vaccine. It should be stated also that every epidemic of viral disease treated by the writer followed vaccination within a few months, when protection should have been had instead of an epidemic. This was so in Brazil, in Aftosa, Cinemosa, Hog Cholera and Rabies, and in Cuba in Hog Cholera.
The question arises then as to how one accounts for the decrease in the incidence of Smallpox, since vaccination was instituted. The question is not easy to settle, since the hygienic improvements in sewage disposal has wiped out the means of spread of intestine carried viral infections. In the great Smallpox days, excreta were thrown out of the window into the streets, and then the outhouse was invented with its flies, etc. Today modern sewage is an obvious advantage, and soap and water are available even for washing the fingers of cooks and waiters in restaurants, and inspections by Public Health Officers help greatly in keeping down the spread of infection. It must be recalled that viruses integrate with bacteria and when these form spores, the integrated virus shares the protection of the spore against sterilization by chemicals and heat. They can thus survive for many months or years with full virulence. The intestinal tract is known to be a favorable habitat for such integrated viruses, so the hygienic measures of today would wipe out small-pox anyway without the benefit of vaccination, if there is any when carried on commercially. The present-day kitchen garbage disposal sink apparatus has cut down the incidence of the house fly so much that its universal adoption should become the greatest health booster of the century. In the writer’s experience, vaccination is a laboratory success when the technique is correct all the way through. Commer cially the statistics do not look so favorable when other variables are encountered.
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CHAPTER 3
CANCER
Glover showed in 1923 that the cancer virus existed in a pleomorphic germ that was bacillus in one phase and coccus in another, and virus in the third phase. He also showed it could exist in a fungus or mycelium phase. The latter form has been identified lately by Irene Diller, and some others, and the whole chain of forms was independently proved by von Brehmer, in the last few decades as well. The work was thoroughly repeated and proved by my friend Jacob Engel and George Clark, at the U.S. P.H.S. laboratories, but, for reasons we will not discuss, they were not allowed to publish their findings. The infectious nature of natural cancer was thus proven beyond any doubt by carefully following the four laws of Robert Koch. Doctor Clark was able to get a paper read on this confirmation in 1953, at Rome, Italy, at the Sixth International Congress of Microbiology. So at last the facts are recorded in the archives of orthodox scientific literature.
In the usual viral infections, the host cell material and energy are used to build the viral colony with terrific multiplication of new viruses. In cancer, both nutrition and energy go into the building of new cancer cells and perhaps only an equal number of integrated viruses. For this reason it has been difficult to demonstrate the virus in certain cancer growths. Synthetic carcin ogens numbering over two hundred have been tried out. One sees that the same two atomic units required for viral integration with the host cell are to be found. These are:
(a) the activated amine group, and
(b) the highly mobile hydrogen atom alpha to a double bond in the most exposed area, the “K region”, as it is now named.
When dehydrogenated during anoxia it adds to the FCG activating unit. Carcinogens carrying the amine group that integrates with the host cell FCG to start the pathogenesis, as in acetyl amino-fluorene, and in Butter Yellow, and its analogues, hold the amine group in a protected state until the agent enters the body and hydrolysis or oxidation frees it of its protection, so it can make the azomethine condensation. Some experts think that the synthetic carcinogen prepares the cell for the virus carcinogen, but give no explanation of how this is done. Our Postulate, on the other hand, shows that the amine group of synthetic carcinogens or of the fungus always found in cancer can play a part by inactivating the cell’s FCG. The blocking of the oxidations that results brings about the colloidal gelling that causes the anoxia necessary for addition of the free radical (brought about in the virus by dehydrogenation) to the double bond that activates the FCG. Our Thesis also shows how the carcinogen can produce cancer without the aid of a virus by addition of either pathogenic atomic unit.Some animal experiments with neoplastic transplants, and some with carcinogenic agents are reported here for comparison to show that the same reagent gave protection and cured in high percentage in each set. The parathyroidectomy experiments should be recalled in connection with the pathogenesis and the anoxia involved. This is a main pillar of our Thesis as based upon our earliest findings that, of course, took considerable thought to be appreciated. They are not even appreciated today in the orthodox circles, although Warburg, the Nestor of the biochemical profession, has championed the fact that anoxia is the cause of cancer for decades. He is the pioneer who developed methods of study of the oxidations in tissues. However, Warburg has not yet appreciated the place of the free radical in the process. It will be seen that it is this position of orthodoxy that has limited progress in the explanation of the mechanism of anoxia in causing cancer, and the true nature of the carcinogenic change. Nevertheless, his contributions that won for him the Nobel Prize in Medicine on this subject are a monument of support to our Postulate. Hence we give some quotations from his most recent summary in “Naturwissenschaften,” Vol. 42 — p. 401, 1955:
If one examines them in the light of the data we have presented in the preceding pages, it will be evident that they confirm our own Thesis on the pathogenesis of cancer and disease, in general. They point out the essential status of anoxia, which we have claimed is necessary for the pathogen to be changed by dehydrogenation (of the tissue metabolism) to a free radical which instead of being burned and disposed of as fuel in the presence of oxygen, is not burned in its absence but is able to add to the cell grana and do so at the very point where the activation of the oxidations is generated, namely the double bonds that activate the Carbonyl group, which we credit with initiating the tissue oxidations by serving as a dehydrogenator of fuels and pathogens. Thus anoxia is essential to the pathogenesis, as it disposes the pathogen, carcinogen, virus or what not, to be able to integrate with the host cell and block grana function.The following quotations support our Thesis as far as they go.
“One method for the destruction of the respiration of the body cells is removal of oxygen. If, for example embryonal tissue is exposed to an oxygen deficiency for some hours and then is placed in oxygen again, 50 percent or more of the respiration is usually destroyed. The cause of this destruction of respira tion is lack of energy. As a matter of fact, the cells need their respiration energy to preserve their structure, and if respiration is inhibited, both structure and respiration disappear.” If one estimates the amount of normal function, one sees how the pathogenesis we have described will accomplish what Warburg reports here. Again, “If an injury to respiration is to produce cancer, this injury must, as already mentioned, be irreversible. We understand by this not only that the inhibition of respiration remains after the removal of the respiratory poison but, even more, that the inhibition of respiration also continues through all the following cell divisions, for measurements of metabolism in transplanted tumors have shown that cancer cells can not regain normal respiration, even in the course of many decades, once they have lost it.”
“But why are the body cells dedifferentiated when their respiration energy is replaced by fermentation energy? At first, one would think that it is immaterial to the cells whether they obtain their energy from respiration or from fermentation, since the energy of both reactions is transformed into the energy of adenosine triphosphate, and yet adenosine triphosphate = adenosine triphosphate. This equation is certainly correct chemically and energetically, but it is incorrect morphologically, because, although respiration takes place for the most part in the structure of the grana, the fermentation enzymes are found for a greater part in the fluid of the protoplasm. The adenosine triphosphate synthesized by respiration therefore involves more structure than the adenosine triphosphate synthesized by fermentation.” Since the enzymes and intermediaries of fermentation, which biochemists accept as playing a big part also in the cell respiration, bathe the grana and the grana do not use them, as the quotation shows, then the conventionally accepted process is not correct, and a different process and different set of enzymes and intermediaries are involved. This process must be one, which inactivates the grana when oxygen is missing; hence the logical deduction is that the free radical is an essential part of an early intermediary as we have hypothesized for so long.
Further, “The first notable experimental induction of cancer by oxygen deficiency was described by Goldblatt and Cameron, who exposed heart fibro blasts in tissue culture to intermittent oxygen deficiency for long periods and finally obtained transplantable cancer cells, whereas in control cultures that were maintained without oxygen deficiency, no cancer cells resulted. Clinical experiences along these lines are innumerable.” Warburg emphasizes, “but there is only one common cause into which all other causes of cancer merge, the irreversible injuring of respiration.” He states, “In recent years it has been recognized that subnarcotic doses of urethane cause lung cancer in mice in 100 percent of treatments. Urethane is particularly suitable as a carcinogen, because, in contrast to alcohol, it is not itself burned up on the respiring surfaces and, unlike ether and chloroform, it does not cytolyze the cells. Any narcotic that has these properties may cause cancer upon chronic administration in small doses.” So Warburg recognizes that a carcinogen must be not destructible by the cell’s oxidative mechanism or otherwise. It can then become integrated with the cell and become a part of it, and can become accumulative as the disposing anoxia provides occasion. Warburg states in this connection, “Any respiratory injury due to lack of energy, however, whether it is produced by oxygen deficiency or by respiratory poisons, must be cumulative since it is irreversible.”
The essential nature of the process of fermentation subjects it only to control by the circumstances that control any enzyme action. These are tem perature, the pH reaction of the medium, the concentration of the ferment and of the substrate. Besides such accessories as the magnesium ion or when needed, a co-enzyme will determine the speed and extent of the reaction. Fermentation progresses as well in a test tube as in a living cell. No physiological control of these qualities for the specific service of the cell economy are known, except one, and that is the presence of the oxidation process. Normally this is the presence or absence of oxygen. Pasteur was first to observe this relationship, and the great Warburg named it after this supreme observer, — the Pasteur Effect. This phenomenon was first described by him when observed in yeast cultures, but it is a common property to all cells that are obligatively aerobic. He reported that if a culture of yeast is deprived of oxygen, fermentation comes to the aid of the cell to supply the energy for vital processes, and if oxygen is again admitted to the culture, the fermentation ceases and oxidation takes its place. Fermentation is very wasteful and less than one-fifteenth as efficient as oxidation in the use of fuel material. The mechanism of the Pasteur Effect has never been explained by orthodox biochemistry. However, one will see that our Postulate incorporates its explanation as a function of the Functional Carbonyl Group.
Oxidation has several positions of control in its process in line with our Postulate. The first is the potency of the FCG, which must start the process by dehydrogenating the fuel. When this Carbonyl group is not free, as when the hydrogen it removes from the fuel is not taken away by some electron acceptor system, then oxidation is blocked. And for this, oxygen is essential as the ultimate electron acceptor in aerobic organisms. So lack of oxygen has two steps in blocking oxidation or hindering it. Another position of control is the inactivation of the FCG by additions to the double bonds that activate it. This would happen as we explained when anoxia prevents the free radical formed by FCG action from becoming a peroxide free radical so it must add to some position as that of the activating double bond. When this happens the FCG is inactivated and the starting of another oxidation progression is blocked. Fuels so added, may easily be burned away by the process we outlined for removal of pathogens, but normally it is not accomplished by FCG action when oxygen is again admitted unless the FCG belongs to a different unhindered structure. If a pathogen has been added the SSR is needed to free it. * However, when oxygen is lacking the FCG as a rule will not be relieved of its hydrogen atom and can not form a free radical in the fuel until oxygen is admitted, and this is a protection to the mechanism.
* The SSR is a synthetically produced Carbonyl compound of high Oxidative-Reduction potential, used as a therapeutic agent.
Physiologically, however, the control that is designed to serve the economy of the tissue itself and the organism as a whole is regulated by the need for energy production. Oxidation is regulated so quantatively but fermentation is not. The need for energy is determined by the work to be done by a functional unit, and this is regulated by nerve or some hormone action, which releases the phosphate’s stored energy to become work energy. This creates a deficit of stored phosphate energy, and oxidation must get going to replenish the supply. We explained elsewhere how the FCG accomplishes this act. So physiologically, oxidation is controlled by the need of energy for work, and the substances concerned in the process in addition to oxygen and the fuel are the FCG, creatine, and phosphoric acid. Therefore free creatine and free phosphoric acid and possibly some calcium balancing factor will give the free FCG a chance to start oxidation progressions that will yield the energy to form energy carrying creatine-phosphoric acid, as we explained before. Dehydrogenation and FCG action are concerned in oxidation only, and not in fermentation. Therefore, fermentation is probably blocked by inactivating its initiating enzyme by the act of dehydrogenation to form an active free radical in it, so that it makes an inactivating addition that is split by phosphoric acid set free when it is liberated from an energy carrying ester. The ferment would then act through its restored hydroxyl group when energy fails, — a possibility only, as the need for energy production would be indicated by an accumulation of phosphoric acid, the first indicator for the need of fermentation, that is also able to liberate the ferment’s bound hydroxyl group, that was inactivated by oxidation (dehydrogenation) during anoxia. Aside from such automatic control, there is the nerve and hormone control of the FCG and its azomethine double bond with the amine group of creatine where the nerve impulse determines its rupture to form the phosphate energy carrier, or its formation to discharge the energy load into the working mechanism. The phosphate energy bonds of fermentation are not formed or split in that way. Their energy must enter the functional mechanism through a different door. Mass action and energy transferred by photosensitiza tion may determine such activity. There is no data on which to base a decision.
Fermentation need not be a general affair, but may be localized in some particular tissue where the FCG function is hindered. Function forced by fermentation energy beyond physiological control is the characteristic of all allergies including cancer. The type of allergy is determined by the functional unit involved, secreting fibrillae in hay fever, contractible fibrillae in asthma, conducting-synapse fibrillae in compulsion neuroses, mitotic fibrillae in cancer, etc. However, FCG block is necessary as described before. And the permanent block is done by a condensation with a firmly bonding amine as guanidine, or of some virus or an amine produced by decarboxylase action on some amino acid. When Victor C. Vaughan demonstrated in 1910 that the alkaline hydrolysis of various proteins gave rise to a toxic fraction that caused anaphylaxis, the writer was privileged to work in this kindly scientist’s laboratory and isolated several toxic amines from his alkaline hydrolysate. They produced the allergic changes of fatal anaphylaxis. Later on it dawned on the writer that if his Postulated FCG were blocked by toxic amines produced in a tissue by their decarboxylases that operate best in an alkaline medium, fermenta tion would be the result that could force the allergic responses that occur in anaphylaxis, and the type of response would depend upon the functional unit acted upon, while the amount of amine could be very small.
To check up on this a large number of allergy cases were treated with the SSR by the writer and several hundred collaborators. The results reported were about 85% recoveries obtained on one or two doses. These included the intractable asthmas and hay fever cases as well as the infantile eczemas that fail to respond to known methods. Some guinea pigs sensitized to egg white by the Vaughan method were also treated with success, but such experiments are not determinative unless all variables can be excluded, and they cannot. At any rate, one sees here the practical meaning of the Pasteur Effect as modified by a pathogen. Physiologically, fermentation stops in an anoxic tissue when oxygen is admitted, but here pathologically, the use of oxygen was blocked until the hindrance to the FCG was removed by use of a “super” Carbonyl group, the SSR. Though in orthodox biochemistry the explanation of the Pasteur Effect has not yet been made, we see that the Carbonyl group is the key to the situation both normally and in pathological processes. Our Postulate is thus strengthened by its broad utility.
