Category Archives: Acidity

CDC confirms 62 cases of Post-Polio illness or Acute Flaccid Paralysis (AFP)!

The Centers for Disease Control and Prevention has confirmed 62 cases of a post polio neurological condition called acute flaccid myelitis, also known as AFM.  So far this year in the U.S. more than 90 percent of the cases involved children 18 or younger, with an average age of just 4 years old.

AFM is an illness that affects the nervous system, specifically the area of spinal cord called gray matter. It causes the muscles and reflexes in the body to become weak or even paralyzed. Cases of AFM are characterized by a sudden onset of arm or leg weakness and loss of muscle tone and reflexes.

Its symptoms are identical to those of poliomyelitis or polio which is associated with a so-called virus.  Years of research have shown that these cases of polio and post-polio are associated with chemical poisoning or organochlorines used as a pesticide in farming found in all of our food sources (except for organically grown food).

Table 1: This graph shows polio in the United States in a context rarely (if ever) portrayed since Dr. Morton Biskind, the environmental context. [1] “DDT” and “DDT-like chemicals” are selected for this graph as the least complex way to represent a broad overview of the evolution of the technology of, and potential for, mass acidic chemical poisoning. (US Vital Statistics, US Government Printing Office, Washington, D.C.) [2][6]

Additional symptoms can include facial drooping or weakness, difficulty swallowing and slurred speech.

This condition, which may be caused by acidic poisoning from DDT like chemicals found in all non-organic fruit, vegetables, poultry and meat can lead to paralysis and even death, but no deaths have been reported so far this year.

Some prominent organochlorines are chlorobenzene, PCBs (polychlorinated biphenyls) and DDT (dichloro-diphenyl-trichloroethane). [3] Chlorobenzene is a precursor, a foundational compound used in the production of many industrial organochlorines as a chemical pesticide. [4] In the U.S., high production of chlorobenzene began in 1915, soon after the beginning of World War I. [5]

The above graph is a compilation of new cases per year (not incidence, as portrayed elsewhere herein). The data for the last half of the 20th century was gathered from U.S. Vital Statistics. [6] The very earliest numbers, from 1887 to about 1904, and the post polio numbers, are interpolated from the general historical commentary regarding those periods. [7] (see bibliography on Homepage and NYC Health Commissioner Haden Emerson’s compilations). While the graph is not perfectly accurate, due to changing methods of diagnoses and record-keeping within the medical system, it does give a reliable overall picture of Polio cases in terms of known literature and records.

The source for the U.S. and Swiss discoveries of paralysis in calves is from Van Nostrand’s Encyclopedia of Science and Engineering (1995), vol. 5, p1725. The phrase “Pesticides as a Panacea: 1942-1962” is a subtitle found in Encyclopedia Britannica, Macropaedia (1986). [8] Refer to other graphs (Overview) for specific pesticide comparisons with Polio incidence.

In 1915 Hooker Electrochemical began massive, unprecedented production of chlorobenzene (8,200 metric tons per year) and Dow Chemical began large-scale production soon thereafter. [9]

Chlorobenzenes are the basis for picric acid explosive used in World War I. [10] They have also been used in the manufacture of wood treatments, war gas, herbicides, insecticides, bactericide, moth control, and polymer resins. [11] (Mono) chlorobenzene is the base compound for DDT production. [12] Currently in the U.S., 15 million pounds of p- dichlorobenzene production goes into room deodorants. [13] According to Peter Duesberg, CDC’s investigation into Legionnaires disease ignored toxic chemical causes and created a new false field of study regarding the Legionella bacterium. [[4]

The sudden surge of chlorobenzene production coincides in time and place (1915, Niagara Falls) to be considered as probable cause for the epidemic of central nervous system diseases that followed the next year in the New York City region. [15] This epidemic lasted only six months, June to November, with 82% of the cases occurring in just 8 weeks. [16] While Polio literature terms this a world-wide Polio epidemic, it was peculiarly a phenomena of the U.S. and was especially prominent in the New York City region. [17] This is strange behavior for a supposedly so-called predatory Poliovirus, in an era, a continent, wholly unprotected by so-called miracle vaccines!

The number of new cases for 1916 (40,485) were calculated by multiplying the U.S. incidence rate by the U.S. population. [18] The number seems too high because of Naomi Rogers’ statements that worldwide new cases in 1916 were 27,000, that two-thirds of world Polio new cases were in the U.S. and that New York City new cases were 9,000. [19] While this discrepancy exists, the data is still useful for showing relative case numbers and/or incidence for the early 20th century. [See Tables 1,3,4,5,8,9,10 and 11]

Both Polio epidemics occurred two years after the beginning of World War I and World War II, if we use the dates of the epidemics, 1916 and 1942. [20]

DDT and “DDT-like chemicals” are used to represent the major organochlorine pesticides and organochlorines of similar neurotoxic character. [21] Most of the industrial organochlorines can produce CNS disease symptoms similar to Polio. [22] [Refer to Tables 2, 3, 5, 6, 7, 8, 9,10 and 11] below to see the relationship between DDT and DDT-like chemical production and the incidence of Polio.

Other Poisonous DDT-Like Pesticide Composite

Just over three billion pounds of persistent pesticides are represented in the Table 2 above and 3 below. Virtually all peaks and valleys correlate with a direct one-to-one relationship with each pesticide as it enters and leaves the US market. Generally, pesticide production precedes polio incidence by 1 to 2 years. The variation may be to variations in reporting methods and the time it takes to move pesticides from factory to warehouse, through distribution channels, onto the food crops and to the dinner table. A composite of these graphs, of the persistent pesticides–lead, arsenic, and the dominant organochlorines (DDT and BHC) is presented in Table 10.

The four chemicals were not selected arbitrarily. These are representative of the major pesticides in use during the last major polio epidemic. They persist in the environment as neurotoxins that cause polio-like symptoms, polio-like physiology, and were dumped onto and into human food at dosage levels far above that approved by the FDA. They directly correlate with the incidence of various neurological diseases called “polio” before 1965. They were utilized, according to Dr. Biskind, in the “most intensive campaign of mass poisoning in known human history.” [23]

Critique of Pesticides and Polio Vaccination

It certainly appears, from the above graphs, that the vaccination programs arrived a few years too late to be credited for declining polio case numbers. The programs were close enough, however, for media to shoehorn them into their historical position. This quote from Time Magazine (March 28, 1994) is a typical example:

“The great postwar epidemic peaked in the U.S. in 1952, when more than 20,000 children were paralyzed by polio and it tapered off in the early ’60s, after the Salk vaccine and then the Sabin oral version were introduced.” [23]

This smooth, loaded phrase, framed with glossy photos and clever captions, goes down like several shots of Vodka and with the same physiological effects. However, if we contain our admiration, and review the actual data, we realize that the great Polio epidemic actually occurred from 1942 (or gradually, beginning decades earlier) to 1962, that is, it was not a “postwar epidemic”. (Refer to Table 1) The epidemic declined not “in the early ’60s”, but a full decade earlier, in the early 1950s. Polio cases per year did not “taper off… after the Salk vaccine” as Time would have us believe — new cases per year dove resolutely downward two years before the Salk vaccine field trials and four years before the vaccination programs were firmly underway. The decline of Polio actually occurred after heated discussions regarding the dangers of DDT that began with in-house government/industry reviews of DDT in 1951, following Dr. Morton Biskind and other’s criticism of pesticides which began in 1945. [23 to 85] These discussions were followed by a phase-out through industry compliance, a huge shift of sales to third-world countries, a phase-in of less-persistent pesticides, which was facilitated by legislation in 1954 and 1956, (86) a renewed public image regarding the proper use and dangers of pesticides, [87] the cancellation of DDT registration by 1968, [88] and eventually the official ban of many of the persistent organochlorine pesticides by 1972 (in U.S. and developed countries). [89]

Notice that while pesticide production directly correlates with new polio cases per year through every peak and valley, the Salk vaccine enters only after Polio’s decline. (Refer to Tables 1 and 4) Salk’s point of entry is not sufficient evidence to be routinely offered as proof for the victory of vaccines over the Poliovirus, as Time implies, [90] and as implied by Hayes and Laws, [91] and virtually all other presentations of polio history in whatever media or educational forum.

The molecular biologist, Peter Duesberg, in his attempt to give Modern Medicine some credence with regard to virus causality (before refuting HIV causality with AIDS), [92] apparently felt he could assume, in Inventing the AIDS Virus, that, …the sudden, frightening polio epidemic that exploded in the Western nations, brought home by troops returning from the Pacific theater in 1945. [93]

Yet a glance at the graphs in Tables 1 and 4 shows his statement to be inaccurate. Polio was entrenched in the U.S. long before returning troops, and the increased Polio cases per year correlate much more consistently with pesticide production than returning troops. A rise in new cases per year that peaked in 1945 can be clearly attributed to the government’s release of war surplus DDT to the public market in 1945, not vague data about “troops returning from the Pacific theater in 1945”. The troops were heavily treated with DDT years before the U.S. civilian population and as can be expected, in light of the acidic chemical poison-theory, the troops suffered unusually high Polio incidence rates when compared to the non-treated populations where they were stationed, and soldiers based in the U.S.. [94] The unusual drama and rash assumption that fills this excerpt of Peter Duesberg’s writings gives a sense that he has taken the whole package of ingrained Polio images for granted. [95]

Pesticide Phase-Out and Vaccinations Phase-In

DDT and BHC were phased out from the developed nations and at the same time vaccination programs were dramatically credited with saving these countries from the ravages of the Poliovirus. (96) However, the banned pesticides continued with higher than ever total distribution in the under-developed countries thanks to W.H.O.’s anti-mosquito campaigns, where to this day acute flaccid paralysis (AFP), Polio, and DDT/BHC still prevail. (97) DDT application, DDT phase-out programs, and Polio vaccination programs are all being directed in these countries concurrently by the World Health Organization with little or no success. (98)

Registration for DDT was canceled in 1968, and DDT was banned by the EPA in 1972 — after the major organochlorines (DDT, BHC) had been gradually phased out of the U.S. market by the chemical industry and replaced with the less environmentally persistent pesticides, the organophosphates. (99)

Post-Polio Pesticides

In 1983, via new legislation, DDT was allowed back into the U.S. marketplace, but only in pesticide blends. (100) Within only a few months of this re-entry, a new kind of polio epidemic suddenly occurred. (101) It was labeled “Post-Polio”, the re-emergence of Polio symptoms in former victims. (102) This has involved approximately 600,000 victims and is shown in Table I above. Like most of the data, this correlation is not even a whisper in the mainstream media.

Central nervous system diseases other than Polio continues in the U.S. and throughout the world: acute flaccid paralysis, chronic fatigue syndrome, encephalitis, meningitis, muscular sclerosis, and rarely in humans, rabies. (103)

The harsh realities of government policy are stated in Casarett and Doull’s Toxicology (1996): “Although government agencies and industry have been slow in their re-evaluation of a vast array of pesticides in use, reassessment often comes in the wake of or concomitant with some recently disclosed adverse environmental or health effect.” (104) This after-the-fact approach to pesticide poisoning is puzzling enough without questioning Casarett and Doull’s careful usage of the words: “often”, “some”, “recently”, and “disclosed”. The acidic chemical environmental correlations of “Post-Polio are overlooked.

Searching PubMed has not been successful. However, an online a paper entitled “The Environmental Aspects of The “Post-Polio” Syndrome”, was found. This article establishes a strong correlation between environmental acidic chemical factors and “Post-Polio”. (105)

No other similar articles are to be found, and no abstracts were available, although it can be ordered from PubMed. Poliovirus presence in “Post-Polio” according to immunity and vaccination theories, if anyone should be immune to Polio, it should be former Polio victims, however, numerous studies of “Post-Polio” victims have found evidence of active Poliovirus. (106) (107) (108)

Polio images are projected as if this data doesn’t exist. It does not appear that money is being directed into these kinds of research studies.