That the narcotic action promotes neoplastic behavior is only too well known to the clinician. Especially is this true of the oxides of nitrogen that present permanent free radicals that can block respiration and promote cancer growth most disastrously. Their essential action is to hinder cell respirations. Other confirmatory quotations in support of our Postulate could be given, but this is enough.
While it was important to recognize the essential role of oxygen lack in carcinogenesis, the observation is of no practical use until one understands the mechanism whereby the anoxia disposes to neoplasia. It is too bad that Warburg was not aware of our findings after parathyroidectomy, the action of high-energy amino groups in attacking the oxidation initiating Carbonyl group of the grana as we Postulated, and that thereby the oxidation mechanism was blocked. It is too bad he gave no thought to the position of the free radical formed by these dehydrogenations and the absolute need of molecular oxygen to carry the oxidation progression forward, and that when the substrate acted upon could find no oxygen to combine, it must combine an appropriate double bond, and thus integrate with the cell’s energy producing mechanism. It is too bad that he did not make these steps and then the third step to recognize that the very integration of the pathogen with the host cell invited the oxidative separation of both leaving the host cell in good functional status, while the pathogen was destroyed. He therefore missed the essence of the reversibility of carcinogenesis, and the means of bringing it about.
We will give the details as we go along, and the substantiating proof for each step. However, what Warburg did establish was a great advance in cancerology and his prestige as a biochemist makes this support to our Thesis, a most valuable one.
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ment at Detroit, are given below. Since the only variable that entered the picture was our own therapy, we take the credit for the drop in the death rate in Detroit and its lesser increase in cities that sent us patients, as compared to the high increase in death rate in all largest cities that did not send us patients. While Philadelphia and Los Angeles showed a 30% increase in this decade, Detroit showed a drop of over 20%, and it was the only large city that showed any fall whatever in the death rate from cancer.
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National Statistics
Individual case studies that support this thesis are taken from the testimony of collaborating physicians in the U.S. Federal Court where they were proven factually incontestable. They demonstrate the different features of the reversibility.
UTILITY IN GENERAL PRACTICE
What is most important to the physician is the field of utility of Synthetic Survival Factor Therapy. The following table is contributed by Dr. Wendell Hendricks as part of a paper given before a convention of collaborators who were making observations with this Therapy. The best showing is in the viral diseases which gave a 100% recovery rate, measles, mumps, infantile paralysis, and the acute infections as gonorrhea, rheumatic fever, sinusitis, etc., and influenza. The poorest showing was in Arthritis Deformans which gave only a 50% cure rate. This disease is 100% incurable otherwise, however, and perhaps the patients did not stay with the Treatment long enough to give it a chance. In the 100% incurable hyperthropic type of arthritis a cure rate of 82% of 144 cases is certainly a good service with observations showing the permanency of the cures over a period of 4 years of checkup.
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CHAPTER 5
ANIMAL EXPERIMENTS
When presenting a Thesis such as this, it is good policy to eliminate superstitions and misinterpretations. For example, the idea that the cures we will report were secured by psychology or suggestion, or that after all the disease was not Cancer, Infantile Paralysis, Tuberculosis, or what it is represented as being. That the diagnoses were uncontradictable is established, and the pretreatment control period showing the downward course of the patient was also proven uncontradictable. The recoveries were established for many years, even several decades in some cases. It was also proven that no other remedy was used, and the sharp contrast between the pretreatment control period and the characteristic cyclic recovery that characterizes the recovery process after the Survival Factor Reagent was used settles the credit according to modern scientific procedures in drug testing. Because of the many short comings in the collateral control system when humans are under treatment, it has been discarded long ago, and the ACTH and Cortisone experiments show the clinical procedure of using an adequate pretreatment observation period to compare with the post-treatment period is the only reliable procedure known, and it is the procedure used by all highest rating clinicians for clinical tests. This is the system we use throughout, and each case should be studied with this in mind.
However, to remove any doubts about etiological and psychic factors we offer a few animal experiments, in which transplantable C 57 Breast Cancer was inoculated into mice, and also transplantable Sarcoma 37 was inoculated into mice, all at the Jackson Memorial Laboratory at Bar Harbor, Maine. The inoculated animals were then sent to Dr. Stanley Bandeen, of Louisville, Ken tucky for Treatment and observation. The C 57 inoculations were made on May 7th and the Sarcoma 37 on June 30, 1950. The experiment was terminated by a frost on November 13, 1950, that killed most of the cured animals and those undergoing recovery. The details are given below. Since the etiological factors in these experiments are uncontradictable, the diagnoses of the conditions treated are also uncontradictable. Some mice were killed by fighting. They are excluded from the statistics, even though they appeared cured. The Treatment used was the 10-(12) concentration of the serial system of Carbonyl groups with free radical terminals, which we designate as the Synthetic Survival Reagent (SSR). We sometimes call it the Survival Factor Reagent or Remedy. The chemical formula is stated a little farther along. The dose is that equal to the smaller dosage of Vitamin B (12) proven clinically active.
EXPERIMENT I
Twenty-five mice C 57 breast tumor transplantation, May 7, 1950. Five were held as controls, and the rest were divided into two sections: (a) 8 mice each receiving 4 minims of the Reagent by injection, and (b) 12 mice each receiving 6 minims of the Reagent. Treatment was given three days after tumor transplantation.
RESULTS
Controls: Five mice. All of the controls died of cancer from the 12th to the 24th day following tumor inoculation. Average length of life: 17 days after inoculation.
Section (a): Eight mice, 4 minims each, the third day after inoculation. All tumors had ruptured through on the 11th day and started to heal on the 12th day. They were completely healed on the 15th day. One of the mice had recurrence which proved fatal on the 44th day. On the 64th day one mouse gave birth to 3 young which lived until killed by frost on the 126th day after birth. Three mice died on the 64th and 66th days tumor free. One was killed fighting on the 32nd day. Three lived cured until killed by frost on the 190th day.
Death from cancer: 1
Death from fighting: 1
Recoveries: 6
Average length of life of those which recovered: 127 days.
Section (b): Twelve mice, 6 minims each, third day after inoculation. All tumors ruptured through from the 9th to the 10th day. All tumors were healed between the 13th and 14th days. Three mice died fighting, one on the 4th day, one on the 32nd day, and one on the 36th day. One died of cancer on the 38th day via recurrence. (On the 62nd day one mouse gave birth to 4 young. On the 112th day she gave birth to 3 young, her 2nd set). The rest, 8 cured mice lived to the 190th day when killed by frost, cancer free.
Death from cancer: 1
Death from fighting: 3
Recoveries: 8
Average length of life of those which recovered: 190 days.
EXPERIMENT II
Twenty-five mice were inoculated with C 57 Breast Cancer by trans plantation on May 26, 1950. Five were used as controls. Four were treated with 2 minims, 8 were treated with 4 minims and 8 were treated with 6 minims of Reagent.
RESULTS
Controls: One died fighting the third day. The other four died from cancer between the 12th and 18th days. Average length of life: l5 1/2 days.
Section (a): Four mice treated with 2 minims of Reagent. One died of cancer on the 24th day. Another died of cancer on the 26th day. On the 30th day and the 32nd day the other two tumors healed. One died cancer free on the 104th day amid the other died cancer free on the 128th day.
Death from cancer: 2
Death from fighting: 0
Recoveries: 2
Average length of life of those which recovered: 116 days.
Section (b): Eight mice were treated with 4 minims of Reagent. Three tumors healed on the 13th day, the others on the 11th, 12th, and 16th days. Three mice with healed tumors were killed fighting. One died on the 44th day, one on the 135th day, one on the 139th day, and two were killed by frost on the 177th day, cancer free.
Death from cancer: 0
Death from fighting: 3
Recoveries: 5
Average length of life of those that recovered: 135 2/5 days.
Section (c): Eight mice treated with 6 minims of Reagent. On the 12th day 4 tumors were healed, and on the 15th day the other 4 tumors were healed. Two mice were killed fighting on the 16th day. One was killed on the 24th day, tumor recurrent. One died with cancer on the 34th day, tumor recurrent. One died on the 128th day and three were killed by frost on the 177th day, all four being cancer free.
Death from cancer: 2 (including the one killed fighting on the 24th day).
Death from fighting: 3
Recoveries: 4
Average length of life of those which recovered: 164 3/4 days.
EXPERIMENT III
Sixteen mice received by transplantation Sarcoma 37 on June 30, 1950. Four were used as controls, and the rest were divided into three sections: (a) 4 mice received 4 minims each of the Reagent, (b) 4 mice received 6 minims, and (c) 4 mice received 8 minims.
RESULTS
Controls: Four mice. All of the controls died of cancer between the 12th and the 20th day. Average length of life: 16 1/2 days.
Section (a): Four mice, 4 minims each. Two died fighting on the 10th day and the 14th day before tumors were healed. The tumors healed on the other two on the 16th and 17th days; one died on the 110th day and the other on the 125th day, both cancer-free.
Death from cancer: 0
Death from fighting: 2
Recoveries: 2
Average length of life of those which recovered: 117 1/2 days.
Section (b): Four mice 6 minims each. One died from cancer on the 18th day. Three tumors healed on the 35th day. They lived cured until killed by frost on the 136th day.
Death from cancer: 1
Death from fighting: 0
Recoveries: 3
Average length of life of those that recovered: 136 days.
Section (c): Four mice, 8 minims each. All 4 tumors healed on the 30th day. On the 84th day one mouse died fighting, this animal being cured. The other 3 remained cured until killed by frost on the 136th day.
Death from cancer: 0
Death from fighting: 1
Recoveries: 3 (4 if one includes the mouse killed fighting on the 84th day).
Average length of life of those which recovered: 136 days.
EXPERIMENT IV
Twenty-four mice were inoculated with Sarcoma 37 on July 28, 1950 and were treated with the Reagent 5 days later. Four mice were held for controls, and the rest were divided into three sections: (a) 8 mice receiving 4 minims each, (b) 8 mice receiving 6 minims each, and (c) 4 mice receiving 8 minims each.
RESULTS
Controls: Four mice. Two mice died from cancer on the 31st day, and two died from cancer on the 36th day. Average length of life: 33 1/2 days.
Section (a): Eight mice, 4 minims each. Two died fighting on the 11th day and on the 28th day after inoculation. Two died on the 84th day, cancer free. Two were killed by frost on the 108th day, cancer free.
Death from cancer: 0
Death from fighting: 4
Recoveries: 4
Average length of life of those that recovered: 96 days.
Section (b): Eight mice, 6 minims each. All tumors healed from the 18th day to the 23rd day. Two mice died cancer-free, one on the 83rd day, the other on the 101st day. Five of the others lived until the 108th day and were killed from frost. One survived the frost and lived to the 411th day.
Death from cancer: 0
Death from fighting: 0
Recoveries: 8
Average length of life of those that recovered: 142 days.
Section (c): Four mice, 8 minims each. Two tumors were healed on the 10th day, and two were healed on the 12th day. All continued in good health, cured, until the 108th day when 3 were killed by frost. One survived the frost and lived to the 412th day.
Death from cancer: 0
Death from fighting: 0
Recoveries: 4
Average length of life of those that recovered: 184 days.
It should be noted that the two mice that survived the frost, lived for an average of 411 1/2 days and died free of cancer. This is equivalent to 41 years after cure on the human scale. One of the mice received 6 minims of the Reagent and the other received 8 minims.
DISCUSSION:
The average length of life of the untreated controls was 20½ days, that of the treated animals that survived the frost was 411½ days, and those that lived up to the frost and were killed by it was 190, 177, 136, and 108 days for the different groups. We see that the frost reduced the possible life of the recoveries on an average from 411½ days to 153 days. When considering the average of Groups II, III, and IV, it must be remembered that the animals killed by freezing were all killed by the same freeze that killed those in Group I, and that those mice in the last three groups were treated 21, 56, and 84 days after those in Group I were treated. Therefore, the average length of life, while it appears to be shortened in the last 3 groups, actually was not shortened.
However, the frost experience makes this experiment valuable in that it showed the effect of dosage, for the only frost survivors were those that received 6 and 8 minims, and those that lived to the frost were those that received the heavier dosage for the largest part.
Two minims showed very poor results as compared with the 6 and 8 minim dosages, but even the 2 minims gave cures, while the controls all died of cancer within three weeks. Hence a minim of a solution of one part to a trillion of water is a great deal of material when one considers the effects. It is just a few millions of molecules, that is all, and only one molecule should be able to start a chain reaction under ideal conditions.
As a comparison of cure rate, with the controls showing 100% deaths from cancer and 0 cures, in spite of the frost, the experiment is decisive, if any such experiments mean anything and it shows the effect of higher oxidation catalysis from the heavier dosage in
fighting the cold.
In other experiments we took accounting on the 100th day or the 200th day instead of letting the frost set the limit as in this experiment. The end result runs about the same as the others.
A matter of interest here is the recurrences of the tumor after it healed pre-eminently in 3 cases that received more than 4 minims each. There were two such that received 6 minims in one group, and one in another. The explanation can be found in the text. In these animal experiments the word “cure” is used to indicate the complete absorption of all tumors, visibly and palpably, the healing of the lesion, and the return of health to the animal.
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CHAPTER 6
ENERGY PRODUCTION
In order to explain the therapeutic procedure and reasons for certain features controlling the care of the patient, a consideration of the energy producing mechanism will be helpful.
We do not know what energy is, but we can differentiate several forms, and measure them in various ways. It is the consensus that all energy produced in the cell, whether by oxidation — namely the Krebs tricarboxylic acid process—or by fermentation, is the same and is stored as ATP (Adenosin triphos phate) high-energy bonds, before it is transferred to the working elements of the cell to be transformed into the energy of work. No other mechanisms of energy production are recognized, simply because no intermediaries identifiable with any other processes have been encountered. However, there is plenty of room for the operation of a far more efficient process than the Krebs Cycle, which indeed is a decarboxylation process nicely adapted to the lower forms of life. The clinical data show that the Krebs system does not fulfill the requirements of the oxidations that maintain health and that some other process of higher efficiency is present that provides the Survival Factor we have identified and reproduced for four decades for clinical use. The intermediaries of this High Efficiency Process are not to be trapped. They constitute the “smokeless flame” that supplies the energy as a preferred process. This is our Postulate that will be supported by practical proof later.
Ochoa and others have calculated that the combustion of a gram mol. of glucose in the tissues yields 450,000 calories of energy as the total from the various steps of the Krebs Cycle. This gives 36 (38) high-energy phosphate bonds with a P/O ratio of three. The free energy ^ F of glucose is, however,—691,000calories, and the energy of combustion ^ H is —673,000 calories. Thus, 18,100 calories are consumed in the process. The energy calculated as —450,000 calories from the Krebs process of oxidations is therefore —220,000 calories shy of the —673,000 calories available for work, and that are not accounted for in anyway. Therefore, some other process of higher efficiency than the Krebs Cycle has plenty of room to operate. Further, the highly inefficient Krebs process (65%) offers no protection against pathogens as it provides no O/R potentials high enough to start their combustions, but supports viral and neoplastic processes instead. It thus does not account for the survival oxidations that are clinically demonstrated. This process we identify with the FCG dehydrogenations that start a chain of oxidations via the free radical formed and its addition of oxygen to produce a peroxide free radical as carrier of the process. In free circulating toxins the reaction may be pictured thus:
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Where TH is the toxin, and RCO the Survival Reagent Carbonyl Group.
In combined or integrated toxins, the most mobile hydrogen atom is alpha to a double bond in the most activated region which would be adjacent to the position of integration with the FCG or its activating double bond. Free radical production where this hydrogen is removed and addition of molecular oxygen to form a peroxide free radical causes cleavage into two parts with Carbonyl terminals. The azomethine double bond is broken, and the nitrogen oxidized away. The double bond of the new Carbonyl groups formed by the cleavage activate alpha positioned hydrogen atoms where further dehydrogena tions repeat the process forming more peroxide free radicals that are the best dehydrogenators and carriers of the oxidation chains to new molecules of fuel or toxin that enter the field. All of the peroxide free radicals serve destructively to toxins therefore and constitute what we referred to as the antitoxic state of structure of the toxin after the Synthetic Antitoxic Reagent worked on it. Koch, “Cancer Journal,” October 1924; Philadelphia; “Koch, Investigations,” 1924. Here the process was described as converting toxin into antitoxin.
Our Postulate required that the FCG is activated by conjugation with the double bonds of an ethylene linkage from which it receives electrons. These two atomic groups are the center of romance in the maintenance of function and in the protection against toxins that enter the field. They are also the centers of attack of pathogens in viral, neoplastic and degenerative diseases. Whether or not a pathogenic response is to be had will depend upon:
(a) the presence or absence of a normal quota of molecular oxygen, and
(b) upon the firmness of condensation of an amine with the FCG, that guarantees or destroys its potency.
In case the normal range of energy production cannot cleave the bond, FCG function is destroyed and disease results. Then a superiorly efficient dehydrogenator Carbonyl group must be supplied to burn off the pathogen as previously stated. This restores the FCG for normal function. This super dehydrogenator is our Therapeutic Synthetic Survival Factor, (SSR).
The adequate oxygen supply plays two parts:
(1) it is the ultimate electron acceptor when the hydrogen atom removed from fuel or toxins by FCG is transferred to some oxidase system so the FCG is free to start new oxidations, and
(2) after the fuel or toxin is dehydrogenated to become a free radical, molecular oxygen must be at hand to convert it into a peroxide free radical to continue the oxidation process.
Otherwise the free radical would under hypoxia add to the closest reactive group that would accept it, and this is the double bond of the ethylene linkage that activates the FCG. The pathogen would thus integrate with the host cell’s energy producing mechanism where it would draw off energy for its own vegetation or to transfer ectopically, and produce disease, and at the same time block the activation of the FCG and stop further FCG dehydrogenations. Thus oxidation is blocked and the consequent colloidal degenerations would follow to produce further anoxia. Thus anoxia is essential to the integration of the pathogen with the grana when the FCG is still operating. However, the moment the pathogen is added to its ethylenic activating double bond, electrons are no longer contributed to it, so the FCG is no longer able to dehydrogenate, and the grana appears to be out of commission, destroyed and lost. Ectopic uncontrolled transfer of energy to various secreting and contractile or conducting functional systems referred to above we hold to be the cause of allergy.
Since creatine did not interfere with FCG function as did guanidine, and since it is the only amine possibly that forms high-energy phosphate bonds, it was easy to assume that it played a role in the transfer of energy produced from the oxidation of fuel to high-energy phosphate bonds as of ATP. It would accommodate this transfer by condensing with the FCG to form an azomethine bond until enough energy had been generated to admit phosphoric acid into the bond and unite it with the amine group of creatine sending the creatine phosphate off as a high-energy carrier. The FCG is thus free to start further dehydrogenations physiologically. However, if the amine condensed with the FCG forms a tight bond not separable under normal ranges of energy production, as did guanidine in the parathyroid experiments, the whole train of pathological events must follow. For this reason it is well to inquire into the sources of such pathogenic amines. One is the production of toxic amines in the acid colon by various bacteria that decarboxylate amino acids. In many people, the intestinal flora is firmly entrenched and converts the food into one’s poisons that serve as the vanguard of disease. Animal proteins are the main sources of these toxic amines, and sulfides, while vegetables, cereals, and fruits supply plenty of protein and at the same time do not support decarboxy lating germs. The intestine must be kept at a range of pH above 7, since the decarboxylations progress best at a pH of 3.5 to 6 when mediated by the Streptococcus fecalis and so many others.
The fungus found always in cancer is an amine producer that could initiate the pathogenesis as explained above, with its whole train of symptoms. And the modern antibiotic amine poisons, especially those that attack the liver and cause suspensions of consciousness like the sulfa drugs, and any in fact, are to be scrutinized with great suspicion as the cancer death rate his increased so greatly since they have become so widely used. Sulfides and sulfhydryl derived from food add to the double bonds that activate the FCG and thus block its activation powers. The intestinal flora again is to be considered with the diet if one is to maintain a normal function of the FCG as an energy producer and protector against pathogens. Especially during the Treatment period, when a dehydrogenator Carbonyl group of highest efficiency has been administered, one must protect the oxidation progression that follows from being blocked, as can take place through permanent free radicals as the oxides of nitrogen. Gas anesthesia should never be used in connection with this Therapy. Highly polar double bonds can also add to and quench the free radicals of the recovery process and block it, so certain terpenoids and even perfumes, and especially acrolein and polymerizing acrylic aldehydes from frying pans, are to be avoided in this regime. The proofs of our Postulate are serious practical facts.
Some medications absorbed into the tissue colloids may alter the steric set-up so that the remedial Carbonyl group which ordinarily could attack the hydrogen atom to be removed perpendicularly to the plane of the conjugation of its carrier carbon atom with the double bond that activates it, now finds a distortion that hinders this line of attack. Opiates and coal tar drugs, and especially aspirin, appear to interfere in this way.
The atomic set-up of the Reagent itself that carries the Super-high-efficiency Carbonyl group must offer a steric advantage in each disease where it is applied. For example: in Hog Cholera, diphenoquinone proved 100% efficient in several epidemics, while it proved 100% worthless in Rabies, and the serial system of Carbonyl groups used in Hog Cholera proved 100% worthless, while it was 86% efficient in Rabies in terminal cases. Both diseases kill 100%, within 3 to 5 days. Rabies is neurotropic always and Hog Cholera rarely before the terminal hours. Our search has been for a molecule carrier of the Survival Efficient Carbonyl group that is equally applicable in all diseases where drug interference has not modified the steric set-up. This will be discussed later on. It will be seen, however, that to identify the high efficiency oxidation system, we consider normal to the cell, as of the same order as the therapeutic substitute used to rescue the FCG and restore normal function and structure, a few comparisons will have to be made. For example: that they are of the same order is seen in being blocked by the same agencies as anoxia, sulfhydryl, and that their processes are blocked by permanent free radicals, highly polar double bonds, etc. Likewise, the restitution program, that follows the freeing of the FCG system of its pathogen by the Synthetic Reagent, is the normal process. So the Synthetic Reagent fits into the mechanism with equal grace, as did the FCG before it was attacked by the pathogen. Likewise, since recoveries from viral and neoplastic diseases that could never be combated successfully before are accomplished by the natural resources of the body after the Synthetic Survival Reagent is used, they both fit the cell chemistry, but each in its respective capacity for survival. Since the recovery mechanism includes cyclic reactions at definite periods never seen in medicine before, just as the cure of the pathologies involved were never seen before, a deeper grasp on tissue physiology is made possible and a wider range of expertness can be acquired. Any successful clinician will recognize that expertness in this Therapy depends upon study and experience, and some new viewpoints must be adopted. To illustrate let us review a few toxic cases.
These cases show the characteristics of the recovery process, which itself gives evidence as to the nature of the etiological factor. Only the most pertinent data is used. It will be seen that each case presents a long pretreatment control period that definitely established the downward trend of health with the steady and often rapid advance of the diseases. Thus the best possible control for comparison of pretreatment and post-treatment progress was followed, and no confusing variables were permitted, as for example, other medications or treatment measures. Likewise factors that interfere with recovery were eliminated, so that the contest lay plainly between the Therapy, the patient’s cooperation, and physical advantage on the one hand, and the disease forces on the other. The Remedy is named the Synthetic Survival Reagent (SSR). There are two forms, the Quinone form which when used is so named, and the Carbonyl group chain form with free radical terminals. This is simply called the Synthetic Survival Reagent (SSR) or given a similar appellation. The quinone dose is two micrograms, and the SSR, two micrograms, millimicro grams and micro micrograms in water, given intramuscularly or under the skin.
With few exceptions, the case records are taken from Federal Court and Federal Trade Commission Testimony, where they were proven factually uncontradictable. Some of the exhibits have been reproduced for use in this book. This policy was adopted to give the student full confidence in the proofs of a Thesis as unusual as this one.
A case of toxic nodular goiter illustrates some of the main features of the oxidation mechanism of our Postulate.
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CHAPTER 7
CLINICAL PROOFS OF HIGH EFFICIENCY AND SSR OXIDATIONS
TOXIC NODULAR GOITRE
CASE No. 1
Dr. Baldor
Mrs. M. J. was 35 years of age in July, 1943, when she came to Dr. Julian Baldor for treatment of a rapidly developing weakness, tremor, sweating, a big change in her appearance, loss of weight, twitching of her muscles, continual excitement, excessive nervousness, pains in her legs, terrific heart palpitation, and shortness of breath. She noticed her eyes were “popping out”, and that her neck had become enlarged by a number of hard nodular tumors. Although the situation had only started a few months previously it had advanced rapidly until she was almost helpless. Examination by Doctor Baldor showed a very rapid pulse, a blood pressure of 190/110 and the other symptoms mentioned, and the Basal Metabolism Rate was found to be plus 104, instead of plus 4 or 6 which would be normal. He noted the nodular develop ment of the goitre which meant that iodine therapy would not help as it does in other cases without this pathognomonic change. The exophthalmia was excessive, and meant an advanced stage of toxicity. Operation could not be done under the circumstances, without first reducing the symptoms to the limit and, in the only way this is attempted, he gave her the iodine therapy with ice bags to the neck and quiet, on July 8, 1943. This treatment was continued until October 30th when it was discontinued as a failure. Indeed her whole condition had become so much worse, she was about wild with excitement and nervousness, she experienced things that made her think she was losing her mind, the muscle tremors increased and jerked uncontrollably, besides. She had become so weak she had to be carried and had lost control of her hands and feet. The exophthalmus and the tumors of the neck had increased exceedingly, the heart showed signs of failing in the weakness of the ever rapid pulse, and the drop in the systolic pressure from 190 to 170, while the diastolic stayed at 110 showing that the toxic cause of the high blood pressure was still as bad as ever. Operation was out of the question, so Dr. Baldor decided to use the Reagent discussed in this book. The iodine therapy was stopped two weeks, so she would be ready for the SSR Treatment. In these two weeks, she became worse at the same speed as previously. Thus the pretreatment control period showed a steady advance of the disease.
She was so weak by Nov. 10th that she had to be carried into the car and into Dr. Baldor’s office to be given the Treatment, an injection of 2 micro micrograms of the Synthetic Survival Reagent (SSR). Every physician knows the value of the patient’s own description of her symptoms and status, so we will let a few words from her personal report emphasize some of the points we wish to establish. She stated:
“First my trouble started in my finger tips with throbbing. It seemed as if the blood circulation was half stopped. My hands began to swell and I could not wear my rings any more. I had terrific pains and then I began having trouble with my legs. I began to have contraction of the muscles, my toes would draw up into knots. I went to Dr. Baldor about it. He gave me one thing after another, but I did not improve any. He sent me to the clinic for the metabolism test, and after that he started a different treatment. It was some drops. All the time I was taking on like crazy. I could not sleep at night. My husband had to lift me up in bed. My hands and legs got steadily worse. Finally I got so bad, my husband had to pick me up and put me in the car. I could not get in. My legs would just turn to water. Dr. Baldor gave me the Koch Treat ment. About two or three weeks later, I felt like a new woman. My strength came back, my legs and hands cleared up, and I can use them again. I now have a job demonstrating. I carry a suit case weighing fifty pounds in and out of homes.”
The Basal Metabolism Rate was taken three months after the Treatment, and found to be perfectly normal, namely plus 6, and physical examination showed her normal in all other respects, no sweating, no jerking, no tremor, no muscle twitches. The exophthalmus had completely disappeared, and so had the thyroid tumors. The thyroid gland was normal on palpation, inspection and function. The pulse was normal 80 to 90, and so was the blood pressure, 140/80. She was strong, slept well, and without any trace of the former disease.
An analysis and interpretation of this case notes two toxic states — one that is the result of the forced secretion of the thyroid cells, the thyrotoxicosis that nearly killed the patient. The other is the toxin that blocked the regulated energy production and the regulated energy acceptance and utilization in both the thyroid cells and the tissues in general. This is the pathogen toxin, which the Postulate identifies as an amine of higher O/R potential than the functional Carbonyl (FCG) group of the tissue cells that could dehydrogenate and thus burn out of the way. The pathogen toxin therefore had the upper hand and as it was being increased in amount, its effects were also increasing as the block to energy production and energy acceptance by the tissue functional Carbonyl groups. These normally initiated oxidations that produce energy efficiently, and received energy in a regulated way to perform work.