Farr’s Law

Farr’s Law requires, for an epidemic to be a valid example of contagion, that the epidemic increase its incidence rates exponentially. (109) Since Polio has been ubiquitous since the beginning of human history, its incidence rate should have peaked long ago and universal immunity conferred, if immunity was ever required, and if the Poliovirus was actually a predator or even existed! Polio’s non-compliance with Farr’s Law is explained by viro pathologists with a unique argument, the inverse of the argument usually given to support so-called germ theory. (110) The argument is that the Poliovirus, which has been intimate with mankind since the beginning of history, suddenly became estranged from humans because of modern hygiene, and thus humans lost their natural immunity to the virus. (111) So it is modern hygiene and the resulting lack of exposure to the virus that is said to have caused the Polio epidemics to rage as never before. (112) It is interesting that for only one brief moment, viro-pathologists are willing to become eco-nutritional types who appreciate the value of natural breast feeding and the importance of the internal microbiological ecology conferred positively upon humans as I have suggested in my pH Miracle books and other published articles. (113)

Three different promotions of their inverse or perverse argument follows:

1)   The prominent book on polio history by Naomi Rogers, where the inverse argument resides in the title, Dirt and Disease: Polio Before FDR. (114) The language style here is popular. (115)

2)   In Textbook of Child Neurology (1995), John H. Menkes promotes the inverse argument with scientific language style: “Poliomyelitis… is less likely to be symptomatic in areas with inadequate sanitation, because poor sanitation is conducive to exposure at an age when lingering

transferred maternal immunity can attenuate the clinical picture.” (116)

3)   In the propaganda film, A Paralyzing Fear: The Story of Polio in America. This was funded by the government and pharmaceutical firms and released in 1998. (117)

The New York Times (March 4, 1998) reviews the film. It reinforces the fundamental tenets of the Polio culture, beginning with a quotation from a section that portrays a “vintage film clip”: “My name is virus Poliomyelitis,” intones a cultivated, sinister male voice, as a camera pans over fair-weather clouds from which a hollow shadow emerges carrying the silhouette of a crutch. “I consider myself quite an artist, a sort of sculptor,” the voice continues. “I specialize in grotesques, twisting and deforming human bodies. That’s why I’m called The Crippler.”

Having dramatically demonized the Poliovirus, the medical cavalry rides to the rescue: …the epidemics grew steadily worse each year, with the number of new cases climbing from 5,000 in 1933 to 59,000 in 1952. (Refer to Tables 1 and 4)

Salvation came in 1954 with the Salk vaccine…And the inverse argument is now fit to print:

“The irony of the rise of polio in the 20th century, the movie reports, is that its prevalence was a result of improved sanitation. In grubbier times, babies and very young children developed antibodies to the disease, which had been around forever. A cleaner environment left increasing numbers of children with no natural immunity. (118)

So The New York Times review concisely presents the standard Polio images:

“the predatory virus, paralytic horror, epidemics, salvation via the Salk vaccine, and a unique exception from Farr’s Law.” (119)

I have my own personal concerns that anyone at NYT actually wrote this article, rather that it was probably supplied to the journalist as a suggested article, to be adjusted to the author’s style, thus essentially a customized press release.

The Epidemic Intelligence, Inventing The AIDS Virus (1996): The CDC’s disease-control mission was increasingly being regarded as obsolete, prompting serious discussions about abolishing the CDC altogether. (120) The situation changed in 1949 when the CDC brought on board Alexander Langmuir, an associate professor at the Johns Hopkins University School of Hygiene and Public Health. (121) Langmuir was the CDC’s first VIP, bringing with him both his expertise in epidemiology (the statistical study of epidemics) and his high-level connections — including his security clearance as one of the few scientists privy to the Defense Department’s biological warfare program……Langmuir and talked public officials and Congress into giving the CDC contingent powers to deal with potential emergencies… (122)

In July of 1951 he assembled the first class of the Epidemic Intelligence Service (EIS), composed of twenty-three young medical or public health graduates. After six weeks of intensive epidemiological training, these EIS officers were assigned for two years to hospitals or state and local health departments around the country. Upon completing their field experience, EIS alumni were free to pursue any career they desired, on the assumption that their loyalties would remain with the CDC and that they would permanently act as its eyes and ears. (123) The focus of this elite unit was on activism rather than research and was expressed in its symbol — a shoe sole worn through with a hole. According to British epidemiologist Gordon Stewart, a former CDC consultant, the EIS was nicknamed the “medical CIA.” (124)

To read and understand more about the Phantom virus called Polio please order Dr. Young’s book by clicking here: https://www.amazon.com/…/ref=dbs_a_def_rwt_hsch_vapi_taft_p…

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Do YOU Believe the Polio Viral Theory?

The first isolation of a virus was achieved in 1892 by Russian bacteria hunter Dimitri Iwanowski, who gathered fluid from diseased tobacco plants. He passed this liquid through a filter fine enough to retain bacteria; yet to Iwanowski’s surprise, the bacteria-free filtrate easily made healthy plants sick. In 1898 a Dutch botanist, Martinus Willem Beijerinck, repeating the experiment, also recognized that there was an invisible cause and named the infectious agent “tobacco mosaic virus.” In the same year as Beijerinck’s report, two German scientists purified a liquid containing filterable viruses that caused foot-and-mouth disease in cattle (viruses were at one time called “filterable viruses,” but eventually the term “filterable” came to apply only to viruses, and was dropped). Walter Reed followed in 1901 with a filtrate responsible for yellow fever, and soon dozens of other disease-causing viruses were found.

In 1935 another American, Wendell M. Stanley, went back to the beginning and created pure crystals of tobacco mosaic virus from a filtered liquid solution. He affirmed that these crystals could easily infect plants, and concluded that a virus was not a living organism, since it could be crystallized like salt and yet remained infectious. Subsequently, bacteriologists all over the world began filtering for viruses, and a new area of biology was born-virology.

Historically, medical science has vacillated on the question of whether a virus is alive. Originally it was described as nonliving, but is currently said to be an extremely complex molecule or an extremely simple microorganism, and is usually referred to as a parasite having a cycle of life. (The term “killed” is applied to certain viral vaccines, thus implying an official conviction that viruses live.) Commonly composed of either DNA or RNA cores with protein coverings, and having no inherent reproductive ability, viruses depend upon the host for replication. They must utilize the nucleic acids of living cells they infect to reproduce their proteins (i.e., trick the host into producing them), which are then assembled into new viruses like cars on an assembly line. Theoretically, this is their only means of surviving and infecting new cells or hosts.

The Replicating Virus Theory

Then it was discovered that, when bacteria slowly begin to die, bacteria create tiny, apparently lifeless forms of survival, the so-called spores. It was then suspected that these spores were toxic and that they were the so-called pathogenic poisons. This was then refuted, since the spores are rapidly developing into bacteria when their vital resources are being restored. When scientists in the laboratory observed that the weak, highly inbred bacteria perished very quickly while turning into much smaller structures than the spores, it was first believed that the bacteria were being killed by the alleged pathogenic poisons, called viruses, and that the viruses were thereby replicating.

The Replicating Virus Theory

Then it was discovered that, when bacteria slowly begin to die, bacteria create tiny, apparently lifeless forms of survival, the so-called spores. It was then suspected that these spores were toxic and that they were the so-called pathogenic poisons. This was then refuted, since the spores are rapidly developing into bacteria when their vital resources are being restored. When scientists in the laboratory observed that the weak, highly inbred bacteria perished very quickly while turning into much smaller structures than the spores, it was first believed that the bacteria were being killed by the alleged pathogenic poisons, called viruses, and that the viruses were thereby replicating.

The Invention of Bacterial Viruses

Due to the belief that these – at the time of their discovery still invisible- structures were killing the bacteria, they were called phages/bacteriophages, “eaters of bacteria”. Only later it was determined that merely highly inbred and therefore almost non-viable bacteria can be made to turn into phages, or bacteria which are being destroyed so fast that they do not have time to form spores.

The introduction of the electron microscopy led to the discovery of the structures resulting from the biological transformation or pleomorphism of bacteria when these were suddenly dying or when the metabolism of the highly inbred germs was overwhelmed by processes triggered by the adding of “phages”. It was also discovered that there are hundreds of types of different-looking “phages”. The discovery of phages, the so-called bacterial “viruses”, reinforced the wrong assumption and the belief that there were human and animal viruses that looked the same and had the same structure. This is not and cannot be the case, for several different reasons.

After introducing chemical examination techniques in biology, it was discovered that there are thousands of types of phages and that phages of one type always have the same structure. They consist of a particular molecule, made of nucleic acid, which is covered in a shell of proteins of a given number and composition. It was only later discovered that merely the bacteria which had been highly inbred in the test tube could turn into phages themselves, by contact with phages, but this never applied to natural bacteria or bacteria which had just been isolated from their natural environment. In this process, it was discovered that these “bacterial viruses” actually serve to provide other bacteria with important molecules and proteins, and that the bacteria themselves emerged from such structures.

Before it could be established that the “bacterial viruses” cannot kill natural bacteria, but they are instead helping them to live and that bacteria themselves emerge from such structures, these “phages” were already used as models for the alleged human and animal viruses. It was assumed that the human and animal viruses looked like the “phages”, were allegedly killing cells and thereby causing diseases, while at the same time producing new disease poisons and in this way transmitting the diseases. To date, many new or apparently new diseases have been attributed to viruses if their origin is unknown or not acknowledged. This reflex found an apparent confirmation in the discovery of the “bacterial viruses”.

It is important to note that the theories of fight and infection were accepted and highly praised by a majority of the specialists only if and when the countries or regions where they lived were also suffering from war and adversity. In times of peace, other concepts dominated the world of science.[272]

It is very important to note that the theory of infection – starting from Germany – has only been globalized through the third Reich, when the Jewish researchers, most of which had opposed and refuted the politically exploited theories of infection, were removed from their positions.[273]

The Detection of Phages and Biological Transformation

The existence of phages can be proved rapidly

First step: their presence is confirmed through an effect, namely the transformation of bacteria into phages, and also through an electron micrograph of those phages. The control experiments show that phages do not appear if bacteria do not change or if bacteria randomly start decomposing due to extrinsic sudden annihilation, without forming phages.

Second step: the liquid containing the phages is concentrated and applied on another liquid, which has a high concentration at the bottom of the test tube and a low concentration at the top of the test tube. The test tube with the phages is then powerfully spun (centrifuged) and all the particles gather according to their mass and weight to the place of their own density. The density is the ratio of weight (mass) per unit of volume, expressed as Kg/l or g/mg, respectively. That is why this concentration and purification step for particles with the same density is called density gradient centrifugation.

The layer where many particles of the same density gather becomes “cloudy”, which is called a “band.” This step is being documented, then the particles concentrated, purified and sedimented in a “band” are removed with a syringe needle. The extracted concentrated amount of particles is called an isolate. A fast and simple electron micrograph will confirm the presence of phages in the isolate, which at the same time is an indication for the purity of the isolate, if the micrograph shows no other particles but the phages. The appearance and the diameter of the phages will also be established with the help of this micrograph.

The control experiment performed for this step consists in treating and centrifuging the liquid from bacteria which did not form any phages, where no phages appear at the end of the procedure.

After the step of successfully isolating the phages, the decisive biochemical characterization of the phages follows. The biochemical characterization of their composition is essential for identifying the specific type of phage, since different types of phages often appear to be similar. The isolate obtained through the density gradient centrifugation is now divided in two parts. One part is used to determine the size, type and composition of the nucleic acid; in a separate procedure, the other part is used to determine the amount, size and morphology of the proteins of the phages. Since the 1970s, these tests have been simple standard techniques that are learned by every biology student in their first semesters.

These tests represent the biochemical characterization of the phages. In almost every case, these results have been and are being published in only one publication, since a phage has a very simple structure which is very easy to analyze. The control experiments for these tests use liquid from bacteria which do not form phages and thus cannot present any biochemical proof. The existence of approximately two thousand different types of phages have been scientifically demonstrated this way

The So-Called Pathogenic Viruses

The “bacteriophages,” correctly defined as incomplete mini spores and building blocks of the bacteria, have been scientifically isolated, while the so-called pathogenic viruses have never been observed in humans or animals or in their body fluids and have never been isolated and subsequently biochemically analyzed. To date, none of the researchers involved in virology research seems to have realized this very important point.

The use of electron microscopy and the biochemistry were very slowly returning to normal after 1945 and no one had realized that not one pathogenic virus had ever been isolated in humans or animals; thus, as of 1949 researchers started applying the same idea used for the (bacterio) phages, in order to replicate the human and animal “viruses.” John Franklin Enders, born in 1897 in the family of a rich financier, was active in various fraternities after having finished his studies, then he worked as a real estate agent and studied foreign languages for four years before turning to bacterial virology, which fascinated him. He then simply transferred the ideas and concepts that he learned in this area of research to the supposed pathogenic viruses in humans.

UnScientific Experiments and Interpretations Gave Birth to Virology

With his unscientific experiments and interpretations that he had never confirmed through negative controls, Enders brought the entire “viral” infectious medicine to a dead end. It is important to note at this point that Enders, like many infectious diseases specialists, worked for the U.S. military, which had always been and remains to date a huge victim of the fear of contagions. It was mainly the U.S. military which spread its erroneous belief that besides chemical weapons there were also biological weapons in the form of bacteria and viruses.

In 1949, Enders announced that he had managed to cultivate and grow the alleged polio virus in vitro on various tissues. The American expert opinion believed everything immediately. What Enders did was to add fluids from patients with poliomyelitis to tissue cultures which he claimed to have had sterilized, then he alleged that the cells were dying because of the virus, that the virus was replicating in this way and that a vaccine could be harvested from the respective culture. At that time, summer polio epidemics (polio = flaccid paralysis) were very frequent during summer and they were believed to be caused by the polio virus. A vaccine was to help eradicate the alleged virus. After the polio vaccine was introduced, the symptoms were then re-diagnosed among other things as multiple sclerosis, flaccid acute paralysis, aseptic meningitis etc. and later polio was claimed to have been eradicated. During his experiments, Enders et al. sterilized the tissue cultures in order to exclude the possibility of bacteria killing the cells. What he didn’t take into consideration was that the sterilization and the treatment of the cell culture when preparing it for the alleged infection was exactly what was destroying and killing the cells. Instead, he interpreted the cytopathic effects as the existence and the action of a so-called polio virus, without ever having isolated a single virus and describing its biochemistry. The necessary negative control experiments, which would have shown that the sterilization and the treatment of the cells prior to the “infection” in the test tube was killing the cells, have never been performed. However, for this “performance” Enders received the Nobel prize in 1954.

The Invention of the Polio Virus and ‘YES” the Measles Virus Too!

1954 is also the year in which Enders applied and introduced the same technique in order to allegedly replicate the measles virus. As he had been awarded the Nobel prize for the alleged polio virus the same year, all researchers believed his technique to be scientifically valid. Thus, to date, the entire concept of polio and measles has been based upon this unscientific technique and fraud.

Thus, the polio and measles vaccines do not contain viruses, but particles of dead monkey kidney tissue or human cancerous body cells. To date, no negative control experiments have been done with respect to the so-called polio and measles viruses either, which would have shown that it was the laboratory procedures that lead to the cytopathic effects on the cells.

Additionally, all claims and experiments made by Enders et al. and subsequent researchers lead to the only objective conclusion, that in fact they were observing and analyzing the cellular particles or fragments and the activity thereof in the test tube, misinterpreting these as particles and characteristics of the alleged polio and/or measles viruses.

ALL Viruses from HIV, EBV, CMV, Hepatitis C, West Nile Virus, Ebola, Zika Virus, etc. are ALL Phantom Viruses

Their Existence Has NEVER Been Scientifically Demonstrated!

The following explanations applies to all the so-called (human or animal) “pathogenic viruses”. The six papers provided by Dr. Bardens in the course of the “measles trial” as proof for the existence of the measles virus described in a didactically ideal way the various steps of the chain of misinterpretations up to the belief in the existence of a measles virus.

The first paper was published in 1954 by Enders et al.: “Propagation in tissue cultures of cytopathogenic agents from patients with measles” (Proc Soc Exp Biol Med. 1954 Jun; 86 (2): 277–286).

This publication can be found on the internet, like all the other publications presented at the measles trial. In that experiment, Enders et al. cut down dramatically on the nutrient solution and added cell-destroying antibiotics to the cell culture before introducing the allegedly infected fluid. The subsequent dying of the cells was then misinterpreted as presence and also isolation of the measles virus. No control experiments were performed to exclude the possibility that it was the deprivation of nutrients as well as the antibiotics which led to the cytopathic effects.

Enders’ and his colleagues’ blindness can be explained by the fact that he truly wanted to help people, while the ‘virus hysteria’ was intensifying after the war and during the cold war. It can also be explained by the fact that Enders and many of his colleagues had no idea about medicine or biochemistry and they were competing with the Soviet Union for the development of the first measles vaccine. Such a pressure for success can also explain why Enders and his colleagues ignored their own reservations and cautions expressed in 1954, when they had observed and noted that many cells also died after being treated normally (i.e. without being “infected”), which they thought to have been caused by unknown viruses and other factors.  All these facts and cautions were subsequently disregarded.

The second paper presented by the claimant in the ‘measles trial’ was published in 1959[274] and, for the reasons presented above, the authors concluded that the technique introduced by Enders was not appropriate for the isolation of ANY virus. This rebuttal is not only NOT being discussed by ALL the other researchers, but it is being ignored completely!

The ‘Viral Dogma’ of Pathogenic Viruses is Still Being Promoted Today!

In a third paper[275], the authors photographed typical cellular particles inside the cells and misinterpreted these as measles virus. They did not isolate any virus. For unexplained reasons, they failed to determine and describe the biochemical structure of what they were presenting as a virus in a separate experiment. In the short description of the methods used, one can read that the authors did not apply the standard isolation technique for viruses, i.e. the density gradient centrifugation. They simply centrifuged fragments of dead cells at the bottom of a test tube and then, without describing their biochemical structure, they misinterpreted the cellular debris as viruses.

From the way the experiments were performed, one can only conclude that cellular particles were misinterpreted as viruses. We find the same situation in the fourth[276] and the sixth[277] publication put forward by the claimant as proof of the existence of a measles virus. The fifth publication[278] is a review describing the consensus process as to which nucleic acid molecules from the dead cells would represent the so-called genome of the polio or measles virus. The result is that dozens of research teams work with short pieces of cell-specific molecules, after which -following a given model – they put all the pieces together on paper. However, this jigsaw puzzle made of so many pieces was never scientifically proven to exist as a whole and was never isolated from a virus, for a polio, measles, HIV or Hepatitis C, Ebola or Zika viruses have never been seen, neither in humans nor in a test tube. Referring to this publication, the court-appointed expert stated that it described the gold standard, i.e. the entire virus genome. It is obvious that the expert did not read this paper, whose authors stated that the exact molecular composition and functions of the measles virus genome will have to be the object of further research, which is why they had to rely on other virus models in order to achieve a consensus on the structure and functions of ANY virus genome. The easiest thing for anyone to notice is that in all of these publications, as well as in all other publications on the “measles virus” and other pathogenic viruses, including HIV, EBV, CMV, Ebola and Zika, no control experiments have ever been performed. No researchers used the density gradient centrifugation technique; instead, they only centrifuged cellular debris at the bottom of a test tube. This technique, used to collect all the particles from a fluid, is called pelletizing. From a logical and scientific perspective, it can be said that in all publications on the so-called “pathogenic viruses”, the researchers demonstrated in fact only particles and characteristics of cells. I would also like to point out that the so-called giant viruses[279] , i.e. an enwrapped nucleic acid can be found everywhere in the sea and in basic organisms. Like all bacterial phages, not only are they harmless, but they have beneficial functions. They can be also isolated by using the density gradient centrifugation, which proves their existence (see the graphic above).

I also recommend Prof. Lüdtke’s relevant review (1999).[280] He noted that at the early beginnings of virology, the majority of virologists always concluded that the structures they had mistaken for viruses turned out to be components of the cells and thus, they were only the result of the experiment and not the cause of the changes observed.

After the discovery and characterization of the phages and after introducing the dogma that the nucleic acid was the genome of all cells and viruses, the consensus was born, according to which such viruses must exist in humans and animals as well. In 1992, the dogma stating that the nucleic acid is the genotype of all cells was retracted in the scientific community. The ‘viral dogma’ of pathogenic viruses, however, is still being promoted today to the harm of billions of people. – for what?

The Bottom Line Concerning Phantom Viruses and the Polio Virus

My bottom line still holds the truth that the terrain or internal environment is everything and the germ or so-called virus is NOTHING! The germ or so-called virus can only be a symptom of cellular breakdown due to an imbalance of the delicate alkaline pH balance of the body fluids and NOT the cause of that breakdown. That is why years ago I offered any scientist in the World a finders fee of 5 million US dollars if they could prove the existence of the HIV virus using Koch’s postulates. It has now been over 20 years and I am still waiting even though currently I no longer have the funds to pay the prize due to political assassination! It is unfortunate that a former 5 million US dollar prize offered 20 years ago was not enough money to change the current medical viral dogma that is currently paying out trillions of dollars to guess who?

Click here to read more: http://medcraveonline.com/IJVV/IJVV-02-00032.php

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Lecture in Dubai – The Annual Conference on Bacterial, Viral and Infectious Diseases

http://www.drrobertyoung.com/events.html

Join Robert O Young PhD and Galina Migalko MD in Dubai on December 5th and 6th, 2018 for the Annual Conference on Bacterial, Viral and Infectious Diseases. They will be Key Note Speakers and doing a workshop on the New Biology.

For more information and to register go to: https://bacterialdiseases.infectiousconferences.com/organiz…

The following is the abstract for Dr. Young’s lecture:

The Dismantling of the Viral Theory

Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner

Abstract

There is now over 100 years of documented history and research on the Polio virus and whether or not its treatment by inoculation has been successful in eradicating Polio. I am suggesting in this article and in my lecture that there are significant findings based on historical and past and current research, including my own that the viral theory of Polio and possibly other modern-day diseases, such as Post-Polio Syndrome, Polio Vaccine-Induced Paralysis, Legionnaires, CNS disease, Cancer, HIV/AIDS and now Zika may be caused by acidic chemical poisoning from DDT (dichloro-diphenyl-trichloroethane) and other related DDT pesticides, acidic vaccinations, and other factors including lifestyle and dietary factors rather than from a lone infectious virus. I will present ten historical graphs outlining the history of Polio, the production of DDT, BHC, Lead, Arsenic, Polio vaccinations and the author’s theory that chemical poisoning, vaccination, and lifestyle and dietary choices are a more likely causes for the symptoms of Polio, neurological diseases, Cancer, HIV/AIDS and now Zika.

https://www.linkedin.com/…/lecture-dubai-annual-conference…/
https://bacterialdiseases.infectiousconferences.com/organiz…

References:

[1] Morton S. Biskind, MD. “Public Health Aspects of the New Insecticides”. American Journal of Digestive Diseases, New York, 1953, v 20, p331.

[2] Handbook of Pesticide Toxicology, edited by Wayland J. Hayes, Jr. and Edward R. Laws, Academic Press Inc., Harcourt Brace Jovanovich, Publishers, San Diego, 1991, p769

[3] Toxicological Profile: for DDT, DDE, and DDE. Agency for Toxic Substances and Disease Registry, September 2002.

[4] U. Beck, E. Löser “Chlorinated Benzenes and other Nucleus-Chlorinated Aromatic Hydrocarbons” Ullmann’s Encyclopedia of Industrial Chemistry, 2012, Wiley-VCH, Weinheim.

[5] Chlorobenzene”. Immediately Dangerous to Life and Health. National Institute for Occupational Safety and Health (NIOSH)

[6] U.S. Vital Statistics, U.S. Government Printing Office, Washington, D.C.

[7] Historical Statistics of the U.S., The U.S. Government Printing Office, Washington, D.C.

[8] Van Nostrand’s Encyclopedia of Science and Engineering (1995), vol. 5, p1725. The phrase “Pesticides As A Panacea: 1942-1962” is a subtitle found in Encyclopedia Britannica, Macropaedia (1986).

[9] Thomas, Robert E. (1955), Salt & Water, Power & People: A Short History of Hooker Electrochemical Co. Niagara Falls, NY: Hooker Chemical Co.

[10] Booth, Gerald (2000), “Ullmann’s Encyclopedia of Industrial Chemistry – Nitro Compounds, Aromatic”. doi:10.1002/14356007.a17_411. ISBN 3527306730

[11] Weber, Manfred; Weber, Markus; Kleine-Boymann, Michael (2004). “Ullmann’s Encyclopedia of Industrial Chemistry – Phenol”. doi:10.1002/14356007.a19_299.pub2. ISBN 3527306730.

[12] Haller, H. L., Bartlett, P. D., Drake, N. L., and others: The Chemical Composition of Technical DDT, American Chemical Society, Journal, volume 67, pages 1591- 1602, 1945.

[13] Jo-Yu Chin, Christopher Godwin, Chunrong Jia, Thomas Robins, Toby Lewis, Edith Parker, Paul Max, and Stuart Batterman, “Concentrations and Risks of p-Dichlorobenzene in Indoor and Outdoor Air,” Indoor Air, 2013 Feb; 23(1): 40–49, Published online 2012 Jul 18. doi: 10.1111/j.1600-0668.2012.00796.x.

[14] Duesberg, PH, “Inventing the AIDS Virus,” Regnery, (1996). ISBN 0-89526-399-8. [15] Icon Group International (Author), Chlorobenzene: Webster’s Timeline History, 1851 – 2007 May 17, 2010

[16] Ibid [17] Ibid

[18] Risse, GB (1988). Fee E, Fox DM, eds. Epidemics and History: Ecological Perspectives. in AIDS: The Burden of History. University of California Press, Berkeley. ISBN 0-520-06396-1.