As a result the Krebs Cycle energy production took over, and had already largely replaced the high efficiency oxidations of the FCG’s, when the patient came under observation of Dr. Baldor. If the toxic amine pathogen had been subject to dehydrogenation at the hands of the FCG, like the usual run of pathogens and fuel substrates, it would have been burned out of the way and would not have condensed with the FCG of either the high efficiency energy producing system, or the FCG of the energy accepting system of the cell, and blocked their functions.
It was evident clinically that energy was not reaching the working mechanisms. This was seen in the steadily increasing weakness of the skeletal and heart muscles and nervous system. It was also clinically evident that energy production was going on at the highest rate shown by the BMR of 104%. It was also seen that the thyroid gland was forced to the limit in producing its secretion to push cell activity to evolve more energy. But no matter how much was produced even to the exhaustion of the patient, none was used by the energy-starved cells. The patient lost weight rapidly and to the extreme to supply material for energy production, but it could not get into the working mechanism via the blocked Carbonyl groups of the energy accepting system of the Postulate. The basic pathology then was the block to energy acceptance by vital working units. Since one toxin, an amine of high activation was the pathogen, it is also evident that the FCG’s of energy production and energy acceptance are similar atomic groups and since these are dehydrogenators, the Postulate identifies them as highly activated Carbonyl groups. This conclusion is supported by the type of response to oxidation the integrated toxin gives, after it is condensed with the tissue cell FCG’s. That is, the type of cleavage observed is that of an azomethine double bond when its alpha positioned hydrogen atom actually invites dehydrogenation and is removed so a free radical can be formed and add molecular oxygen to become a peroxide free radical which, accomplishes the oxidative separation with restoration of the functional Carbonyl groups of the tissue cell and the toxic amine group is burned away. The facts of the case history support this explanation. (See Appendix).
It is seen here that the pathologic state actually invites correction, and any clinician would suggest correctly how it could be done. He would say, since the FCG cannot dehydrogenate the toxin and start its combustion, because its O/R potential is too low, then the thing to do is to offer a Carbonyl group of higher activation with a potential equal to the job. This is what was done in this case. A molecule of correct steric advantage carrying a Carbonyl group of high O/R potential was used. The results were the rapid reversal of the pathogenesis. As soon as the integrated toxin was burned out of the way, energy could enter the cell working units, and the urgent call for more energy stopped. The thyroid was not called upon to whip up the tissues to do more oxidizing, and the nodules it had developed to aid its work subsided and disappeared. The BMR dropped to a normal of plus 6%, and all of the symptoms of the thyrotoxicosis, and of the basic pathogen disappeared. The woman was normal in 3 months after one dose of a highly activated Carbonyl compound.
This case proved a few things in the Koch Postulate, and it also shows that the thyroid secretion takes no part in the oxidation process, any more than the poisonous nitrophenol series, that some have classified as accelerators of the oxidations. As we pointed out here, the thyroid function is to whip up the cells to put their oxidation apparatus to work to supply the energy needed for the occasion. It itself does not enter the oxidation process. Nitrophenol blocks various esterifications with phosphoric acid which normally form high energy carrying phosphate bonds. Thus it starves the cells of energy and the tissues are whipped up to produce more energy for survival, just as in the case at hand. Nitrophenol thus works as an “uncoupler” and is so classified. It prevents the energy accepting mechanisms from receiving the energy. In the case at hand, the energy came to the doors of the energy accepting mechanism, the FCG of energy acceptance, but the door was closed, — blocked by the condensation with the amine compound.
Thus the Carbonyl group of energy acceptance was already occupied and could not condense with the amine of the ATP that carried the energy that would be liberated by ATP-ase with the help of calcium. Our Postulate goes on to explain that with the liberation of energy by the hydrolysis of the ATP to ADP, the phosphoric acid set free can split the azomethine bond setting the ADP free to again do another cycle of energy transport with the acid.
One sees that there is no similarity in the actions of the thyroid secretion, the nitrophenols and the highly activated dehydrogenator Carbonyl compound (SSR) used to oxidize the pathogen out of the way. The SSR actually took the leading part in the oxidation mechanism and did the work the normal oxidation initiator would have done, if it had an adequate O/R potential. It is not possible to compare a reagent that prevents energy storage for use in work, with an agent that produces energy for use in work, and besides, actually starts the oxidation process in the cell by burning away the pathogen that was blocking energy production.
Further, the nitrophenols are pathogens whose action can wear out, if not forced too long. But if they are forced too long, they are subject to reduction to aminophenols, which would then act much like the pathogen in this case, and block the initiation of the oxidation progression, and bring about a dangerous situation much like in the case at hand. The nitrophenols proved to be pathogens in the attempt to beautify obese patients. The reduction in weight took place but, in too many, the destructive action continued because of the situation that existed in the case we are discussing, and these victims went on to their deaths. They need their FCG’s freed from the obstructive amine as was accomplished in this case. However, the experts are still at sea with regard to the true action that caused the fatalities.
The block in the use of the energy of oxidation by dinitrophenol is seen also in its inhibition of mitosis in Sea Urchin eggs reported by Clowos (1951 Ann. N. Y. Acad. of Science). Even though the dinitrophenol in doses of .01 mm concentration caused a fourfold increase in the consumption of oxygen, the mitosis and phosphorylation was cut in half, and further increase in the concentration of the poison completely blocked mitosis and phosphory lation. So whether the oxidation process is blocked in producing energy, in transferring and carrying energy in phosphate bonds, or in receiving this energy, the reactive response is to produce more energy to make up for the energy starvation, in the tissues whose working mechanisms do not receive the energy. Thus an analysis of effects of toxic amines and nitrophenols shows they do not give impetus to the oxidation mechanism, but block its ultimate purpose—the supply of energy to the vital mechanisms of the tissues. Here we find in 1951, a nice confirmation of our Postulate measured with micro scopic accuracy.
The thyroid secretion is a hormone whose intimate action is still unknown. However, it does not take any part in the oxidation process itself. Comparing its action with that of the SSR, one sees that the latter took the leading part in the oxidation mechanism. Further the action of nitrophenol and of thyroid extract are of different orders and challenge comparison. The former always has a toxic action, the latter is physiological, but the action of both, as explained before, is very different from that of the SSR. The high BMR in the case at hand, has a pathologic cause depending on the pathogen that blocked energy acceptance by the cell’s working mechanism.
The statement of some biochemists that the oxidation process has no immunological significance is based on the fact that the Krebs Cycle has none. We gave the reasons before. The O/R potentials of the participants are too low. Then these biochemists also hold that the Krebs Cycle is the only mechanism concerned in the tissue oxidations, and is all sufficient. They do not consider that the Krebs Cycle is a hang-over from the process used by primitive forms as bacteria and though it is retained by the higher forms as animals and man, it is only used by such as an alternative pathway, when the High Efficiency System already explained is inactivated for a time. That it offers no protection is seen. Moreover, it gives no clues to the explanation of the Pasteur Effect. The early Chapters of “The Survival Factor in Neoplastic and Viral Diseases” show how both depend on the action of the FCG. While the Carbonyl group that initiates the oxidations of the High Efficiency Smokeless System, lacks the high O/R potential Carbonyl dehydrogenator, that some pathogens require for their destruction, yet its range of O/R potentials is twice as high (0.7 v) as that of the Krebs Cycle participants (0.3 v). So the opportunity to give protection by the High Efficiency System is consider able, — enough to maintain good health under the usual circumstances. The use of a Super-high Carbonyl dehydrogenator of correct steric advantage is proven, in this case, to offer protection by way of an oxidation process that imitates that Postulated for the High Efficiency System, and a close analysis of this case is all that is needed to prove the existence of the High Efficiency System.
However, two more cases will be submitted to show that the toxic basis for malfunction can be removed, and the pathology corrected by the processes of adequate dehydrogenating efficiency, started by the Super-high dehydrogenator, and continued by the natural dehydrogenator (FCG) system.
POST-PNEUMONIA NEPHRITIS
CASE No. 2
Dr. Evans
Tom E. 4 years old, was recovering from bilateral bronchopneumonia, when suddenly he took a convulsion of considerable severity. Oedema rapidly developed with blurred vision, headache, dizziness, delirium, etc. The urine secretion diminished as the oedema rapidly increased. The blood pressure was found to be 146/68, and the blood non-protein nitrogen 74.6 mgms %. Twelve hours later the pressure rose to 160/100, and two days later it was 180/130 showing a rapid development of the pressor substance that blocked the kidney elimination. The oedema had developed by then to the point where the contours of the chin and neck were obliterated, and very little urine was passed. Then the second convulsion took place. It was severe and the boy passed into coma. It was in this condition that he received the Synthetic Survival Reagent. A few hours later, the mental symptoms had improved, he came out of the coma; soon the headache, blurred vision, delirium, etc., gave way to rational mental comfort, the blood pressure steadily dropped and the urine increased as the oedema disappeared. The blood pressure was found normal in a few days with a normal non-protein blood nitrogen of 25 mgms.%. The correction was completed by rescuing the FCG so it would go back to work again. The pressor substance is well known now to be a toxic amine, so our Thesis is supported nicely by this case also.
ECLAMPSIA
CASE No. 3
Dr. Baldor
Mrs. D. was married seven years and could never carry a baby to term. Abortion was required before the end of the second month of pregnancy each time, and the period was shorter each time. This was the 4th pregnancy, and they all followed the same course and symptoms but with increasing severity. In each instance she vomited profusely, with much salivation constantly; the urine was progressively decreased until only blood came, just as in the last hours of the parathyroidectomy intoxication. Convulsions followed by coma called for immediate abortion, if life was to be saved. This time, however, Dr. Baldor tried the Synthetic Survival Reagent as her big ambition in life was to have a baby. Twenty hours after the injection was given, vomiting had decreased from 20 times a day to twice per day. The urine increased and, in 72 hours, she was passing half a liter a day. This urine still carried blood and albumen. In four days, she passed a full quart of urine per day. The vomiting disappeared entirely within two weeks, but the salivation had continued and, during the third week, vomiting started again. She was given another dose of the Survival Reagent, and all cleared up quickly thereafter. No more symptoms of eclampsia returned. She carried her baby comfortably into the seventh month, when she had an automobile accident, and spontaneous abortion threatened, so she was delivered of a 5½ pound baby that thrived well. She had no return of eclampsia symptoms and gained full health quickly.
Here we see again that the toxin that blocked the oxidations of function and the regulated energy acceptance by the working mechanisms, could be removed by an atomic group similar in kind but of higher O/R potential. The allergic uncontrolled spasms of the small blood vessels, and the anoxia caused by colloidal gellation, had to yield to restored efficient FCG function. The basic pathology was met and corrected, at its very inception. Still, some of America’s greatest biochemists and clinical experts claim that “the oxidation mechanism has no significant action or position in the maintenance of health or in the combat against disease.” They are limited, of course, by the performances of the Krebs Cycle, which to them is the whole oxidation mechanism. But, if one were to accept such a dictum, one would have to add, “it is impossible to die of asphyxia.” The predicament is rather contrary to progress.
TOXIC GOITRE AND CANCER OF THE STOMACH
CASE No. 4
To show that one toxic agent (removable by one corrective attack) can cause a toxic hyper-function as in Case I, and also cause a very high-grade malignant neoplasm of the stomach in the same person and at the same time, the case of Mrs. W. is offered.
At the time this patient was treated, the Geiger Counter had not yet been invented, so it was impossible to estimate the earth’s irradiations in her environ ment. However, it is noted that she lived in what is known as the goitre belt, a region of iodine deficiency and also of high cancer mortality rate. Her daughter had been treated for a rapidly developing brain tumor. Many other patients came from this region for Treatment. However, one thing this study lacks is a systematic correlation of the terrestrial radiations with cancer incidence and also the number of conditions allied to cancer to be met; and most of all, how the terrestrial rays affect the recovery rates both of the neoplasms and of the allied diseases.
There was no history of cancer in the ancestry, but her husband died of cancer 8 years previously, and her daughter, with a very malignant tumor, was only 28 years of age as compared with the patient’s age of 58 years, at her first visit. One recognizes here the vigor of the carcinogenic flux of this region. Both the mother and daughter made typical recoveries under the Treatment. There was nothing in the geophysical environment that interfered with the cyclic reactions and the steady progress of the recovery process. One feature to be noted is that as cancer is associated with aging processes, this patient, at only 58 years of age, looked like a person twenty to thirty years older. The skin and tissues in general were senile, though the hair was not grey. During the recovery process the senility changes disappeared. The main features were as follows:
The disease started two and one-half years previously as a steadily increasing nervousness, progressive cardiac weakness, tachycardia, increasing ease of perspiration, loose bowels, and tremor of characteristic hyperthyroid type. Radiographs showed considerable enlargement of the heart and mediastinal shadows early in 1927. There was dyspnoea on slight exertion or lying down. Exophthalmus developed rapidly, the skin was bronzed, and gastric distress and inefficiency set in. The feet and ankles swelled considerably, yet she lost weight, falling from 150 pounds to 108 pounds in less than nine months.
The physical examination revealed the exophthalmus as shown in the photograph before Treatment. There was also a greatly enlarged lymph gland (walnut size) in the left supraclavicular space; the veins of the head and neck engorged with blood when she laid down, and percussion showed a marked increase in the mediastinal dullness.
Examination showed the epigastrium and the whole area below the costal border down to two centimeters below the umbilicus on the right side to be occupied by a huge, bulging, solid, fixed, irregular tumor. The stools showed decomposed and occult blood. There was vomiting and great weakness and considerable pain throughout the abdomen. Thus the stomach, the liver, and probably the suprarenal glands were involved by the neoplasm. At the time of this examination she was very weak.
Mrs. W. before Treatment showing the exophthalmus from toxic goitre excited by
the carcinogenic toxin.
(Left photo)
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Mrs. W. after Treatment and re covery from cancer of the stomach, and toxic goitre as
secured from one chemical reagent. The ex ophthalmus is gone for good. (Right photo)
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One dose of two cc. of a 10-(12) solution of the (SSR) serial Carbonyl system was used on September 28, 1929. The recovery process exhibited the usual cyclic three-week reactions, with chills, fever, and general aching, and with improvement following each reaction until the recovery became complete. At last report, ten years later, she was in good health. We lost track of her thereafter.