[19] A Disease of Cleanliness: Polio in New York City, 1900-1990, in David Rosner, ed., Hives of Sickness: Public Health and Epidemics in New York City Rutgers University Press, 1995, pp. 115-130.

[20] McDonough, F., The Origins of the First and Second World Wars (Cambridge Perspectives in History), Cambridge University Press, August 28, 1997.

[21] Goel, A, Aggarwal, P, “Pesticide Poisoning,” Natl Med J India. 2007 Jul-Aug; 20(4):182-91.

[22] Ibid.

[23] Biskind, MS (1953) “Public Health Aspects of the New Insecticides,” American Journal of Digestive Diseases 20: 331-341.

[24] TIME Magazine, U.S. Edition, March 14, 1994 Vol. 143 No. 11. [25] Baily, J. W.: J. Am. Vet. M. A. 113: 251, Sept. 1948.

[26] Biden-Steele, K. and Stuckey, R. E.: “Poisoning by DDT Emulsion: Report of a Fatal Case”, Lancet, 2: 235-236, Aug. 17, 1946.

[27] Biskind, M. S.: “DDT Poisoning and X Disease in Cattle”, J. Am. Vet. M. A. 114: 20, Jan. 1949.

[28] Biskind, M. S.: “DDT Poisoning a Serious Public Health Hazard”, Am. J. Dig. Dis. 16: 73, Feb. 1949.

[29] Biskind, M. S.: “DDT Poisoning and the Elusive ‘Virus X’: A New Cause for Gastro- Enteritis”, Am. J. Dig. Dis. 16: 79, March 1949.

[30] Boyd, C. L.: “A Report on “XX Disease in Texas”, J. Am. Vet. M. A. 113: 463, Nov. 1948.

[31] Cameron, C. R., and Burgess, F.: “The Toxicity of DDT”, Brit. M. J. 1: 865-871, June 23, 1945.

[32] Carte; R. H., Hubanks, P. E., et al: “Effect of Cooking on the DDT Content of Beef”, Science, 107: 347, April 2, 1948.

[33] Case, R. A. M.: Toxic Effects of DDT in Man”, Brit. M. J., 2: 842-845, Dec. 15, 1945.

[34] Council on Pharmacy and Chemistry, A. M. A.: “Health Hazards of Pesticides”, J. A. M. A. 137: 1603, Aug. 28, 1948.

[35] Crescitelli, F., and Gillman, A.: “Electrical Manifestations of Cerebellum and Cerebral Cortex Following DDT Administration to Cats and Monkeys”, Am. J. Physiol., 147: 127- 137, Sept. 1946.

[36] Deederer, C.: “DDT Toxicity”, M.Rec. 161: 216-220, April 1948

[37] Domenici, T. J.: “Hepatitis without Jaundice and without Hepatomegaly”, N. Eng. J. Med. 240: 88, Jan. 20, 1949

[38] Dunn, J. E., Dunn, J. C., and Smith, R. S.: “Skin Sensitising Properties of DDT for 31

Guinea Pig”, Pub. Health Rep. 61: 1614-1620, 1949.

[39] Editorial: Pesticides: “Chemical Contaminants of Foods”, J.A.M.A. 137: 1604, Aug. 28, 1948.

[40] Fitzhugh, O. G., and Nelson, A. A.: “The Chronic Oral Toxicity of DDT”, J. Pharm.acol. and Exper. Therap. 89: 18-30, Jan. 1947.

[41] Gamier, G.: “Treatment of Scabies with DDT”, .Presse Med. 56: 458, June 23, 1948. [42] Garett, ii. M., “Toxicity of DDT for Man”, Alabama St. M. A. J., 17: 74, Aug. 1947.

[43] Globus, J. H.: “DDT Poisoning; Histopathologic Observations on the Central Nervous System in So-Treated Monkeys, Dogs, Cats and Rats”, J. Neuropath. 7: 418-431, Oct. 1948.

[44] Haymaker, W., Ginzler, A. M., and Ferguson, J. L.: “Toxic Effects of Prolonged Ingestion of DDT on Dogs, with Special Reference to Lesions in Brain”, Am. J. M. Sc. 212: 423, Oct. 1946.

[45] Hill, K. R., and Daniiani, C. R.: “Death Following Exposure to DDT, Report of a Case”, New Eng. J. Med., 235: 897-899, Dec. 19, 1946.

[46] Hill, K. 3. and Robinson, G.: “A Fatal Case of DDT Poisoning in a Child, with an Account of Two Accidental Deaths in Dogs”. Brit. M. J. 2: 845-847, Dee. 15, 1945.

[47] Ingle, L.: “Toxicity of Chlordane to White Rats”, J. Econ. Entomol. 40: 264-268, 1947.

[48] Jandorf, B. J;. Sanett, H. P., and Bodansky, Oscar: “Effect of Oral Administration of DDT on Metabolism of Glucose and Pyruvie Acid in Rat Tissues”, J. Pharmaeol. and Exper. Therap. 88: 333-337, Dec. 1946.

[49] Jenkins, D. W.: “A Review of the Insecticide Hexachloro-cyclohexane (‘666’)”, Office of Technical Services, U. S. Dept of Commerce, Washington, D • C., No. PB 4034, Med. Div. Rept. No. 56, Sept. 26, 1945.

[50] Kempe, H. E.: “Progress Report on Benzene Hexachloride for the Destruction of Sheep Scab Mites”, Vet. Med., Feb. 1948, pp. 76-79.

[51] Kirk, H.: Vet. Red. 58: 43, 1946.

[52] Kirk, H.: “DDT in Canine Practice”, Vet. Med. Feb. 1947, PP. 76-78.

[53] Lawhon, G. J., Jr.: “X Disease in South Carolina”, N. Am. Vet. 29: 643, Oct. 1948.

[54] Leider, M.: “Allergenic Eczematous Contact-Type Dermatitis Caused by DDT”, J. Invest. Dermatol. 8: 125-126., March 1947.

[55] Lillie, R. D., Smith, M. I., and Stohlman, E. F.: Pathologic Action of DDT and Certain of its Analogs and Derivatives”, Arch. Path. 43: 127-142, Feb. 1947.

[56] Mackerras, I. M., and West, R. F. K.: “DDT Poisoning in Man”, M. J. Australia, 1: 400-401, March 23, 1946.

[57] Mobbs, J. F.:” Toxicity of Hexaehloroeyclohexane in Scabies, J.A.M.A. 138: 1253, Dec. 25, 1948. Personal Communication.

[58] Morrill, C. C.: “Hyperkeratosi.s or X Disease”, N. Am. Vet. 29: 642, Oct. 1948.

[59] Neal, P. A., Sweeney, T. B., Spicer, S. S., and von Oettingen, W. F.: “The Excretion of DDT in Man, Together with Clinical Observations”, Pub. Health Rep., 61: 403, March 22, 1946.

[60] Neal, P. A., von Oettingen, W. F., Smith, W. W., et al: Toxicology and Potential Dangers of Aerosols, Mists and Dusting Powders Containing DDT”, Pub. Health Rep. Suppl. 177, 1944.

[61] Neal, P. A., von Oettingeu, W. F., Dunn, R. C., and Sharpless, N. E.: “Toxicology and Potential Dangers of Aerosols and Residues from Aerosols Containing 3 Percent of DDT. Second Report, ibid., Suppl. 183, 1945.

[62] Nelson, A. A., Draize, 3. H., Woodard, G., et al: “Histopathological Changes Following Administration of DDT to Several Species of Animals”, U. S. Pub. Health Rep. 59: 1009, Aug. 4, 1944.

[63] Neve, Helen: “Toxic Effects of DDT on a Cat”, Vet. Rec. 58: 43, 1946. Vet. Med., Feb. 1947, p. 78.

[64] Niedelman, M. L.: “Contact Dermatitis Due to DDT”, Occup. Med. 1: 391-395, April 1946.

[65] Radeleff, R. D.: “DDT Spray Outmodes Dipping Vat”, Vet. Med. Oct. 1947, pp. 372- 373.

[66] Radeleff, R. D.: “Chlordane Poisoning: Symptomatology and Pathology, Vet. Med. Aug. 1948, pp. 342-347.

[67] Robinson, J. H.: “Harvest Analysis of DDT Residues”, Food Packer, 29: 50-53, 1948.

[68] Riker, W. F., Jr., Huebner, Virginia, R., Raska, S. B., and Cattell, McKeen: “Studies on DDT, Effects on Oxidative Metabolism”, J. Pharmacol. and, Exper. Therap., 88: 327- 332, Dec. 1946.

[69] Sarrett, H. P., and Jandorf, B. J.: “Effects of Chronic DDT Intoxication in Rats on Lipids and Other Constituents of Liver”, ibid., 91: 340-344, Dec. 1947.

[70] Smith, M. I.: “Accidental Ingestion of DDT, with a Note on its Metabolism in Man”, J.A.M.A., 131: 519-520, Juno 8, 1946.

[71] Smith, M. I., and Stohlnian, E. F.: “Pharmacologic Action of 2, 2 his (p-Chlorophenyl) 1,1,1-Trichloroethane and its Estimation in the Tissues and Body Fluid”, Pub. Health Rep., 59: 984, July 28, 1944.

[72] SmIth, M. I., and Stohlman, E. F.: “Further Studies on the Pharmacologic Action of DDT”, ibid., 60: 289, March 16, 1945.

[73] Smith, N. 3.: “Death Following Accidental Ingestion of DDT”, J.A.M.A., 136: 469- 471, Feb. 14, 1948.

[74] Smith, R. F., Fullmes, O. H., and Messenger, P. S.: “DDT Residues on Alfalfa Hay and Seed Chaff”, J. Econ. Entomol. 41: 755-8, 1948.

[75] Strycker, G. V., and Godfroy, B.: “Dermatitis Resulting from Exposure to DDT”, J. Missouri St. M. A., 43: 384-386, June 1948.

[76] Taylor, E. L.: “Danger of Ununction with DDT”, Lancet, 2: 320, Sept. 8, 1945.

[77] Telford, H. S., and Guthrie, J. E.: “Transmission of the Toxicity of DDT Through the Milk of White Rats and Goats”, Science, 102: 647, Dec. 21, 1945.

[78] Thoungh, TI. C.: “Poisonous Effects of DDT on Humans”, Indian M. Ga:. 81: 432, Oct. 1946.

[79] U. S. Dept. Agriculture, “Bureau of Entomology and Plant Quarantine: Now Insecticides in Grasshopper Control”, Bull. E-722, May 1947. Bull. EC.1, March 1948.

[80] U. S. Dept. Agriculture, Bureau of Entomology and Plant Quarantine: “New Insecticides for Controlling External Parasites of Livestock”, Bull. E. 762, Dec. 1948.

[81] Westerfteld, C.: “The Use of DDT in Medicine-A Review”, Vet. Med., Oct. 1946, pp. 355-360.

[82] Wigglesworth, V. D.: “A Case of DDT Poisoning in Man”, Brit M. J. 1: 517, April 14, 1945.

[83] Wilson, J. B.: Are Pesticides Making Your Food Unsafer? Hygiea, Jan. 1949. p. 44.

[84] Woodard, G., Ofner, Ruth B., and Montgomery, C. M.: “Accumulation of DDT in the Body Fat and its Appearance in the Milk of Dogs”, Science, 102: 177-178, Aug. 17, 1945.

[85] Wright, C. S., Doan, C. A., and Haynie, H. C.: “Agranulocytosis Occurring after Exposure to DDT Pyrethrum Aerosol Bomb”, Am. J. Med., 1: 562-567, Nov. 1946.

[86] The Pesticide Residues Amendment of 1954, Pub. L. No. 83-518, ch. 559, 68 Stat. 511 [codified at 21 USC § 346a (1981)]; and the Food Additives Amendments of 1958, Pub. L. No. 85-529, Ch. 4.72 Stat. 1785 [codified at 21 USC § 348 (1981)], respectively.

[87] 20 Fed. Reg. 750 (1955) [codified until repealed at 21 CFR § 120. 1(f) (1956). [88] DDT Regulatory History: A Brief Survey (to 1975). United States Environmental

Protection Agency (EPA).

[89] Ibid.

[90] TIME Magazine, U.S. Edition, March 14, 1994 Vol. 143 No. 11.

(91] Handbook of Pesticide Toxicology, edited by Wayland J. Hayes, Jr. and Edward R. Laws, Academic Press Inc., Harcourt Brace Jovanovich, Publishers, San Diego, 1991.

[92] Peter Duesberg and Brian J. Ellison, Inventing the AIDS Virus, Regnery Pub.,1996. [93] Ibid.

[94] Biskind, MS (1953) “Public Health Aspects of the New Insecticides,” American Journal of Digestive Diseases 20: 331-341.

[95] Peter Duesberg and Brian J. Ellison, Inventing the AIDS Virus, Regnery Pub.,1996. [96] DDT Regulatory History: A Brief Survey (to 1975). United States Environmental

Protection Agency (EPA).

[97] Poliomyelitis: Fact sheet N°114″. World Health Organization. Sep 2016. Retrieved 14 Sep 2016.

[98] Ibid.

[99] DDT Regulatory History: A Brief Survey (to 1975). United States Environmental

Protection Agency (EPA).

[100] Ibid.

[101] Handbook of Pesticide Toxicology, edited by Wayland J. Hayes, Jr. and Edward R.

Laws, Academic Press Inc., Harcourt Brace Jovanovich, Publishers, San Diego, 1991.

[102] Rea WJ, Johnson AR, Fenyves E, Butler J. Related Articles: The environmental aspects of the post-polio syndrome. Birth Defects Orig Artic Ser. 1987;23(4):173-81. No abstract available. Pub Med ID: 3620615; UI: 87299998.

[103] Ibid.

[104] Casarett and Doull’s Toxicology (1996).

[105) Rea WJ, Johnson AR, Fenyves E, Butler J. Related Articles: The environmental aspects of the post-polio syndrome. Birth Defects Orig Artic Ser. 1987;23(4):173-81. No abstract available. Pub Med ID: 3620615; UI: 87299998.

[106] PubMed ID: 7611631, UI: 95336052 (London, May, 1995)

[107] Pub Med ID: 7611630, UI: 95336051 (Bethesda, MA, May, 1995)

[108] Pub Med ID: 8818905, UI: 96415998 (Lyon, France, Aug., 1996)

[109] Alfredo Morabia (1 January 2004). A History of Epidemiologic Methods and Concepts. Springer. pp. 133–4. ISBN 978-3-7643-6818-0. Retrieved 22 June 2013.

[110] Ibid.

[111] Morton S. Biskind, MD. “Public Health Aspects of the New Insecticides”. American

Journal of Digestive Diseases, New York, 1953, v 20, p331. [112] Ibid.

[113] Young RO (2016) Second Thoughts Concerning Viruses, Vaccines and the HIV/AIDS Hypothesis – Part 2. Int J Vaccines Vaccin 2(3): 00034. DOI: 10.15406/ijvv.2016.02.00034

[114] Dirt and Disease: Polio before FDR Rutgers University Press, 1992. [115] Ibid.

[116] Menkes, John H., Child Neurology, pg. 420, (1995).

[117] A Paralyzing Fear: The Story of Polio in America. Produced by Paul Wagner, Nina Gilden Seavey. Directed, written by Nina Gilden Seavey. Narration written by Stephen Chodorov. With: Narrator: Olympia Dukakis. Camera (Colorlab color), Allen Moore, Reuben Aaronson; editor, Catherine Shields; music, Paul Christianson; associate producers, Tom Wentworth, Malvina Anderson Martin. Reviewed on videocassette, N.Y., March 3, 1998. Running time: 90 min.

[118] FILM REVIEW; Once a Fear Beyond Fear Itself, by STEPHEN HOLDEN, Published: March 4, 1998, New York Times.

[119] Ibid.

[120] Duesberg, Peter and Ellison, Brian J., Inventing the AIDS Virus, Regnery Pub.,1996.

[121] Ibid.

[122] Ibid.

[123] Ibid.

[124] Ibid.

[125] Rose DR (2004). “Fact Sheet—Polio Vaccine Field Trial of 1954.” March of Dimes Archives. (2004).

[126] Ibid.

[127] American Journal of Digestive Diseases, 1953 20:330 [128] Ibid.

[129] Ibid.

[130] Jenkins, D. W.: “A Review of the Insecticide Hexachloro-cyclohexane (‘666’)”, Office of Technical Services, U. S. Department of Commerce, Washington, D.C., No. PB 4034, Med. Div. Rept. No. 56, Sept. 26, 1945.

[131] Biskind, M., “DDT Poisoning and the Elusive ‘Virus X’.” A New Cause for Gastroenteritis.” Am. J. Dig., Vol. 16, Num 3, pg. 79-84, (1949).

[132] Biskind, MS, Bieber, I, “DDT Poisoning A New Syndrome With Neuropsychiatric Manifestations,” American Journal of Psychotherapy, p261, (1949).

[133] Presented before the Select Committee to Investigate the Use of Chemicals in Food Products, United States House of Representatives, U.S. December 12, 1950 Westport, Conn.

[134] “Salk and Sabin: poliomyelitis immunisation”. J Neurol Neurosurg Psychiatry. 75 (11): 1552. doi:10.1136/jnnp.2003.028530. PMC 1738787. PMID 15489385.

[135] H. Rept. No. 2356, 82d Cong., 2d sess. 1 (1952), reprinted in A Legislative History of the Federal Food, Drug and Cosmetic Act and Its Amendments 499 (hereinafter Legislative History)

[136] Scobey, RR, “Is The Public Health Law Responsible For The Poliomyelitis Mystery?” Syracuse, N.Y., Archive of Pediatrics (May, 1951).

[137] White, Mark; Sharon M. McDonnell; Denise H.Werker; Victor M. Cardenas; Stephen B. Thacker (2001). “Partnerships in International Applied Epidemiology Training and Service,”. American Journal of Epidemiology 154 (11): 993–999. doi:10.1093/aje/154.11.993.

[138] Van Nostrand’s Encyclopedia of Science and Engineering, Van Nostrand Reinhold 1995, v 5, p1775

[139] “Salk and Sabin: poliomyelitis immunisation”. J Neurol Neurosurg Psychiatry. 75 (11): 1552. doi:10.1136/jnnp.2003.028530. PMC 1738787. PMID 15489385.

[140] Ralph R. Scobey, MD. “The Poison Cause of Poliomyelitis and Obstructions to Its Investigation.” Archive of Pediatrics, April 1952.

[141] The National Adipose Tissue Survey, reported in Handbook of Pesticide Toxicology, edited by Wayland J. Hayes, Jr. and Edward R. Laws, Academic Press Inc., Harcourt Brace Jovanovich, Publishers, San Diego, 1991, pg. 303.

[142] The National Adipose Tissue Survey, reported in Handbook of Pesticide Toxicology, edited by Wayland J. Hayes, Jr. and Edward R. Laws, Academic Press Inc., Harcourt Brace Jovanovich, Publishers, San Diego, 1991, pg. 303.

[143] Van Nostrand’s Encyclopedia of Science and Engineering (1995), vol. 5, pg.1725. [144] Offit, Paul A. (2007). The Cutter Incident: How America’s First Polio Vaccine Led to

the Growing Vaccine Crisis. Yale University Press. p. 38. ISBN 0-300-12605-0. [145] Albert Sabin to Henry Kumm, Sabin Papers, UC, Pittsburgh Press, 1954. [146] American Journal of Digestive Diseases, 1953 20:330.

[147] Trevelyan, B., Smallman-Raynor, M. and Cliff, A.D., The Spatial Dynamics of Poliomyelitis in the United States: From Epidemic Emergence to Vaccine-Induced Retreat, 1910–1971, Ann Assoc Am Geogr. 2005 Jun; 95(2): 269–293.

[148] Baicus, A., History of Polio Vaccination, World J Virol. 2012 Aug 12; 1(4): 108–114. Published online 2012 Aug 12. doi: 10.5501/wjv.v1.i4.108.

[149] Ibid.

[150] Women’s History Month: “Oveta Culp Hobby” by Senator Kay Bailey Hutchison

Humanities Texas, March 2012.

[151] Harry M. Marks, “The 1954 Salk Poliomyelitis Vaccine Field Trial,” Institute of the History of Medicine, Johns Hopkins University, Baltimore, MD: 2008.

152[ National Museum of American History, “Whatever Happened to Polio?” Time line, http://americanhistory.si.edu/polio/timeline/index.htm (accessed March 28,, 2012).

[153] Abid.

[154] Norrby E., Prusiner S.B., Polio and Nobel Prizes: looking vack 50 years. Ann Neurol.

2007 May;61(5):385-95.

[155] Eloise Batic, You Are There 1955: Ending Polio exhibit text (2012).

[156] Boston Herald newspaper, April 18, 1955, “Drug Companies Expecting Big Profit on

Salk Vaccine”,

[157] Washington Bureau of the Detroit Free Press reports, June 3, 1955.

[158] Michigan University. Poliomyelitis Evaluation Center (1955), An evaluation mof the 1954 poliomyelitis vaccine trials; summary report. Ann Arbor: n.p. , pp. 17-18 as quoted in Marks, Harry M. “The 1954 Salk Poliomyelitis Vaccine Field Trial.” Institute of the History of Medicine, Johns Hopkins University. Baltimore: 2008, p. 20.

[160] McBean E. The Poisoned Needle. Mokelumne Hill, California: Health Research,1957:1

[161] McBean E. The Poisoned Needle. Mokelumne Hill, California: Health Research, 1957:119.

[162] McBean E. The Poisoned Needle. Mokelumne Hill, California: Health Research,1957:1

[163] Offit, Paul A. The Cutter Incident: How America’s First Polio Vaccine Led to the Growing Vaccine Crisis, Yale University Press, 2005, pp. 100, 116–19, 133. ISBN 0-300- 10864-8

[164] Ibid.

[165] Smith, JS, “Patenting the Sun: Polio and the Salk Vaccine,” 1st Edition, William

Morrow & Co; 1st edition (April 1990).

[166] Offit PA (2005), “The Cutter incident, 50 years later” (PDF). N. Engl. J. Med. 352 (14): 1411–1412. doi:10.1056/NEJMp048180. PMID 15814877

[167] McBean E., The Poisoned Needle. Mokelumne Hill, California: Health Research,1957:1.

[168] Harris RJ et al Contaminant viruses in two live vaccines produced in chick cells. J Hyg (London) 1966 Mar:64(1) : 1-7

[169] McBean E. The Poisoned Needle. Mokelumne Hill, California: Health Research,1957:1

[170] Ibid.

[171] Ibid.

[172] Ibid.

[173] Ii. Results. American journal of public health and the nation’s health. 1955;45:15–48. [PMC free article] [PubMed]

[174] Harper’s Magazine. “’Who is responsible, and why, for the chaotic confusion over the polio inoculations?’ A noted medical journalist disentangles the essential facts.” August, 1955.

[175] Ibid.

[176] Ibid.

[177] American Cancer Society, Volume 8, Issue 1, Pages 1–218, (1955).

[178] Paul JR. A history of poliomyelitis. New Haven, CT: Yale University Press; 1971.

[179] Ibid.

[180] Ibid.

[181] Ibid.

[182] Rogers N. Dirt and disease: Polio before fdr. New Brunswick, NJ: Rutgers University Press; 1992.

[183] Ibid.

[184] Smith, Derek R; Leggat Peter A (2005). “Pioneering figures in medicine: Albert Bruce Sabin–inventor of the oral polio vaccine”. The Kurume medical journal. 52 (3): 111–6. doi:10.2739/kurumemedj.52.111. PMID 16422178

[185] Rose, David, March of Dimes Archives, August 26, 2010. http://www.marchofdimes.org/mission/a-history-of-the-march-of-dimes.aspx

[186] American Journal of Public Health and the Nations Health: May 1956, Vol. 46, No. 5: 547–562. Citation | PDF (2177 KB) | PDF Plus (744 KB)

[187]

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[189] O’Hern M. Profiles: Pioneer Women Scientists. Bethesda, MD: National Institutes of Health.

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[191] Sweet BH, Hilleman MR. The Vacuolating Virus: SV-40. As cited in The polio vaccine and simian virus 40 by Moriarty, T.J. http://www.chronicillnet.org/online/bensweet.html

[192] Moriarty T.J. The polio vaccine and simian virus 40. Online News Index.

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[196] Innis MD. Oncogenesis and poliomyelitis vaccine. Nature, 1968;219:972–3. [197] Soriano F, et al. Simian virus 40 in a human cancer. Nature, 1974; 249:421–4.

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[200] Stoian M, et al. Possible relation between viruses and oromaxillofacial tumors. II. Research on the presence of SV40 antigen and specific antibodies in patients with oromaxillofacial tumors. Virologie, 1987;38:35–40.