Regular FCG function, both for producing and using ATP energy, was blocked and this showed for the thyroid cells, the stomach growth mitotic mechanisms and the general tissue oxidations as demonstrated by the senility changes. Still the Krebs Cycle oxidations went on, and fermentation supported the neoplastic cells. Had we supplied a Carbonyl group of FCG oxidation potential, we probably would have gained nothing. However, a Carbonyl group of boosted O/R potential cleared the inactivator of FCG functions away so normal FCG metabolism (in contrast with the Krebs metabolism) was restored, senility, toxic goitre, and cancer all faded away permanently.
TOXIC GOITRE AND ETIOLOGICAL TOXIC FOCI
CASE No. 5
Dr. Jayme Treiger
In this case the pretreatment control or observation period lasted from September 12, 1953 until March 13, 1958. The development of the etiological factors with the progress of the disease itself was well noted.
Mrs. D. S., F. 27 years old, married, a thin brunette woman, very nervous, complained of dyspnoea, cold sweating, pharyngeal spasm (sensation of an egg in her throat), able to bear heavy duties but not simple ones, urine sometimes fetid and strongly colored, acne, leukorrhea, sometimes bloody, and painful nodules in the right breast. These breast symptoms arrived after a second electro-coagulation of an ulcer on the cervix uteri, produced after the second childbirth. These nodules were helped by hormone treatment for a while but had returned, with further toxic symptoms as a tachycardia of 106 per minute, and slight thyroid enlargement, that started nine years previously. She had pertussis, measles and vericella during childhood.
During and since childhood, she had periodic crises of angina with high temperature and pus from the tonsils. Homeopathic treatment helped the tachycardia and the throat spasms and made her feel much better, but the basic pathology was not retarded, and she went to a gland specialist who treated her from November 1954 to January 1956. From him she received Dexamyl, Somniphene, Prometron, Ovocycline, Diiodotyrosine, Apliotil, Thiouracil, and Nodular on different occasions. She did not improve on this series of modified benzene rings, though enough were tried. This shows that the therapeutic conception was not based on physiological considerations, but was the fruit of modern pharmacology.
Feeling worse, she returned to Petropolis. The B.M.R. by Dr. T. showed a plus 45 and Cholesterol of 122 mgms. % on 3/12/58. She was now exhausted, extraordinarily excited, always tired, difficult to sleep, with frequent nightmares, pulse 106 per minute, and her blood pressure in a low range. She was given 2 millimicrograms of the SSR intramuscularly on March 13, 1958, and the reactions that followed are indicative of the sources of her toxins.
Reactions: Tonsillitis that was suppressed from activity while under the phenolic treatments mentioned above, started to be active with high fever, pus discharge and pain in violent periodic crises. The bloody drainage from the cervix uteri that was suppressed by the cautery started up again. However, one week after the Treatment in spite of the strong angina crises, she was feeling very well, as if with renewed vitality. A few weeks later she reported again. The pulse was normal, 82 per minute, the blood pressure normal 120/90, and as her good health was being restored, old symptoms of years of little difficulties returned briefly and disappeared. She felt good enough to not need a doctor. The throat had normalized and the cervix uteri had healed, and she did not return for more observation. She had received two injections of the SSR, the second one a year after the first, for while the cervix showed no abnormality on examination, there were symptoms suggesting reaction in the deep scars within. The BMR in February, 1960 showed 6% over normal, the breasts, tonsils, uterus, nerve responses were normal, temperature 36.7°C, pulse 60, the B.P. 110/70, and she enjoying the best health she had ever experienced.
In this case the etiological lesions that brewed the toxins that attacked the breast tissues and the thyroid gland were respectively the cervix infection and the tonsil infection. The cautery sealed up the drainage facilities, and made the scar tissue that was infected more anoxic. The reactivity of the reticuloen dothelial cells of the tonsils to their contained infections was suppressed by the phenolic derivatives, so the thyroid was poisoned all the more. Further, the poisons from the cervix and those from the tonsils while showing some speci ficity to the thyroid and breast tissues were also general poisons and affected all of the tissues making her nervous and weak aside from a special thyroxin effect. Here the relation of the reactions (following the Treatment with the SSR Reagent, which were severe) to her improvement in tissue function showed that these reactions were not of a vaccination nature, but were actual reticuloendothelial battles against the disease agents going on in conjunction with the chain oxidation of these agents. Then, too, as the various FCG units were liberated from combined toxins and went back to work, she started to feel normal and her various functions behaved normally again. It is to be recalled that after the SSR was given the tonsils became acutely inflamed, and the cervix lesion broke loose with a strong inflammatory process. Thereby both lesions were cleared of their imprisoned germs and fibrosis integrated pathogens, and as the induced oxidations burned the pathogens away, the fibrosis disappeared also. The anoxic centers were wiped out, so the disease was cured right at its very inception. She has no more sore throats nor cervix troubles, and no more secondary effects, as thyroid enlargement or abnormal function. The breasts have no more nodules either. Her general health is normal. Her nervous system is steady. She sleeps normally and does not sweat as she formerly did. In other words, the pathology was fully reversed and discarded. This same course will be seen in the other cases reported here, and in all others when one takes the trouble to thoroughly check the recovery course.
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CHAPTER 8
ATROPHY, ANAPLASIA, AND NEOPLASIA
One may compare the correction of nerve atrophy and neoplasia very nicely in retinal cases where cell reconstruction can go on, but not cell reproduction; we may also compare the corrective responses of anaplastic and neoplastic tissues in reproductive cells. In all four situations, the correction is had by restoring normal FCG function and thus a Least Common Denominator is established in these supposedly widely varying conditions. So the basic pathology is the same. There is a suggestion that the requirement for neoplasia is the loss of the functional mechanism.
In Glioma, there is no development of functional mechanism, because the cells are too embryonic and immature or undifferentiated. In the Sympathicogonioma case, one sees how the nucleus is separated from the functional mechanism, the fibrillar structure. The latter lays separated as a fibrillar syncitium supported by cytoplasm, while the reproductive portion is separated off as individual entities, — cells. Thus the functional mechanism is discarded. The return to normal which, we are not able to see must be like the maintenance of the normal; a correct balance and interaction of the reproductive and functional mechanisms. Thus the energy production in nerve cells must serve their work of repair and Nissle substance synthesis only to keep them normal. But when these systems are blocked, the energy has only one place to go and that is mitosis. When the working part is shed as in Sympathicogonioma, of course, there is the visible separation. The very high-grade malignancy of such neoplasms may therefore be understood.
In this case of Neuroblastoma, which will be detailed a few pages further on, visible separation of reproductive and functional elements of the cell is demonstrated, even though the child is born with the neoplasm, latent in his system. In the Retinoblastoma case, the functional mechanism did not exist in the cells that went malignant, so the mitotic mechanism had no other course than to use the energy produced in the nucleus for reproduction. There was no other path for it to follow. It appears from these two cases alone, that energy production is primarily evolved in the nucleus, even though the nucleo protein grana are found throughout the cytoplasm. In the Glioma case, these granules did not exist, while in the Neuroblastoma case their connections with the nucleus were severed.
In the Optic atrophy case to follow, complete atrophy was not possible as yet, as a result of the Retino-choroiditis, for regeneration of the affected cells took place with restoration of function. A bacterial origin, of the toxic injury, is of concerned here.
There is another situation due to toxic injury, that of chronic alcoholism, where this weakness can be transmitted from parent to child for several generations. A case of Delirium tremens presented on this topic, should interest the geneticist, in view of the foregoing remarks, for indeed hereditary transmission is concerned in all of these conditions. Even in this case of Delirium tremens, the effect of a toxin on the cerebral cells, the connection between the genes and the functioning elements is concerned, — the nucleus and the mitochondria. Evidently, this is the toxin that caused the cancer in this case, for the Delirium tremens returned during the 12th week reaction in his recovery from cancer of the face. The patient himself had never used alcoholic drinks but his father, and other predecessors, did drink themselves to death. Still, the patient gave the D.T. symptoms during the correction of the neoplastic defect. Both defects were corrected by the Reagent, which corrected the hereditary Neuroblastoma defect, in the case to follow very shortly.
This case, with its high malignancy characteristics, teaches another very important fact; namely that trauma, with its circulatory injury and consequent anoxia alone, is not sufficient to cause cancer. Also it teaches that the recovery from this disease removed the carcinogenic factor that requires anoxia to become effective as our Postulate outlines. For as will be seen this boy, after being cured by restoration of his FCG Survival Factor, did not again get cancer after being severely injured by the automobile accident that bruised him at the site of the former rumor. This case repeats the lesson learned from case No. 11 to follow.
Recovery Reactions
Cyclic reactions: 1) often characterized by the symptoms of the pathogenesis showing up in the reverse sequence to their coming, 2) accompanied by a local congestion at the lesion, 3) as well as constitutional symptoms of grippiness, as occurs in so many virus infections, are to be expected periodically, while recovery is in progress. The cycles run in a definite periodicity, in which a three-hour unit, or more often, a twelve, twenty-four, thirty-six, seventy-two, or eighty-four hour interval, is usually observed. Thus a reaction of chills, fever and achiness can show up twenty-four, seventy-two or eighty-four hours after the Treatment. Or, it may come the third week, the sixth week, the ninth week, or the twelfth, twenty-fourth, thirty-sixth, sixtieth, seventy-second, eighty-fourth, ninety-sixth, hundred and eighth, or even later multiples of twelve weeks.
The local features in the lesion are: congestion, swelling, hyperasthenias, hyperreflexia, more or less pain, local heat, and maybe some bleeding. But this passes off in three hours or a multiple thereof, and improvement is then noted. When biopsies are taken of the lesion undergoing recovery in this way, it will be found to undergo: 1) a coagulation necrosis, 2) then a calcification, much like accompanies or mediates the digestion of a blood clot or of milk, 3) vascular in-growth is observed, first angioblastic and fibroblastic tissue, and 4) mast cells or other white blood cells to help carry off the debris. (Koch,New York, Medical Record, October 30, 1920) 4) Angioblastic tissue finally replaces the growth, and then 5) functionating parenchyma grows in to reform the organ on physiological lines. The cure is therefore complete, as it could not start without preliminary elimination of the pathogen, and its functional status is returned. The sequence of events during reconstruction is exceedingly interesting and will be discussed.
PRIMARY ATROPHY OF THE OPTIC NERVE AND RETINA SEQUEL TO SCARLET FEVER
CASE No. 6
R. J., 14 years old, gave a family history negative to tuberculosis and cancer. The pretreatment control period and diagnosis are well described in the correspondence between the Henry Ford Hospital and Jennings Hospital experts as follows:
HENRY FORD HOSPITAL
DETROIT, MICHIGAN
Henry A. Du----, M.D. September 10,1946
7815 E. Jefferson Ave., Detroit, Michigan
Case No. 453242 Re: R. J.
Dear Dr. Du----:
Our first contact with the above named child, according to our records, was a precamp examination done by Dr. J. A. Jo---, of the Division of Pediatrics, in July, 1945. At this time his vision was recorded as being 20/20 bilaterally. He was seen by us April 15, 1946, at which time he had developed a scotoma in the right eye. Vision without correction on the right was 8/200, left 20/20. External examination of both eyes revealed them to be normal. Funduscopic examination of the right eye revealed a normal lens. In the macular area there was a chorioretinitis which fits the description given by you in your letter. The left eye was normal to Fundascopic. Tangent screen examination was done which showed an absolute scotoma in the supracentral region. The periphery was normal; red field was reduced.
He returned to Pediatrics for a general physical examination by Dr. Jo----April 17. Dr. Jo---- noted that the child had been seen by Dr. Ca--- who had applied .1 mgm. of 1/10,000 O.T. He had been negative to 0.01 mgm. when seen by Dr. Jo---- the previous year.
Sinus and chest X-Rays were made. Dr. Do--- reported them as showing chronic pathology of both antra and probably the ethmoids and frontals as well, and were suggestive of a pan sinusitis. There was only a moderate increase in the broncho-vascular markings in the bases.
Blood count showed on 4-16-46 a hemoglobin of 13.5, white blood cells 10,100, red blood cells 4.66, polymorphonuclears 46, small lymphocytes 52, monocytes 2.
He was last seen April 20 by Dr. Di---- for ear, nose, and throat consulta tion. No foci of infection were found in the ears, nose or throat to account for his eye condition. Dr. Di---- reviewed the sinus X-Rays and washed out the left antrum. The return flow was clear.
He did not return for follow-up eye appointment, and we have not seen him since. Trusting this information will aid you in your studies, we are,
Sincerely yours,
Henry Ford Hospital
Per; /s/ E. L. W.----, M.D.
M. W. S---, M.D. Surgeon-in-Charge
rms. Division of Ophthalmology.
Our History
Our examination made April 26, 1946, gave a history of headaches and chronic sinus drainage with acute exacerbations, sore throats often, and a history of exposure to scarlet fever that did not take on him. He was slightly sick, but had no rash and did not peel. He noticed the eye condition when at a shooting gallery he aimed a gun using the right eye and found he could not see with it. Thus in one year exactly, a 20/20 vision went to zero so far as practical use was concerned. He could not make out objects with it nor read any size print. The area of “absolute scotoma” noted by the experts was an area of retinal and optic nerve “atrophy” that involved the upper half of the retina and the central field. There was some peripheral vision but it did not help much.
We gave him a 2 cc. injection of the 10-(12) solution of the serial system of Carbonyl groups (SSR), the Synthetic Survival Reagent, on April 26th. The sinus drainage and headaches soon ceased. The sore throats returned only twice during two reaction periods. But the other symptoms were aggravated during the 12th, 24th, 36th, and 60th weeks. During this last reaction the throat was most sore, and he had a fever of 103° F. as well as a typical scarlet fever rash that lasted only 12 hours. His health was perfect after that.
Examinations of the eye by the same experts found that the vision in the right eye was 20/400 in August 1946, that is four months after Treatment. Thus a definite improvement had taken place. In June, 1948, it was 20/100, and in October 27th, 1948, it was 20/40. Thus the improvement was continuing. Further reports, but without examination, claim his eye is perfect so far as reading fine print is concerned or for any other use. Here we see the polymerized scarlet fever toxin causing a degenerative change, and after it was broken down to the monomeric phase, it gave rise to the symptoms of the acute infection transiently. This was burned away in only twelve hours, and the recovery was complete. Other similar occurrences could be reported.