[201] Stoian M, et al. Possible relation between viruses and oromaxillofacial tumors. II. Detection of SV40 antigen and of anti-SV40 antibodies in patients with parotid gland tumors. Virologie, 1987;38:41–6.

[202] Bravo MP, et al. Association between the occurrence of antibodies to simian vacuolating virus 40 and bladder cancer in male smokers. Neoplasma, 1988;35:285–8.

[203] O’Connell K, et al. Endothelial cells transformed by SV40 T-antigen causeKaposi’s sarcoma-like tumors in nude mice. American Journal of Pathology, 1991;139(4):743–9.

[204] Weiner LP, et al. Isolation of virus related to SV40 from patients with progressive multifocal leukoencephalopathy. New England Journal of Medicine, 1972;286:385–90.

[205] Tabuchi K. Screening of human brain tumors for SV-40-related T-antigen. International Journal of Cancer 1978;21:12–7.

[206] Meinke W, et al. Simian virus 40-related DNA sequences in a human brain tumor. Neurology 1979;29:1590–4.

[207] Krieg P, et al. Episomal simian virus 40 genomes in human brain tumors. Proceedings of the National Academy of Science 1981; 78:6446-50.

[208] Krieg P, et al. Cloning of SV40 genomes from human brain tumors. Virology 1984;138:336–40.

[209] Geissler E. SV40 in human intracranial tumors: passenger virus or oncogenic >hit- and-run= agent? Z Klin Med, 1986;41:493–5.

[210] Geissler E. SV40 and human brain tumors. Progress in Medical Virology, 1990;37:211–22.

[211] Bergsagel DJ, et al. DNA sequences similar to those of simian virus 40 in ependymomas and choroid plexus tumors of childhood. New England Journal of Medicine, 1992;326:988–93.

[212] Martini, M., et al. Human brain tumors and simian virus 40. Journal of the National Cancer Institute, 1995;87(17):1331.

[213] Lednicky JA, et al. Natural Simian Virus 40 Strains are Present in Human Choroid Plexus and Ependymoma Tumors. Virology, 1995;212(2):710–7.

[214] Tognon M, et al. Large T Antigen Coding Sequence of Two DNA Tumor Viruses, BK and SV-40, and Nonrandom Chromosome Changes in Two Gioblastoma Cell Lines. Cancer Genetics and Cytogenics, 1996;90(1): 17–23.

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[216] Carbone, M., et al. SV-40 Like Sequences in Human Bone Tumors. Oncogene, 1996;13(3):527–35.

[217] Pass, HI, Carbone, M., et al. Evidence For and Implications of SV-40 Like Sequences in Human Mesotheliomas. Important Advances in Oncology, 1996:89-108.

[218] Rock, Andrea. The Lethal Dangers of the Billion Dollar Vaccine Business, Money, December 1996:161.

[219] Carlsen, W. Rogue virus in the vaccine: Early polio vaccine harbored virus now feared to cause cancer in humans. San Francisco Chronicle, July 15,2001:7. Research by Susan Fisher, epidemiologist, Loyola UniversityMedical Center.

[220] National Institutes of Health. Zones of Contamination: Globe Staff Graphic.

[221] Bookchin D, Schumacher J. Tainted polio vaccine still carries its threat 40 years later. The Boston Globe, January 26, 1997.

[222] SV-40 Contamination of Polio Vaccine. Well Within Online, (February 3,2001, updated). http://www.nccn.net/~wwithin/polio.htm

[223] Rosa FW, et al. Absence of antibody response to simian virus 40 afterinoculation with killed-poliovirus vaccine of mothers offspring with neurological tumors. New England Journal of Medicine, 1988;318:1469.

[224] Rosa FW, et al. Response to: Neurological tumors in offspring after inoculation of mothers with killed poliovirus vaccine. New England Journal of Medicine, 1988, 319:1226.

[225] Martini F, et al. SV-40 Early Region and Large T Antigen in Human Brain Tumors, Peripheral Blood Cells, and Sperm Fluids from Healthy Individuals. Cancer Research, 1996;56(20):4820–5.

[226] Fisher, Barbara. Vaccine safety consumer group cites conflict of interest in government report on cancer and contaminated polio vaccine link. National Vaccine Information Center (NVIC); Press Release, January 27, 1998.

[227] National Cancer Institute (June 2001).

[228] The Landsteiner and Popper study, first published in Germany, was reported in Robert W Lovett, MD. The Occurrence of Infantile Paralysis in Massachusetts in 1908. Boston Medical and Surgical Journal, pg. 112, July 22, 1909.

[229] Young, RO (2016) Second Thoughts about Viruses, Vaccines, and the HIV/AIDS Hypothesis – Part 1. Int J Vaccines Vaccin 2(3): 00032. DOI: 10.15406/ijvv.2016.02.00032

[230] Young, RO (2016) Second Thoughts Concerning Viruses, Vaccines and the HIV/AIDS Hypothesis – Part 2. Int J Vaccines Vaccin 2(3): 00034. DOI: 10.15406/ijvv.2016.02.00034

[231] Young RO (2016) Second Thoughts Concerning Viruses, Vaccines and the HIV/AIDS Hypothesis – Part 3 HIV/AIDS and the Monomorphic Disease Model. Int J Vaccines Vaccin 2(3): 00035. DOI: 10.15406/ijvv.2016.02.00035

[232] Young RO (2016) Who Had Their Finger on the Magic of Life – Antoine Bechamp or Louis Pasteur?. Int J Vaccines Vaccin 2(5): 00047. DOI: 10.15406/ijvv.2016.02.00047

[233] Peter Duesberg and Brian J. Ellison, Inventing the AIDS Virus, Regnery Pub., 1996. [234] Gerald L. Geison, The Private Science Of Louis Pasteur, Princeton University Press, 1995.

[235] The Landsteiner and Popper study, first published in Germany, was reported in Robert W Lovett, MD. The Occurrence of Infantile Paralysis in Massachusetts in 1908. Boston Medical and Surgical Journal, pg. 112, July 22, 1909.

[236] Shaw D. Unintended casualties in war on polio. Philadelphia Inquirer June 6, 1993:A1.

[237] Moriarty T.J. The polio vaccine and simian virus 40. Online News Index. http://www.chronicillnet.org/online/bensweet.html

[238] Koprowksi H. Tin anniversary of the development of live virus vaccine. Journal of the American Medical Association 1960;174:972–6.

[239] Hayflick L, Koprowski H, et al. Preparation of poliovirus vaccines in a human fetal diploid cell strain. American J Hyg 1962;75:240–58.

[240] Hayflick L, Koprowski H, et al. Preparation of poliovirus vaccines in a human fetal diploid cell strain. American J Hyg 1962;75:240–58.

[241] Koprowski H. In a letter sent to the Congressional Health and Safety Subcommittee, April 14, 1961.

[242] Rock, Andrea. The Lethal Dangers of the Billion Dollar Vaccine Business, Money, December 1996:161.

[243] Scheibner V. Vaccination: 100 Years of Orthodox Research Shows that Vaccines represent a Medical Assault on the Immune System. Blackheath, NSW, Australia: Scheibner Publications, 1993153.

[244] Curtis T. Expert says test vaccine: backs check of polio stocks for AIDS virus. The Houston Post, March 22, 1992:A-21.

[245] Carlsen, W. Rogue virus in the vaccine: Early polio vaccine harbored virus now feared to cause cancer in humans. San Francisco Chronicle, July 15,2001:7. Research by Susan Fisher, epidemiologist, Loyola UniversityMedical Center.

[246] Neustaedter R. The Vaccine Guide. Berkeley, California: North Atlantic Books, 1996:107–8

[247] Curtis T. Expert says test vaccine: backs check of polio stocks for AIDS virus. The Houston Post, March 22, 1992:A-21.

[248] Essex M, et al. The origin of the AIDS virus. Scientific American, 1988; 259:64–71. [249] Karpas A. Origin and Spread of AIDS. Nature, 1990; 348:578.

[250] Kyle WS. Simian retroviruses, poliovaccine, and origin of AIDS. Lancet, 1992; 339:600–1.

[251] Elswood BF, Stricker RB. Polio vaccines and the origin of AIDS. Medical Hypothesis, 1994:42:347–54.

[252] Myers G, et al. The emergence of simian/human immunodeficiency viruses. AIDS Res Human Retro 1992:8:373–86.

[253] Curtis T. The origin of AIDS: A startling new theory attempts to answer the question “Was it an act of God or an act of man”, Rolling Stone, March 19,1992:57.

[254] O’Hern M. Profiles: Pioneer Women Scientists. Bethesda, MD: National Institutes of Health.

[255] Curtis T. Expert says test vaccine: backs check of polio stocks for AIDS virus. The Houston Post, March 22, 1992:A-21.

[256] Curtis T. Expert says test vaccine: backs check of polio stocks for AIDS virus. The Houston Post, March 22, 1992:A-21.

[257] Essex M, et al. The origin of the AIDS virus. Scientific American, 1988; 259:64–71. [258] Karpas A. Origin and Spread of AIDS. Nature, 1990; 348:578.

[259] Kyle WS. Simian retroviruses, poliovaccine, and origin of AIDS. Lancet, 1992; 339:600–1.

[260] Elswood BF, Stricker RB. Polio vaccines and the origin of AIDS. Medical Hypothesis, 1994:42:347–54.

[261] Workshop on Simian Virus-40 (SV-40): A Possible Human Polyomavirus. National Vaccine Information Center, January 27-28, 1997. http://www.909shot.com/polio197.htm (Includes a summary of evidence presented at the Eighth Annual Houston Conference on AIDS.)

[262] Martin B. Polio vaccines and the origin of AIDS: The career of a threatening idea. Townsend Letter for Doctors, January 1994:97–100.

[263] Curtis T. Did a polio vaccine experiment unleash AIDS in Africa? The Washington Post, April 5, 1992:C3+.

[264] Myers G, et al. The emergence of simian/human immunodeficiency viruses. AIDS Res Human Retro 1992:8:373–86.

[265] World Health Organization. T-lymphotropic retroviruses of nonhuman primates. WHO informal meeting. Weekly Epidemiology Records, 1985; 30:269–70.

[266] Ibid.

[267] Elswood BF, Stricker RB. Polio vaccines and the origin of AIDS. Medical

Hypothesis, 1994:42:347–54.

[268] Ohta Y, et al. No evidence for the contamination of live oral poliomyelitis vaccines with simian immunodeficiency virus. AIDS, 1989; 3:183–5.

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[271] Sabin AB. Properties and behavior of orally administered attenuated poliovirus vaccine. Journal of the American Medical Association, 1957; 164:1216–23.

[272] Siehe Ausführungen zu Virchows Leben und Wirkung in WissenschafftPlus Nr. 5/2015 und Nr. 6/2015. 2 Anticontagionism between 1821 and 1867.

[273] Aufsatz von Erwin H. Ackerknecht in der Zeitschrift Bulletin of the History of Medicine, Volume XXII, The Johns Hopkins Press, 1948.

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[276] Lund GA, Tyrell, DL, Bradley RD, Scraba DG. The molecular length of measles virus RNA and the structural organization of measles nucleocapsids. J. Gen. Virol. 1984 Sep;65 (Pt 9): 1535–42.

[277] Daikoku E, Morita C, Kohno T, Sano K. Analysis of Morphology and Infectivity of Measles Virus Particles. Bulletin of the Osaka Medical College. 2007; 53 (2): 107–14.

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[279] Siehe WissenschafftPlus Nr. 1/2014.

[280] Zur Geschichte der frühen Virusforschung. Übersichtsarbeit von Prof. Karlheinz Lüdtke. Reprint 125 des MAX-PLANCK-INSTITUT FÜR WISSENSCHAFTSGESCHICHTE, 89 Seiten, 1999.

Cancer is a Preventable and Treatable Disease that Requires Major Lifestyle Changes!

“The cure for cancer is NOT found in its treatment but is found in its prevention”  –  Dr. Robert O. Young

Ninety-five-percent (95%) of ALL sickness and diseases are caused by what you eat, what you drink, what you breath and what you think.  Only five-percent (5%) of ALL sickness and diseases are caused by genetics.  The five-percent (5%) of All genetic factors are triggered by the epi-genetics or the alkaline environment of interstitial fluids determined by what you eat, what you drink, what you breath, and what you thing,  Therefore, one-hundred-percent (100%) is caused by what you eat, what you drink, what you breath and what you think.
(Sympathetic Resonance Technology, Scientific Foundations and Summary of Biologic and Clinical Studies, Dec. 2002, Vol. 8, No. 6: 835-842, Alkalizing Nutritional Therapy, medcraveonline.com/IJCAM/IJCAM-02-00046.php Robert O Young and Galina Migalko. Universal Medical Imaging Group, Medical doctor, non-invasive medical diagnostics, USA)

Abstract

This year, more than 1.5 million Americans and more than 18 million people worldwide are expected to be diagnosed with cancer, a disease commonly believed to be preventable. Only 5–10% of all cancer cases can be attributed to genetic defects, whereas the remaining 90–95% have their roots in the environment and lifestyle. The lifestyle factors include cigarette smoking, diet (fried foods, red meat), alcohol, sun exposure, environmental pollutants, infections, stress, obesity, and physical inactivity. The evidence indicates that of all cancer-related deaths, almost 25–30% are due to tobacco, as many as 30–35% are linked to diet, about 15–20% are due to infections, and the remaining percentage are due to other factors like radiation, stress, physical activity, environmental pollutants etc. Therefore, cancer prevention requires smoking cessation, increased ingestion of fruits and vegetables, moderate use of alcohol, caloric restriction, exercise, avoidance of direct exposure to sunlight, minimal meat consumption, use of whole grains, use of vaccinations, and regular check-ups. In this review, we present evidence that inflammation is the link between the agents/factors that cause cancer and the agents that prevent it. In addition, we provide evidence that cancer is a preventable disease that requires major lifestyle changes.

INTRODUCTION

After sequencing his own genome, pioneer genomic researcher Craig Venter remarked at a leadership for the twenty-first century conference, “Human biology is actually far more complicated than we imagine. Everybody talks about the genes that they received from their mother and father, for this trait or the other. But in reality, those genes have very little impact on life outcomes. Our biology is way too complicated for that and deals with hundreds of thousands of independent factors. Genes are absolutely not our fate. They can give us useful information about the increased risk of a disease, but in most cases they will not determine the actual cause of the disease, or the actual incidence of somebody getting it. Most biology will come from the complex interaction of all the proteins and cells working with environmental factors, not driven directly by the genetic code” (http://indiatoday.digitaltoday.in/index.php?

This statement is very important because looking to the human genome for solutions to most chronic illnesses, including the diagnosis, prevention, and treatment of cancer, is overemphasized in today’s world. Observational studies, however, have indicated that as we migrate from one country to another, our chances of being diagnosed with most chronic illnesses are determined not by the country we come from but by the country we migrate to (1–4). In addition, studies with identical twins have suggested that genes are not the source of most chronic illnesses. For instance, the concordance between identical twins for breast cancer was found to be only 20% (5). Instead of our genes, our lifestyle and environment account for 90–95% of our most chronic illnesses.

Cancer continues to be a worldwide killer, despite the enormous amount of research and rapid developments seen during the past decade. According to recent statistics, cancer accounts for about 23% of the total deaths in the USA and is the second most common cause of death after heart disease (6). Death rates for heart disease, however, have been steeply decreasing in both older and younger populations in the USA from 1975 through 2002. In contrast, no appreciable differences in death rates for cancer have been observed in the United States (6).

By 2020, the world population is expected to have increased to 7.5 billion; of this number, approximately 15 million new cancer cases will be diagnosed, and 12 million cancer patients will die (7). These trends of cancer incidence and death rates again remind us of Dr. John Bailer’s May 1985 judgment of the US national cancer program as a “qualified failure,” a judgment made 14 years after President Nixon’s official declaration of the “War on Cancer.” Even after an additional quarter century of extensive research, researchers are still trying to determine whether cancer is preventable and are asking “If it is preventable, why are we losing the war on cancer?” In this review, we attempt to answer this question by analyzing the potential risk factors of cancer and explore our options for modulating these risk factors.

Cancer is caused by both internal factors (such as inherited mutations, hormones, and immune conditions) and environmental/acquired factors (such as tobacco, diet, radiation, and infectious organisms; Fig. 1). The link between diet and cancer is revealed by the large variation in rates of specific cancers in various countries and by the observed changes in the incidence of cancer in migrating. For example, Asians have been shown to have a 25 times lower incidence of prostate cancer and a ten times lower incidence of breast cancer than do residents of Western countries, and the rates for these cancers increase substantially after Asians migrate to the West (http://www.dietandcancerreportorg/?p=ER).

Fig 1

The role of genes and environment in the development of cancer. A The percentage contribution of genetic and environmental factors to cancer. The contribution of genetic factors and environmental factors towards cancer risk is 5–10% and 90–95% respectively. B Family risk ratios for selected cancers. The numbers represent familial risk ratios, defined as the risk to a given type of relative of an affected individual divided by the population prevalence. The data shown here is taken from a study conducted in Utah to determine the frequency of cancer in the first-degree relatives (parents + siblings + offspring). The familial risk ratios were assessed as the ratio of the observed number of cancer cases among the first degree relatives divided by the expected number derived from the control relatives, based on the years of birth (cohort) of the case relatives. In essence, this provides an age-adjusted risk ratio to first-degree relatives of cases compared with the general population.

C Percentage contribution of each environmental factor. The percentages represented here indicate the attributable-fraction of cancer deaths due to the specified environmental risk factor.

The importance of lifestyle factors in the development of cancer was also shown in studies of monozygotic twins (8). Only 5–10% of all cancers are due to an inherited gene defect. Various cancers that have been linked to genetic defects are shown in Fig. 2. Although all cancers are a result of multiple mutations (9, 10), these mutations are due to interaction with the environment (11, 12).

 Fig. 2

Genes associated with risk of different cancers

These observations indicate that most cancers are not of hereditary origin and that lifestyle factors, such as dietary habits, smoking, alcohol consumption, and infections, have a profound influence on their development (13). Although the hereditary factors cannot be modified, the lifestyle and environmental factors are potentially modifiable. The lesser hereditary influence of cancer and the modifiable nature of the environmental factors point to the preventability of cancer. The important lifestyle factors that affect the incidence and mortality of cancer include tobacco, alcohol, diet, obesity, infectious agents, environmental pollutants, and radiation.

RISK FACTORS OF CANCER

Tobacco

Smoking was identified in 1964 as the primary cause of lung cancer in the US Surgeon General’s Advisory Commission Report (http://profiles.nlm.nih.gov/NN/Views/AlphaChron/date/10006/05/01/2008), and ever since, efforts have been ongoing to reduce tobacco use. Tobacco use increases the risk of developing at least 14 types of cancer (Fig. 3). In addition, it accounts for about 25–30% of all deaths from cancer and 87% of deaths from lung cancer. Compared with nonsmokers, male smokers are 23 times and female smokers 17 times more likely to develop lung cancer.

(http://www.cancer.org/docroot/STT/content/STT_1x_Cancer_Facts_and_Figures_2008.asp accessed on 05/01/2008).

The carcinogenic effects of active smoking are well documented; the U. S. Environmental Protection Agency, for example, in 1993 classified environmental tobacco smoke (from passive smoking) as a known (Group A) human lung carcinogen.

(http://cfpub2.epa.gov/ncea/cfm/recordisplay.cfm?deid=2835 accessed on 05/01/2008).

Tobacco contains at least 50 carcinogens. For example, one tobacco metabolite, benzopyrenediol epoxide, has a direct etiologic association with lung cancer (14). Among all developed countries considered in total, the prevalence of smoking has been slowly declining; however, in the developing countries where 85% of the world’s population resides, the prevalence of smoking is increasing. According to studies of recent trends in tobacco usage, developing countries will consume 71% of the world’s tobacco by 2010, with 80% increased usage projected for East Asia.

(http://www.fao.org/DOCREP/006/Y4956E/Y4956E00.HTM accessed on 01/11/08)

The use of accelerated tobacco-control programs, with an emphasis in areas where usage is increasing, will be the only way to reduce the rates of tobacco-related cancer mortality.

 Fig. 3

Cancers that have been linked to alcohol and smoking

Percentages represent the cancer mortality attributable to alcohol and smoking in men and women as reported by Irigaray et al. (see 13).

How smoking contributes to cancer is not fully understood. We do know that smoking can alter a large number of cell-signaling pathways. Results from studies in our group have established a link between cigarette smoke and inflammation. Specifically, we showed that tobacco smoke can induce activation of NF-κB, an inflammatory marker (15,16). Thus, anti-inflammatory agents that can suppress NF-κB activation may have potential applications against cigarette smoke.

We also showed that curcumin, derived from the dietary spice turmeric, can block the NF-κB induced by cigarette smoke (15). In addition to curcumin, we discovered that several natural phytochemicals also inhibit the NF-κB induced by various carcinogens (17). Thus, the carcinogenic effects of tobacco appear to be reduced by these dietary agents. A more detailed discussion of dietary agents that can block inflammation and thereby provide chemopreventive effects is presented in the following section.

Alcohol

The first report of the association between alcohol and an increased risk of esophageal cancer was published in 1910 (18). Since then, a number of studies have revealed that chronic alcohol consumption is a risk factor for cancers of the upper aerodigestive tract, including cancers of the oral cavity, pharynx, hypopharynx, larynx, and esophagus (18–21), as well as for cancers of the liver, pancreas, mouth, and breast (Fig. 3). Williams and Horn (22), for example, reported an increased risk of breast cancer due to alcohol. In addition, a collaborative group who studied hormonal factors in breast cancer published their findings from a reanalysis of more than 80% of individual epidemiological studies that had been conducted worldwide on the association between alcohol and breast cancer risk in women. Their analysis showed a 7.1% increase in relative risk of breast cancer for each additional 10 g/day intake of alcohol (23). In another study, Longnecker et al., (24) showed that 4% of all newly diagnosed cases of breast cancer in the USA are due to alcohol use. In addition to it being a risk factor for breast cancer, heavy intake of alcohol (more than 50–70 g/day) is a well-established risk factor for liver (25) and colorectal (26,27) cancers.

There is also evidence of a synergistic effect between heavy alcohol ingestion and hepatitis C virus (HCV) or hepatitis B virus (HBV), which presumably increases the risk of hepatocellular carcinoma (HCC) by more actively promoting cirrhosis. For example, Donato et al. (28) reported that among alcohol drinkers, HCC risk increased linearly with a daily intake of more than 60 g. However, with the concomitant presence of HCV infection, the risk of HCC was two times greater than that observed with alcohol use alone (i.e., a positive synergistic effect). The relationship between alcohol and inflammation has also been well established, especially in terms of alcohol-induced inflammation of the liver.

How alcohol contributes to carcinogenesis is not fully understood but ethanol may play a role. Study findings suggest that ethanol is not a carcinogen but is a cocarcinogen (29). Specifically, when ethanol is metabolized, acetaldehyde and free radicals are generated; free radicals are believed to be predominantly responsible for alcohol-associated carcinogenesis through their binding to DNA and proteins, which destroys folate and results in secondary hyperproliferation. Other mechanisms by which alcohol stimulates carcinogenesis include the induction of cytochrome P-4502E1, which is associated with enhanced production of free radicals and enhanced activation of various procarcinogens present in alcoholic beverages; a change in metabolism and in the distribution of carcinogens, in association with tobacco smoke and diet; alterations in cell-cycle behavior such as cell-cycle duration leading to hyperproliferation; nutritional deficiencies, for example, of methyl, vitamin E, folate, pyridoxal phosphate, zinc, and selenium; and alterations of the immune system. Tissue injury, such as that occurring with cirrhosis of the liver, is a major prerequisite to HCC. In addition, alcohol can activate the NF-κB proinflammatory pathway (30), which can also contribute to tumorigenesis (31). Furthermore, it has been shown that benzopyrene, a cigarette smoke carcinogen, can penetrate the esophagus when combined with ethanol (32). Thus anti-inflammatory agents may be effective for the treatment of alcohol-induced toxicity.

In the upper aerodigestive tract, 25–68% of cancers are attributable to alcohol, and up to 80% of these tumors can be prevented by abstaining from alcohol and smoking (33). Globally, the attributable fraction of cancer deaths due to alcohol drinking is reported to be 3.5% (34). The number of deaths from cancers known to be related to alcohol consumption in the USA could be as low as 6% (as in Utah) or as high as 28% (as in Puerto Rico). These numbers vary from country to country, and in France have approached 20% in males (18).

Diet

In 1981, Doll and Peto (21) estimated that approximately 30–35% of cancer deaths in the USA were linked to diet (Fig. 4). The extent to which diet contributes to cancer deaths varies a great deal, according to the type of cancer (35). For example, diet is linked to cancer deaths in as many as 70% of colorectal cancer cases. How diet contributes to cancer is not fully understood. Most carcinogens that are ingested, such as nitrates, nitrosamines, pesticides, and dioxins, come from food or food additives or from cooking.