ACUTE CHORIORETINITIS SEQUEL TO PELVIC
AND TONSIL INFECTION
CASE No. 6A
Dr. Jayme Treiger
Mrs. L. P. S., age 35 years. April 9, 1957 when first examined. Her Pretreatment Control Period of observation extended until December 5th, 1958, during which time she received all of the homeopathic remedies, and a course of Cortisone and its derivatives with the most recent and efficient antibiotics. There was a steady downward course in her general health and her two chief areas of infection, the pelvis and the tonsils, and steady deteriora tion of the function and pathology of the retina of the left eye, that developed during the last six months of this period.
Physical Examination on entrance showed, fever of 38.6° C. with a bilateral tonsillitis that had persisted for the past three years, worse at the end of the menses. She was very exhausted because of excessive use of antibiotics and antipyretics. Also there was an inflammatory process in upper and lower abdomen, sequel to violent gynecological infection sustained shortly after marriage. The tonsils—red, hypertrophied; tonsils full of pus, Heart—O.K., Gall Bladder sensitive XXXX, Chaufford Zone XXX, and Ovaries inflammation. The menses were prolonged. There was no benefit from medication followed during the first six months. Indeed headaches, fetid leucorrhea and varicose veins were aggravated. Three months later oedemas of feet and hands on waking, and of the upper eye lid with severe sacro-ovarian pains were added to the symptoms, with severe chest pains, and blurred vision, also cracking of the skin on the palms of her hands. Fundascopic examination by the ophthalmologist showed no retinal pathology at this time, 7/18/58. The examination on 10/28/58 showed the left eyelid congested, vision blurred, photophobia. Fundascopic examination on 11/5/58 showed left eye vision 0.67 fundas turbid with exudate, and a focus of Chorioretinitis in evolution, juxta-papillary. Right eye normal. V--I, Signed Dr. A. H.
Prognosis—Healing with scar causing corresponding scotoma. This Ophthalmologist placed her on Cortisone and its derivatives, anti biotics and topical applications. One month later the eye was strongly congested, much worse than a month previously, and she could see nothing at all with the left eye, much worse than at the beginning when she still had some vision, Her weight was 80 Kilograms. Two millimicrograms of the SSR were given intramuscularly, 12/5/5 8, by Dr. J. Treiger.
Post Treatment Period-12/6/58, swelling of peritonsilar lymph nodes, dizzi ness, uneasiness, and violent pain in the pelvis recalling the time of her acute initial pelvic infection, with exquisite tenderness. Vision more blurred for 2 days. Copious flow of pus from genitals for the past three weeks, 12/31/58. On January 12, 1959, she had severe tonsillitis that lasted for 3 days at the end of her menses, fever 39.5° C., great hypertrophy of the tonsils, weight down to 74 kilos. with terrible vaginal itching, that soon improved. By the middle of 6th week, 1/14/59, much better, temp. 36.7° C. On 2/17/59 her weight was 72 kilos, feels better, and shows cracking in the skin of the palms of hands as of ten years earlier, and skin desquamation. Temporary improvement of left eye vision. On 3/18/59 she reported she spent a wonderful week, including her eye. On 5/5/59 she reported she had two weeks of normal vision and was in good health generally. On 4/9/60 she had three days of reaction with slight swelling of the left tonsil, pain in the left eye, slight blur in vision, and then quickly normalized and has stayed well ever since. The pelvic and throat pathology completely disappeared. This was the 69th week reaction,
Fundascopic examination by Dr. B., reads as follows:
Dr. A. De S. B.
Petropolis
Estado de Rio de Janeiro
December 21, 1959
Dear Dr. Treiger:
The “Fundus Oculi” examination which was done on your recommended patient, Mrs. L. P.S. accused on the left eye an inferior nasal focus, entirely healed of chorioretinitis all the way well into the periphery. There is no abnormality concerning the vascular supply. The visual field through compari son showed no abnormality. Therefore I did not try the instrumental perimetry.
Yours truly,
Dr. B.
Discussion-- No scar was produced as always happens with corresponding blindness. The retina was restored. If or not a scarlet fever infection played a part in the etiology no one can say. However, the cracking of the skin of the palms of the hands and the desquamation that showed up as she finished her recovery may have some indicative value. Even though it may not be scarlet fever, it is a toxic effect of infection antecedent to the retinal lesion. In contrast to the former case which showed no inflammatory change reportable, but only the atrophic changes here the inflammatory changes predominated and the degenerative effects were also in evidence. This woman was also too heavy at first. She lost weight down to 70 kilos and then got thinner without losing more weight, showing a building of solid tissue with functional efficiency that went with her return of happy good health. Both foci of pus infection cleared up, and the non-pusy inflammatory and degenerative changes likewise disappeared. Thus an integration of the toxins of bacterial infection that excite no leukocytosis, as they are bound to and become part of a different tissue, are separated from their host cells by the SSR as we will show viruses are separated and carcinogens are separated, leaving the host cell in good functional status while the pathogen is destroyed. This accompanies destruction of unbound toxins that excite leukocytosis in other parts of the body.
Her reactions occurred typically, twenty-four hours after the Treatment was given and at multiples of three week intervals thereafter for a few times only, the sixth and the 69th weeks. The last reaction occurred after the retina function had returned to normal and examination showed it was structurally normal. Thus the reactions are not to the lesion, but to the cause of the particular lesion, a matter much deeper than the toxic factor of the etiology. One case alone demonstrating this phenomenon, would be good to remember, but many such cases showing reactions for example coming five years after a large cancer of the stomach has been absorbed and health follows a normal course, indicate that a phenomenon is observed that clears up the predilection to the pathological response to the etiological factor rather than an attack on the pathogenic factor which is long out of the system. The correction is more basic than getting rid of the etiological agent and healing the lesions.
Confirming this, one recalls the case of cancer of the face of Dr. M, of a small town in Texas in 1927. He was 81 years old and blind with bilateral retino-choroiditis of several years standing. He was treated with the SSR for the cancer and while that lesion was healing up, the vision returned, so that before the growth had entirely healed, his vision had so perfectly improved that he could see the string that was used to tie up packages in the country store that hung from the ceiling. This was visible to him as he entered the store. He had reactions which he reported long after he considered himself cured. There was high fever, 106.5° F. three years after full recovery. During this fever, which was different from any he had seen in his long practice of medicine, he was surprised by a good appetite and the desire to work and expend effort. Here is food for thought. He reported the best health for years afterward.
Here are three different etiological factors, scarlet fever, a mixed infection of the gonococcus with strep and staph resistant to all latest antibiotics, and the etiological factors in cancer. In the latter case, an infiltrating type of basal cell, solar rays were one big factor and high winds, frost bite, etc. that caused a circulatory injury, anoxia, etc. This circulatory injury was present in the mixed infection case too as scar formation was in progress with the vascular injury that goes with the inflammation, and neuron injury. In Case 6, the inflammatory changes were a minimum but the degenerative changes were neuron loss and scars were most prominent. This is rather strange as there was no inflammatory history, but a very rapid development of the degenerative change. The other cases of this disease, we may review, add nothing to the present meager information. This is unfortunate, since the presence of degenerative change away from the pus forming areas that supported the infection and toxin production gives one a chance to investigate the cause of degenerative disease. If we had sufficient data, we could demonstrate its different steps. This much is brought to mind anyway, it is the job of an Ophthalmologist.
The old doctor had plenty of contact with scarlet fever, and he no doubt had an attack that gave lasting immunity of high degree, but maybe not enough to prevent or clear out a suppressed infection he had carried for some years. Did his immunity lay the foundation for the degenerative change in the retina? If so does vaccination which, brings about comparable condition not play a big role in the great dominance of degenerative diseases of today? We say the virus or the germ toxin must integrate with the cell’s functional structure to bring about the loss of function and its sequel of tissue degeneration and visa versa. Does not vaccination do the same? If vaccination altered the steric set-up of the cell so fresh entrance of the pathogen could not take hold, then the vaccine must persist and do its damage to function. This would lead to degenerative changes with gene effects.
Let us compare this type of immunity with the oxidative protection used in Dr. Treiger’s Case 6A and in the others. The scars did not form or they went away, as they were replaced by functional parenchyma and the distant site of the infection that brewed the toxin, be it scarlet fever, ordinary pus infection, or some other factor that enters the etiology of cancer, was also wiped out.
The cow experiments, a few of which are reported here, show that the most vicious Staphylococci, etc., lose their pathogenicity and maybe become faithful members of the great Biological Economy after they are “cured” by oxidation restoration facilities. Inferior oxidations, it will appear as we go along, are the basis of disease.
RETINOBLASTOMA OF BOTH EYES (GLIOMA)
CASE No. 7
Rita Long was one year of age when the disease first made its appearance. In less than a year the left eye was filled with a tumor mass, irritated, swollen, and blind. The diagnosis was made clinically by Dr. C., a noted Ophthalmologist, of Wichita, Kansas, He removed the eye. The pathological report confirmed his diagnosis of Retinoblastoma. The accompanying document from the court records gives the gross and microscopic pathology. This was in May 1934.
Within a year, the right eye showed the same changes. The same surgeon observed the same disease here and so stated that it was the same disease that had attacked the left eye. This is a well known characteristic of this disease, Prof, Frohlich, of the University of Michigan, testifying as an expert, stated that there is nothing known to scientific medicine that can combat this disease. Even when operated early it returns and kills. She was taken to a renowned Ophthalmologist in Niles, Michigan, who made the same diagnosis and referred her to us.
We examined her with Dr. H., a good specialist, and made the same diagnosis. He found that one-third of the retina was replaced by the neoplasm, including the optic disc. The eyeball was bulging and distorted, the iris dilated and fixed. There was no ability of the iris to move from its infiltrated attachments. Behind the pupil was a yellowish, pinkish reflection to light, showing that a tumor was present within. The area where the left eye was removed was not healthy, but showed neoplastic degeneration, though only in a minor degree. Both foci disturbed her. At this time, November 25, 1935, she was over two years old, and we gave her one cubic centimeter of the 10-(12) solution of the SSR serially arranged Carbonyl groups with free radical terminals by intramuscular injection. The irritation of both foci soon left. Every third week, she exhibited a reaction with general achiness, slight fever, and an aggravation of the irritation of both foci. Each reaction lasted a few days and was followed by improvement.
Examination on August 18, 1936, showed that all visible pathology had been removed. Dr. H---- and Dr. W. made Fundascopic examinations and found the retina normal, fully restored. Since she lived so far away, we gave her another dose for assurance, and no reaction thereto ever developed. She has remained well to date with perfect vision in the right eye. She went through her school courses and college at the head of her classes, is now married and a healthy, happy woman. Reports made in June, 1950, and June, 1953, and September, 1960 confirm her full recovery.
This case along with the cases treated in Canada, all used the same Treatment and are the only cases of Retinoblastoma ever cured. And as Prof. Frohlich, of the University of Michigan Department of Ophthalmology stated, “there is nothing known to scientific medicine that can cope with this disease,” there is no information available as to the changes in the retinoblastoma cells during the recovery process. This is unfortunate for here we have a tumor of a nerve tissue that is supposed not to be able to reproduce in its normal state, even for a reconstructive or compensatory purpose that does reproduce wildly with great stubbornness, as a malignant tissue. In this case and the others, the retina was restored with good vision performance. In this case, the reconstruction was back to 20/20. The question is, where did the new neurons come from, or were they some of the tumor cells that were able to reconstruct functional mechanisms, as soon as the FCG’s were liberated by the SSR? Thus an undifferentiated tissue, probably because of FCG inactivation, went malignant and then underwent normal differentiation so as to be able to again function and take its place in the organism’s economy, after its FCG’s was liberated. This sequence of events calls for deep thought. It shows full reversal of the malignant state.
EUNUCHOIDISM
CASE No. 8
J. S., at age 14, was subject to infections of the respiratory tract and skin, presented marked obesity, female type shape, was very dull mentally, was found to have an infantile penis and undescended testicles. In fact, they had not even descended to the canals. He had been under thyroid and pituitary hormone therapy from the age of 10 in 1931, to age 14, in 1935, without any improvement mentally, physically, or in his resistance to infections. He was closely watched by Dr. S., a relative, who reported that in this time the testicles had not even entered the canals. Thus the disease was classified as the type that is not helped by modern therapy and is permanent.
He received his dose of the SSR serial system of Carbonyl groups in November 1935, and within three months, he lost weight, his infections were gone, and the left testicle had traversed the canal and was entering the scrotum. After the sixth month, both testicles were in the scrotum, the penis was developing, and the pubic hair distribution became masculine. He grew taller, his hips reduced and his shoulders and jaw developed to good proportions. He became very bright in his schoolwork, soon making up for his backward position. He became a good athlete. He entered the army and was soon promoted to a corporal. He is married, and is raising a nice family of children of his own. At the time this Testimony was given, he was in the Army Law School where he was making splendid progress. His boy and girl are physically normal and mentally excellent. Thus his genes were re-established in normal line. One may contrast 14 years of FCG insufficiency with a few months of rescued FCG efficiency, placing him in the normal progression of full health. *
* Photographs and a more complete case history of this patient are included in The Birth of a Science.
CANCER OF THE TESTIS
CASE No. 9
Mr. T., age 38 in June 1925, when treated with SSR serial system of Carbonyl groups with free radical terminals, his testis had become malignant six months previous to its removal. At this operation, no metastases were noted. The biopsy report was “Medullary Carcinoma of the Testis.” Recur rence showed in the groin and scrotum within six months, and another operation revealed that the neoplasm had invaded the abdomen. Removal was attempted and the microscopic report on the material removed read again “Medullary Carcinoma of the Testis.” Recurrence was not long in coming with more rapid spread of the disease. The abdomen was again opened, but was found so inoperably involved and a biopsy is all that was done. This biopsy was reported: “Carcinoma, probably secondary to previous carcinoma of the testis, as the cells are histologically similar.”
At this time he was rather emaciated, exhausted, and a general cachexia called for an early termination, — a hopeless prognosis. Through the intervention of Dr. Alpheus Hoyt, this patient was given the SSR Reagent in June 1925. He regained his health and all tumorous tissues disappeared. He remained well thereafter and in 1946 he offered his report stating he was perfectly well. This was 21 years after he received his Treatment in the terminal phase of the disease. The preceding case of anaplasia and this case of neoplasia were corrected by the same Reagent, which restored good FCG function in both. Here is food for thought.
MALIGNANT SYMPATHICOGONIOMA
CASE No. 10
Dr. Julian Baldor
John L., age 13 months, developed a tumor in the abdomen that required an exploration on September 25th, 1951. A retroperitoneal growth had infiltrated the region too thoroughly to permit removal of any more than a biopsy. On October 6th, examination revealed a visible bulging of the abdomen in the umbilical region which we found on palpation to be the size of an ordinary Florida grapefruit, about 10 to 15 cms. in its diameters, firmly fixed to the surrounding structures. The stools were bloody showing the intestine was invaded, and the blood count agreed with his pallor, — 2,300,000 red cells with a hemoglobin of 52%. The next day he received from Dr. Julian Baldor an injection of the SSR Reagent, the serially arranged system of Carbonyl groups with free radical ends, 2 cc’s 10-(12) solution. Recovery began promptly and at the end of a year no more tumor could be palpated on careful examination.
On May 5th, while in good health he was run over by an automobile and sustained a broken leg and abdominal injuries. While in the hospital for repairs, he was carefully examined by the same surgeons who had removed the biopsy. They found him free of any trace of palpable growth. He made a nice recovery and is in excellent health still. His blood count on April 5, 1953, was 4,750,000 red cells, hemoglobin 87.5%. All the documentation and facts of this case were put in the Florida State Court Records by his surgeons in May 1953. His last report was good health in 1958.
Discussion-
The case of Sympathicogonioma is of interest not only because it is so very highly malignant, but also that the mitotic mechanisms, which are now the malignant cells, are separated from the nerve fibrilla, the functional mechanism, as entities. The functional mechanism is entirely shed or discarded and, of course, as an immature and unorganized fibrillar syncitium. The malignant cells are practically only made of nuclear material. It is unfortunate that periodic sections could not have been taken of the tumor as it normalized, to see if the neoplastic cells made any efforts to form cytoplasm and fibrilla, as a recovery response. In the Retinoblastoma case, the new neurons that restored the retina to normal structure, probably had their origins in the neoplastic cells, as new neurons are supposed never to be formed. In the case of Optic atrophy, this assumption would also have to be made with the conclusion that the new functional retinal neurons were developed from remnants of atrophied cells that probably were integrated with toxin as in symbiotic viral infections, and the atrophy was never complete enough to prevent reconstruction after the FCG was relieved of impediment.
That the FCG is the position that is stopped from functioning to cause the pathology in each condition is quite evident.
Often a biopsy may reveal a tumor to be of grade one or two malignancy, and after the tumor is removed the sections show it is definitely a grade four, thus being changed by the manipulations of the biopsy, the effect of the anesthetic, etc. The case to be reviewed now is one that was exceedingly anaplastic and a grade IV malignancy at biopsy, as the examinations of the specimen by several leading pathologists and many well-trained practitioners of medicine found. Some microphotographs are submitted besides.
This case shows that the Survival chemistry, as established by the high efficiency synthetic Carbonyl activity, may fade out in ten years when the environmental conditions are adverse as they were in this case, and the data should be compared with that of the case that follows it, where a similar neoplasm of malignancy was cured after the Synthetic Reagent was given, and still remains cured 36 years afterward. Here the environmental conditions were satisfactory, even though she was submitted to the trauma of four natural perfect childbirths, and no return of the neoplasm ever threatened. As in the neuroblastoma case just reviewed, trauma alone is not sufficient to cause cancer or its return. The anoxia may thus be established for a sufficient time for the co-factor and the pathogen to make the integration. However, with the improved Carbonyl function established by oxidizing the pathogen away from the FCG system so that the FCG is activated by a Carbonyl group, a sufficiently high O/R potential is established to burn the pathogen, instead of condensing with it. Still the Survival chemistry is a comparative matter, as any other phase of life, and as this case demonstrates.
It will be seen as we go along, as in the above case, that anoxia alone is not sufficient to cause cancer, A CO-FACTOR, be it a virus or another carcinogen, is required. Where trauma is not concerned in causing the anoxia, toxic amines of colonic origin may prepare the soil, and the response may not be neoplastic, but a necrosis instead.
GRADE IV SQUAMOUS CELL CANCER OF THE CERVIX UTERI
CASE No. 11
Mrs. M. W. came under the care of Dr. L----, Dr. H----, and Dr. D- -, of Medford, Oregon, in January, 1940. Dr. L---- examined her and found that she had an enlarged and fixed uterus. She had a cervix that protruded into the vagina and could be seen by a vaginal examination with a speculum; a cervix which was indurated and showed islands of apparent new growth. A diagnosis of far advanced cancer of the uterus was made clinically. Dr. L---- reported that her cancerous condition would probably, if untreated, end her life within a year. That because of the fixation of the uterus and the involvement of the adnexia, it was his opinion, that it was not a surgical case, as surgery would have had to be too extensive. It was too late for that sort of thing. The case had already entered the cachexia stage as Doctor L----’s Testimony reveals:
“She had lost 30 pounds in six weeks, was complaining of general weakness and had a rather poor color at the time.” As Ewing states: “Characteristic cachexia in uterine cancer develops in the terminal stage of the generalized disease, but when the lesion is localized in the pelvis, cachexia is missing.”
Dr. L---- gave the SSR Treatment, 2 cc.’s of the 10-(12) solution on March 20, 1940, December 30, 1940, and October, 1941. His examination made a year and a half later, in the summer of 1942, found that: “She had gained weight, she had gained color, and improved in general appearance. The mass in the abdomen had subsided to the extent that he could no longer palpate it. The appearance of the cervix by examination with the speculum appeared normal.”
Before giving the SSR injection she was placed in the Medford Hospital, and there Dr. L---- removed a specimen from the cervix for microscopic study. The slide was very carefully prepared by Dr. Green, the hospital’s Pathologist, and diagnosed by him as squamous cell cancer of the cervix uteri. But the case was so interesting that he sent the slide to Professor Hunter, the Pathologist at the University, who established the grade of malignancy. Dr. Hunter, in his letter to Dr. Green on January 27, 1940, wrote: “I see a decidedly invasive and anaplastic carcinoma which occupied well over half of the tissue . . . I would if asked to do so, grade this one as a IV.”
The confirmatory diagnosis made by Dr. Weller, professor of Pathology at the University of Michigan, was secured to complete our records. He found the specimen well prepared, and diagnosed it instantly as follows:
Dr. Weller’s statement that the slide was well prepared is incorporated in an Affidavit which reads:
During her fifth year after Treatment, it was desired to ascertain her exact status so an exploratory laparotomy was done by Dr. Haines in June 1944. He found a normal cervix and uterus to which a small fibroid was attached. He removed the body of the uterus and the fibroid, but left the cervix in place as he found it perfectly normal. On gross examination the uterus and fibroid were normal, that is no signs of malignancy were observed but they were both submitted to careful serial section for a thorough microscope search for malignant cells. None were found. Dr. Inskeep, the Pathologist, found no malignant cells and testified that the fibroid was benign.
Here we see, that at the time Dr. Haines operated on Mrs. M. W., there was no evidence of this Grade IV carcinoma present. Dr. Inskeep’s report shows that no cancer cells were found. This indicates that, except for the benign fibroid tumor like so many healthy women carry ordinarily, the uterus was perfectly normal. Thus, we believe, she was found cured several years after being treated in the terminal stage of Grade IV cancer of the cervix when her life expectancy was less than a year.
A photograph of the slide carrying the biopsy specimen well placed under the cover slip is given, and three microphotographs made by the Harper Hospital expert are also submitted for your study.
Photograph of the Biopsy slide showing its perfect condition.
Low Power Magnification of part of specimen Microphotograph by Mr. Rinelander of Harper Hospital. (150X)
Medium Magnification Microphotograph by Mr. Rinelander, of Harper Hospital (200X)
High Power Microphotograph by Mr. Rinelander (675X)
Mrs. M. W. was seen by Dr. L----. again just a few months before her death in December, 1950. At the time of her death he was not aware of the subtotal hysterectomy. Dr. L---- found a very foul smelling friable mass with the gross appearance of a disintegrating carcinoma in the left side of the pelvis and involving the lower end of the large bowel. A complete autopsy was not performed and no biopsy was taken post mortem. He reported that the condition leading to her death was cancer of the uterus.
In light of the whole case history, it is questionable that the original Grade IV squamous cell carcinoma of the cervix uteri in 1940 was the cause of her death in 1950. Her death should have occurred within the year period, had there been a connection between this pathological condition, and her death.
Even though the exact cause of death is not established, this case serves our purpose here, namely to show that the Survival chemistry can be restored to curative efficiency and that it persists for a period of years without further Treatment. That when ill health threatens again, its repetition must be required to restore the desired Survival chemistry again as in the first instance.
This case also illustrates the importance of continued medical observation of a patient even after the accepted five-year period. That the Survival factor, after being restored synthetically, can be subsequently destroyed by inhibiting factors.
This case should be compared with the case of Mrs. T., who also had advanced squamous cell carcinoma of the cervix uteri. Mrs. T. is enjoying best health over thirty years after Treatment. One sees that the Survival chemistry is subjected to environmental influences. In Mrs. W.’s case, they were the worst possible. She was on Welfare for many years prior to her death and the type of care she could receive was limited. In the case of Mrs. T., they were ideal even with the traumata of four childbirths. Thus the physician must carefully measure all influences that may determine health in each case and see that the ideal is maintained, both while the Treatment is followed and after recovery occurs.
SQUAMOUS CELL CANCER OF THE CERVIX UTERI
CASE No. 12
* This case is included in the book, The Birth of a Science.
In August, 1923, Mrs. T. was 31 years old. She could never carry a baby to term and spontaneous abortion took place. For over a year before seeing a physician she had irregular bleeding, mucopurulent discharge and increasing pain with progressive reduction in the capacity of the urinary bladder. She consulted Dr. T. who took a biopsy. A very responsible laboratory in Detroit made the diagnosis of squamous cell cancer of the cervix as follows. Several visiting Pathologists also confirmed this diagnosis as a high grade of malignancy was observed.
My examination was made two weeks later and the findings were those typical of a far advanced widely invading squamous cell type of cancer. It had invaded all the structures of the pelvis, but was more extensive on the right side. All the normal contours were obliterated and the structures hardened by the firm infiltrations. The bladder wall was extremely involved and the mass could be easily palpated above the pubes half way to the umbilicus. Her surgeon did not offer an operation, or recommend any treatment, but watched her progress with interest and took care of her four pregnancies later on.
This case was not so far advanced as the case previously outlined. She bled profusely, especially since the biopsy was made, and she gave a yellow color that one would attribute to the prolonged excessive bleeding aside from the natural cachectic effects of a neoplasm that had broken through into the abdomen.
She received two injections of 2 micro micrograms of the Synthetic Survival Reagent (SSR) on August 7th and 21st, 1923. She had the typical reactions of general achiness as
one observes in most viral infections. The bleeding soon stopped, the pussy drainage soon stopped, and her color took a change for the better. The pain steadily let up and the growth on examination became softer, more elastic and movable, and the normal contours of the pelvic structures returned. After the 36th week, no more evidence of the disease was observable, but the right side of the cervix was a little deficient. This did not fill in fully to make a symmetrical cervix until a few more months had passed.
Her reactions came most vigorously on the twelfth and twenty-fourth weeks. They exhibited chills, fever, achiness, pains in the back, and increased urinary frequency. But after each reaction, her health gained very rapidly and the bladder capacity normalized. She became pregnant and after a normal term of gestation gave birth to a fine healthy boy, with a normal easy delivery, managed by her surgeon, a man of exceeding expertness. Three more children were subsequently born at two-year intervals. All are fine physical specimens, and the births were easy and normal in every way. There was never any return of a neoplastic condition or any other trouble, nor even any serious sickness. She has been remarkably resistant to colds besides, and is still alive in perfect health 36 years after being treated for a terminal stage squamous cell cancer of the cervix that was widespread into the abdomen.
The important lesson from this case is the fact that she had plenty of exercise, taking care of a big strong husband, and four vigorous children. She did the family washing with tub and rubbing board and had plenty of exercise of the abdominal muscles that massaged the intestinal wall, aiding its movements and its circulation. Her diet was well chosen and well prepared, and her life was happy and inspiring. In contrast to the previous case, one sees that the environment was very favorable for the maintenance of a good Survival chemistry.
This case is also interesting in that her husband developed a cancer of the prostate gland 33 years after his wife was cured. The hospital put him through surgical and radiological procedures without offering a diagnosis. Radioactive Cobalt was new then and used vigorously. He quickly suffered widespread bone metastases and died in great agony. The infectious nature of the provocation of neoplasia may be inferred from this history, as well as its conjugal nature. It would have been a helpful observation to remove the cause of the husband’s cancer with the same reagent that cured his wife. But the hospital doctors had no guiding information.
Trauma of four parturitions did not re-excite cancer in her and neither did her exposure to the viral agent that infected her husband. Here is food for thought.
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CHAPTER 9
The Antibiotic Problem
There is no evidence that a high efficiency system of oxidation exists in bacteria, especially in disease germs. However, they do depend upon an unrecognized Carbonyl function that is activated by electrons received from the double bonds of an ethylene linkage, even in the performance of the Krebs Cycle. This is seen where it is necessary to keep the cycle going by supplying the unsaturated dicarboxylic acids, whereas the saturated dicarboxylic acids, as succinic, are of no help. Thus, even in the low level Krebs Cycle, upon which bacteria depend, activated Carbonyl function of this particular order is required. Here, antibiotic activated amine groups have a position in which to produce their toxic effects, and either kill, asphyxiate, or suppress vital activity. The modern antibiotics, in medical use, all contain the toxic amine group and their toxic effects are seen both on the germ and on the host, when used therapeutically. Suspensions of consciousness, injured liver function, and other metabolic injuries are frequently reported, and sometimes, instantaneous death.
Further, the injurious effects on bacteria excite well-proven mutations against the amine poisons. The survival factor in the germ has reached enough success in this combat to excite scientific envy. When the writer balanced up his observations on the reciprocal and antagonistic actions of Carbonyl and amine groups and the reactions of the tissues to them, one experiment that he published in the “Journal of Laboratory and Clinical Medicine” in 1916, exposed the existence of a basis for the mutation against toxic amines. The poison observed was trimethyl melamine. It is probably one of the most toxic substances in existence, and produces instantaneous death when injected in fatal amounts into the blood stream. When sub-fatal doses are injected and the blood pressure recorded on the revolving drum, it is seen that a rapid and sustained fall in blood pressure occurs, but if more of the poison is injected during this period, in amounts that add up to more than the lethal dose, there is no fatal event, but only a minimal decrease in the blood pressure during this period of sustained depression. After the pressure returns to normal for ten minutes, a fatal dose will kill immediately. However, the occurrence of this refractory period indicated to the writer, that a basis for building a resistance to amine toxins and their derivatives existed, and to attack germs via toxic amine therapy would ultimately turn out unsuccessful. He, therefore, decided that for the correction of the basic fault in the host, the boosting of its Carbonyl function would be a preferable means of attack. To the surprise of all observers, it was found that after animals suffering with severe mastitis were given the Synthetic Survival Reagents, the most deadly Staphylococcus Aureus lost its toxic action, and its hemolysins were no longer formed.
Later on, the same was found true for the Streptococcus causing dairy cattle mastitis. It is seen, in the following table, that where gangrenous conditions were caused by the infection after injury had taken place, the bacteria actually increased in numbers while the toxic symptoms disappeared, and rapid healing was going on. But, where no gangrenous condition was present, the infection and its changes subsided together, with rapid decrease in the number of bacteria. Thus, it is evident that the bacteria lost their patho genicity after the host was treated with Survival Carbonyl groups, and became useful in clearing up the debris, they had formerly caused. Evidently they gained also from the Survival Carbonyl chemistry and were apparently enabled to serve constructively in the Great Biological Economy again. There were special studies by the University of British Columbia Veterinary Department on the loss of hemolytic properties of bacteria after the host was Treated, as well as restoration of the calcium balance showing that the tissue colloids were again in good dispersion, in other words, the tissue oxidations were restored. The following table of bacterial counts showings the reductions of bacterial counts and no change or the increase in these counts while healing and constitutional recovery is progressing is taken from the Annual Report (1944) of the Minister of Agriculture to the Parliament of British Columbia. *
* Copies of the Minister of Agriculture’s Reports are available on this web site.
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(Note — These counts were verified by a second laboratory).
It may be noted that cow No. 13 shown above is reported on as drying up with mastitis and ely-4p is shown as improving in udder condition in spite of the high bacterial content. The last-mentioned cow, Vera, had a severe accident to the udder between Treatments which doubtless accounts for the increase in bacteria. However, she was making satisfactory recovery when last reported on.
Other experiments with cultures of the bacteria that caused the lesions, and their high toxicity in comparison to the loss of toxicity of cultures of the same germs planted at different periods after Treatment was given to the host, confirm the observation. This work needs further chemical and clinical investi gation, aside from what is reported here. This is useful in showing how antibiotic resistant gonococci and pneumonococci became nonpathogenic, after contact with the Synthetic Survival Reagent.
In line with our Postulate, the toxic amine groups of intestinal poisons, those present in antibiotics and those produced by fungi, tend to diminish the oxygen supply to the tissues and thus hinder the combat against viral diseases. The toxic amine group also inactivates the FCG and blocks its function so it fails to oxidize pathogens destructively. Altogether the toxic amine tends to favor the integration of the virus with the host cell’s energy producing mechanism. This can be observed practically in the following case of measles.
MEASLES
CASE No. 13
Dr. Jayme Treiger
Baby R., 18 months of age, weight 11,500 grams, was first seen by Dr. J. Treiger 12/3/59. She took sick November 17, 1959, with a terribly itchy rash that was diagnosed an allergy, for which liver extract was given until November 22, when it was seen that it did no good and the condition became worse. Then until December 1, Aminophilin, Streptomycin, and Penicillin were given because of the high fever and aggravation of the rash, acetyl salicylic acid was also given because the pulmonary congestion was increasing. There was no improvement. The rash became worse and so did the other symptoms during these nine days. Further, the child refused all food and drink but allowed sugar water to be put on the tongue. Prostration developed and constipation also as no food was taken.
At his examination the fever was 39.5°C., the rash of measles fully fulminated, there was a bad tonsillitis, pulmonary congestion, and great prostra tion. It was not unconscious, but noticed nothing, and refused food and drink. Homeopathic remedies were given that improved the chest and throat symptoms but the rash, fever and prostration persisted with no improvement in the mental state. The prognosis was very grave. Dr. Treiger gave one micro gram of one of the Survival Factor Remedies, Parabenzoquinone, in one cc. of water, hypodermically, on December 5th to avoid Encephalitis.
Results. In a few hours there was improvement in the fever and rash. In 12 hours, the temperature was a normal 36°C. with the rash and itching about gone. The child asked for food and ate with appetite. During the rest of the day the recovery was completed, with good restoration of bowel function as well. Measles regularly recover under this Treatment in 12 hours. So even here where every toxic amine group available assaulted the body chemistry, the tissues were liberated by the oxidation potential and advantage of Benzo quinone, the weakest of the Survival Factor Reagents. One may contrast the therapeutic effects of toxic amines and constructive Carbonyl in this typical case.
ANTIMITOTIC AGENTS
The approach offered by antimitotic agents to hit the very center of the cancer problem has been most illuminating. This work was started in the past decade, and has been increasing world wide ever since. An excellent review is given by Biesele, of the Sloan Kettering Institution, in “Mitotic Poisons and the Cancer Problem,” Biesele — 1958 — Elsevier. Very interestingly, it will be seen that the antimitotic agents present Carbonyl and amine groups of the same order that we have been studying for the last 49 years. Biesele, while paying no attention to these groups or their action individually, classifies all antimitotics as poisons. It must also be noted that since the antibiotic products of molds and soil bacteria have been studied, inspection of their structural formulae reveals similar active amine and carbonyl groups. In view of our experience, the classification as poisons should be reconsidered to group them as amine poisons and Carbonyl restorative or Survival Agents. Indeed the survival capacity is small because of the structures of the molecules, but for the service of the mold that would protect itself, these groups might have corrected the evil effects of the germ’s toxins, or hindered them when being constantly produced by the mold in fair amounts. Certainly the mold did not attempt to kill the germ by the Carbonyl activity. It might even have tried to correct the germ’s fault and thus showed some therapeutic discretion. Such agents could really be mold hormones designed to serve within its own level of oxidations and reductions — constructively. Representative of Carbonyl containing antibiotics are the substituted quinones, Phoenicin, Citrinin, Clavicin, and Spinulosin. They all offer Carbonyl activated by the double bonds of two ethylene linkages, but this activation is reduced to a low ebb, by the substitutes for the hydrogen atoms that would have allowed splendid antibiotic activity. The representatives of antibiotics carrying highly toxic amine groups are the Sulfa drugs, Streptomycin with its two guanidine groups, and all of the other synthetic products. Some of these, like Terramycin and Penicillin, carry Carbonyl activated by conjugation with an ethylene linkage, as well as the toxic amine groups, and in some, such groups are protected by a substituent as methyl, that can be readily removed leaving the nascent amine group. The amine groups are likewise activated by conjugation with double bonds.
The same active groups are seen in the antimitotic agents, amine and Carbonyl. Maleic acid and Benzoquinone carry the Carbonyl groups, and their activity is measured accurately even in such infinitesimal concentrations as one part to a million, and one part to a billion of water. It would be unreasonable to speak of such high dilutions as being toxic. So, from their own observations, these agents cannot be classified as poisons to the mitotic mechanism.
In 1943, before antimitotic agents were ever studied, we testified in the Federal Court in Detroit on the corrective action of high dilutions of both substances, which we had used therapeutically years earlier and with corrective results. Since no evidence could be found of their injuring any of the participants or any of the processes concerned with mitosis, Biesele gives them a pre-mitotic position, and loses the real action which is to reduce the necessity for mitosis by their protective action against injurious agents, and their rejuvenating vitality, or survival boosts that lengthen the life span and thus reduce the need for reproduction or mitosis to assure the cultured tissue cell’s survival. The tissue culture effect is exactly what we demonstrated in animals and man even under the most adverse circumstances. That the action is attributable to the Carbonyl group as activated by double bonds in conjugation, one sees in the greater activity of Maleic anhydride over that of fumarate which we proved. This is a steric virtue, since in the anhydride both Carbonyl groups are in the same plane with the activating double bonds, whereas in the acid, only one Carbonyl group has that position. This action is, of course, curative and reconstructive in any reasonable dilution up to one part to a billion of water. As to the Carbonyl group working on a physiological and corrective basis that removes the functional and mitotic failure of survival, so well illustrated by cancer, we may refer to the same Court Testimony, which proves the complete permanent cure of far advanced terminal cancer of the liver, accomplished by one dose of two cc. of a dilution of one part of Benzoquinone to a million parts of water. The diagnosis, which was made by a half dozen leading surgeons by laparotomy, and the cure in 1941, is still standing as perfect 18 years later.
A few quotations from Biesele will be helpful, along with some explanatory discussion that we must give. This whole book of Biesele supports our Thesis, in spite of its coming from outside and non-cooperative interests that see nothing in their findings, except cytolytic effects and destructive action. Their observations are well made and accurately recorded, but they lack the physio logical viewpoint that gives these interpretations scientific and therapeutic values.
On page 31, it is reported, “The threshold of mitotic inhibition of chick fibroblast cultures by Benzoquinone was 10-u (Meier and Schar, 1947), or 0.001 ug/mi, the same as for Colchicine.” “The mitosis inhibition caused by some quinones and by Maleic acid has paralleled their uptake of sulfhydryl.” (P. 33).This shows, in line with our Thesis, that the action depends upon the activation of the Carbonyl group as recipient of electrons from its conjugated double bonds and that a physiological rather than a toxic action is to be expected, a dehydrogenating power that can initiate chain oxidation. Our diet has accordingly always eliminated sulfides and sulfhydryl. Lettre’s suggestions, that “quinone blocked sulfhydryl compounds to inhibit mitosis,” Biesele finds “inadequate, as other antimitotics are effective without blocking sulphydryl action.” However, all students of the problem overlook the oxidation catalysis of activated Carbonyl.
On page 30, Meyerhof and Randall (1948) and Burrough (1955) are quoted on the inhibition of epidermal mitosis by adrenaline and adrenochrome in dilutions of one part to a million. They found that “this inhibition occurred not only with glucose as an energy source, but with fructose, lactate and pyruvate… Further experiments indicated that the critical influence on metabolism imposed by epinephrine or adrenochrome was not on glycolysis, the tricarboxylic acid cycle, or the cytochrome system.” Thus, in line with our Thesis, the energy source that is cut off by toxic amines is the unidentified system which we named the “preferred smokeless process” initiated by activated Carbonyl groups, which burns all fuels and even the inhibitors that may be present, but which can be inactivated by highly potent amine groups as of phenylenediamine and epinephrine, which we point out, show reduction potentials of E’o = + 0.38v. and Eo= +0.80v. Other supportive data deserve attention.
Thus on page 50, Biesele reviews the contributions of Gellhorn, Hirschberg and Kream (1952) demonstrating that “the differential susceptibility of various tumors to inhibition by 8-azaguanine was inversely related to their ability to deaminate 8-azaguanine to the non-inhibitory 8-azaxanthine. In tissue culture inhibition by 8-azaguanine and the non-inhibitory effect of 8-azaxanthine on Brown-Pearce tumor were confirmed by Flint, Hirschberg and Murray (1953). Here, again, the inhibitory effect is due to an activated amine group while the protection against the action is a matter of oxidation that removes the amine group and substitutes a Carbonyl group in its place, as we claim happens to viral and other amine poisons during the reversal of carcinogenesis. A further example of this inactivation of toxic amines is found in the observation of Woodside (1953) in “tissues of the mouse in which 8-azaguanine restricted mitotic rates in carcinomas 755 and E0771 but not in tumors C954, C1300, S180 and S91, nor in ileum, jejunum or testis.” It must be recalled that the ileum, jejunum and testis are rich in diamine oxidase, and here a Carbonyl action is also involved in removing the toxic amine group and replacing it with a Carbonyl group in line with our Thesis. Here is another indication that free radicals and peroxide free radicals are involved.
On Page 50, Biesele suggests that the “inhibitory effect of 8-azaguanine may be related to its incorporation into ribonucleic acid, as suggested by Kidder, Dewey, Parks, and Woodside (1949) and demonstrated by Mitchell, Skipper, and Bennett (1950). The latter authors found, however, that the amount of 8-azaguanine incorporated into visceral RNA exceeded the amount incorporated into tumor RNA. This posed a dilemma for which Parks (1955) saw no solution.
However, 8-azaquinine-2-14C was incorporated into RNA of the susceptible mouse leukemia L1210 at a level 100 times that of its incorporation into the derivative azaguanine-dependent leukemia (Bennett, Skipper and Law, 1953). “The incorporation of 8-azaguanine into tumor RNA probably produces defective RNA. It is at this polynucleotide stage that Mandel (1955) envisioned the action of 8-azaguanine as an antimetabolite, rather than as an antagonist of free purines.” Here we see in line with our thesis that normal tissues are armed with many more active Carbonyl groups than are the susceptible tumor tissues and these Carbonyl groups can condense with the toxic amine structures and hold them in combination instead of their oxidative destruction. So our interpretation of the induced antimitotic activities and their prevention is that the same survival factor dealt with in this book is concerned and that the antimitotic data gathered so far, gives further support to our Thesis with measurable proof of the efficacy of high dilutions. Though not recognized by the investigators, their data again show one phase of the interaction of amine and Carbonyl groups dealt with in this book. Their data prove the protective action is an oxidation, though they failed to investigate the whole process.
THE QUINONE STRUCTURE AS AN ELECTRON ACCEPTOR IN NORMAL TISSUE METABOLISM
Recently a fat soluble, moderately substituted for Benzoquinone, has been identified and given intensive study. It is found in all animal and some plant tissues in several modifications and has been named because of its structure and function, Coenzyme Q10. It serves in the electron transport during the oxidation of succinate, and precedes cytochrome C as an obligatory electron carrier in the antimycin A sensitive oxidation of succinate by heart mito chondria. (Ziegler,1959). Ordinarily about one gamma is eliminated in the urine per hour. When a tissue on extraction with acetone and other solvents is made inactive for want of this coenzyme the addition of Coenzyme Q10 restores the oxidative activity. (Crane, 1959). Its structure is, — where n is from 6 to 9. This isoprenoid residue gives it fat-soluble properties, so it works in fatty fractions.
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The kinetics of Coenzyme Q have been worked out by Britton Chance, and the mechanism of its reduction in mitochondria has been investigated by Ziegler, while the specificity of Coenzyme Q homologues in electron transport restorations has been studied by Crane. Thus the physiological position of the quinone structure in metabolism is amply assured, and measured during the past year. This recent work confirms our Postulate, the chemistry of which we put into practical action some decades ago.
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