 Fig. 4

Cancer deaths (%) linked to diet as reported by Willett (see 35)

Heavy consumption of red meat is a risk factor for several cancers, especially for those of the gastrointestinal tract, but also for colorectal (36–38), prostate (39), bladder (40), breast (41), gastric (42), pancreatic, and oral (43) cancers. Although a study by Dosil-Diaz et al., (44) showed that meat consumption reduced the risk of lung cancer, such consumption is commonly regarded as a risk for cancer for the following reasons. The heterocyclic amines produced during the cooking of meat are carcinogens. Charcoal cooking and/or smoke curing of meat produces harmful carbon compounds such as pyrolysates and amino acids, which have a strong cancerous effect. For instance, PhIP (2-amino-1-methyl-6-phenyl-imidazo[4,5-b]pyridine) is the most abundant mutagen by mass in cooked beef and is responsible for ~20% of the total mutagenicity found in fried beef. Daily intake of PhIP among Americans is estimated to be 280–460 ng/day per person (45).

Nitrites and nitrates are used in meat because they bind to myoglobin, inhibiting botulinum exotoxin production; however, they are powerful carcinogens (46). Long-term exposure to food additives such as nitrite preservatives and azo dyes has been associated with the induction of carcinogenesis (47). Furthermore, bisphenol from plastic food containers can migrate into food and may increase the risk of breast (48) and prostate (49) cancers. Ingestion of arsenic may increase the risk of bladder, kidney, liver, and lung cancers (50). Saturated fatty acids, trans fatty acids, and refined sugars and flour present in most foods have also been associated with various cancers. Several food carcinogens have been shown to activate inflammatory pathways.

Obesity

According to an American Cancer Society study (51), obesity has been associated with increased mortality from cancers of the colon, breast (in postmenopausal women), endometrium, kidneys (renal cell), esophagus (adenocarcinoma), gastric cardia, pancreas, prostate, gallbladder, and liver (Fig. 5). Findings from this study suggest that of all deaths from cancer in the United States, 14% in men and 20% in women are attributable to excess weight or obesity. Increased modernization and a Westernized diet and lifestyle have been associated with an increased prevalence of overweight people in many developing countries (52).

 Fig. 5

Various cancers that have been linked to obesity. In the USA overweight and obesity could account for 14% of all deaths from cancer in men and 20% of those in women (see 51).

Studies have shown that the common denominators between obesity and cancer include neurochemicals; hormones such as insulinlike growth factor 1 (IGF-1), insulin, leptin; sex steroids; adiposity; insulin resistance; and inflammation (53).

Involvement of signaling pathways such as the IGF/insulin/Akt signaling pathway, the leptin/JAK/STAT pathway, and other inflammatory cascades have also been linked with both obesity and cancer (53). For instance, hyperglycemia, has been shown to activate NF-κB (54), which could link obesity with cancer. Also known to activate NF-κB are several cytokines produced by adipocytes, such as leptin, tumor necrosis factor (TNF), and interleukin-1 (IL-1) (55). Energy balance and carcinogenesis has been closely linked (53). However, whether inhibitors of these signaling cascades can reduce obesity-related cancer risk remains unanswered. Because of the involvement of multiple signaling pathways, a potential multi-targeting agent will likely be needed to reduce obesity-related cancer risk.

Infectious Agents

Worldwide, an estimated 17.8% of neoplasms are associated with infections; this percentage ranges from less than 10% in high-income countries to 25% in African countries (56, 57). Viruses account for most infection-caused cancers (Fig. 6). Human papillomavirus, Epstein Barr virus, Kaposi’s sarcoma-associated herpes virus, human T-lymphotropic virus 1, HIV, HBV, and HCV are associated with risks for cervical cancer, anogenital cancer, skin cancer, nasopharyngeal cancer, Burkitt’s lymphoma, Hodgkin’s lymphoma, Kaposi’s sarcoma, adult T-cell leukemia, B-cell lymphoma, and liver cancer.

Fig. 6

Various cancers that have been linked to infection. The estimated total of infection attributable cancer in the year 2002 is 17.8% of the global cancer burden. The infectious agents associated with each type of cancer is shown in the bracket. HPV Human papilloma virus, HTLV human T-cell leukemia virus, HIV human immunodeficiency virus, EBV Epstein–Barr virus (see 57).

In Western developed countries, human papillomavirus and HBV are the most frequently encountered oncogenic DNA viruses. Human papillomavirus is directly mutagenic by inducing the viral genes E6 and E7 (58), whereas HBV is believed to be indirectly mutagenic by generating reactive oxygen species through chronic inflammation (59–61). Human T-lymphotropic virus is directly mutagenic, whereas HCV (like HBV) is believed to produce oxidative stress in infected cells and thus to act indirectly through chronic inflammation (62, 63). However, other microorganisms, including selected parasites such as Opisthorchis viverrini or Schistosoma haematobium and bacteria such as Helicobacter pylori, may also be involved, acting as cofactors and/or carcinogens (64).

The mechanisms by which infectious agents promote cancer are becoming increasingly evident. Infection-related inflammation is the major risk factor for cancer, and almost all viruses linked to cancer have been shown to activate the inflammatory marker, NF-κB (65). Similarly, components of Helicobacter pylorihave been shown to activate NF-κB (66). Thus, agents that can block chronic inflammation should be effective in treating these conditions.

Environmental Pollution

Environmental pollution has been linked to various cancers (Fig. 7). It includes outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons (PAHs); indoor air pollution by environmental tobacco smoke, formaldehyde, and volatile organic compounds such as benzene and 1,3-butadiene (which may particularly affect children); food pollution by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins, and other organochlorines; carcinogenic metals and metalloids; pharmaceutical medicines; and cosmetics (64).

Fig. 7

Various cancers that have been linked to environmental carcinogens. The carcinogens linked to each cancer is shown inside bracket. (see 64).

Numerous outdoor air pollutants such as PAHs increase the risk of cancers, especially lung cancer. PAHs can adhere to fine carbon particles in the atmosphere and thus penetrate our bodies primarily through breathing. Long-term exposure to PAH-containing air in polluted cities was found to increase the risk of lung cancer deaths. Aside from PAHs and other fine carbon particles, another environmental pollutant, nitric oxide, was found to increase the risk of lung cancer in a European population of nonsmokers. Other studies have shown that nitric oxide can induce lung cancer and promote metastasis. The increased risk of childhood leukemia associated with exposure to motor vehicle exhaust was also reported (64).

Indoor air pollutants such as volatile organic compounds and pesticides increase the risk of childhood leukemia and lymphoma, and children as well as adults exposed to pesticides have increased risk of brain tumors, Wilm’s tumors, Ewing’s sarcoma, and germ cell tumors. In utero exposure to environmental organic pollutants was found to increase the risk for testicular cancer. In addition, dioxan, an environmental pollutant from incinerators, was found to increase the risk of sarcoma and lymphoma.

Long-term exposure to chlorinated drinking water has been associated with increased risk of cancer. Nitrates, in drinking water, can transform to mutagenic N-nitroso compounds, which increase the risk of lymphoma, leukemia, colorectal cancer, and bladder cancer (64).

Radiation

Up to 10% of total cancer cases may be induced by radiation (64), both ionizing and non-ionizing, typically from radioactive substances and ultraviolet (UV), pulsed electromagnetic fields. Cancers induced by radiation include some types of leukemia, lymphoma, thyroid cancers, skin cancers, sarcomas, lung and breast carcinomas. One of the best examples of increased risk of cancer after exposure to radiation is the increased incidence of total malignancies observed in Sweden after exposure to radioactive fallout from the Chernobyl nuclear power plant. Radon and radon decay products in the home and/or at workplaces (such as mines) are the most common sources of exposure to ionizing radiation. The presence of radioactive nuclei from radon, radium, and uranium was found to increase the risk of gastric cancer in rats. Another source of radiation exposure is x-rays used in medical settings for diagnostic or therapeutic purposes. In fact, the risk of breast cancer from x-rays is highest among girls exposed to chest irradiation at puberty, a time of intense breast development. Other factors associated with radiation-induced cancers in humans are patient age and physiological state, synergistic interactions between radiation and carcinogens, and genetic susceptibility toward radiation.

Non-ionizing radiation derived primarily from sunlight includes UV rays, which are carcinogenic to humans. Exposure to UV radiation is a major risk for various types of skin cancers including basal cell carcinoma, squamous cell carcinoma, and melanoma. Along with UV exposure from sunlight, UV exposure from sun beds for cosmetic tanning may account for the growing incidence of melanoma. Depletion of the ozone layer in the stratosphere can augment the dose-intensity of UVB and UVC, which can further increase the incidence of skin cancer.

Low-frequency electromagnetic fields can cause clastogenic DNA damage. The sources of electromagnetic field exposure are high-voltage power lines, transformers, electric train engines, and more generally, all types of electrical equipments. An increased risk of cancers such as childhood leukemia, brain tumors and breast cancer has been attributed to electromagnetic field exposure. For instance, children living within 200 m of high-voltage power lines have a relative risk of leukemia of 69%, whereas those living between 200 and 600 m from these power lines have a relative risk of 23%. In addition, a recent meta-analysis of all available epidemiologic data showed that daily prolonged use of mobile phones for 10 years or more showed a consistent pattern of an increased risk of brain tumors (64).

Fruits, vegetables, spices, condiments and cereals with potential to prevent cancer. Fruits include 1 apple, 2apricot, 3 banana, 4 blackberry, 5 cherry, 6 citrus fruits, 7 dessert date, 8 durian, 9 grapes, 10 guava, 11 Indian gooseberry, 12 mango, 13 malay apple, 14 mangosteen, 15 pineapple, 16 pomegranate. Vegetables include 1artichok, 2 avocado, 3 brussels sprout, 4 broccoli, 5 cabbage, 6 cauliflower, 7 carrot, 8 daikon 9 kohlrabi, 10onion, 11 tomato, 12 turnip, 13 ulluco, 14 water cress, 15 okra, 16 potato, 17 fiddle head, 18 radicchio, 19komatsuna, 20 salt bush, 21 winter squash, 22 zucchini, 23 lettuce, 24 spinach. Spices and condiments include 1 turmeric, 2 cardamom, 3 coriander, 4 black pepper, 5 clove, 6 fennel, 7 rosemary, 8 sesame seed, 9 mustard, 10 licorice, 11 garlic, 12 ginger, 13 parsley, 14 cinnamon, 15 curry leaves, 16 kalonji, 17 fenugreek, 18camphor, 19 pecan, 20 star anise, 21 flax seed, 22 black mustard, 23 pistachio, 24 walnut, 25 peanut, 26 cashew nut. Cereals include 1 rice, 2 wheat, 3 oats, 4 rye, 5 barley, 6 maize, 7 jowar, 8 pearl millet, 9 proso millet, 10 foxtail millet, 11 little millet, 12 barnyard millet, 13 kidney bean, 14 soybean, 15 mung bean, 16 black bean, 17 pigeon pea, 18 green pea, 19 scarlet runner bean, 20 black beluga, 21 brown spanish pardina, 22green, 23 green (eston), 24 ivory white, 25 multicolored blend, 26 petite crimson, 27 petite golden, 28 red chief.

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To learn more about a healthy lifestyle and diet for the prevention of all sickness and disease read The pH Miracle revised and updated and The pH Miracle for Cancer – http://www.phoreveryoung.com

Lecture in Dubai – The Annual Conference on Bacterial, Viral and Infectious Diseases

Join Robert O Young PhD and Galina Migalko MD in Dubai on December 5th and 6th, 2018 for the Annual Conference on Bacterial, Viral and Infectious Diseases. They will be Key Note Speakers and doing a workshop on the New Biology.

For more information and to register go to: https://bacterialdiseases.infectiousconferences.com/organizing-committee.php

The following is the abstract for Dr. Young’s lecture:

The Dismantling of the Viral Theory

Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner

Abstract

There is now over 100 years of documented history and research on the Polio virus and whether or not its treatment by inoculation has been successful in eradicating Polio. I am suggesting in this article and in my lecture that there are significant findings based on historical and past and current research, including my own that the viral theory of Polio and possibly other modern-day diseases, such as Post-Polio Syndrome, Polio Vaccine-Induced Paralysis, Legionnaires, CNS disease, Cancer, HIV/AIDS and now Zika may be caused by acidic chemical poisoning from DDT (dichloro-diphenyl-trichloroethane) and other related DDT pesticides, acidic vaccinations, and other factors including lifestyle and dietary factors rather than from a lone infectious virus. I will present ten historical graphs outlining the history of Polio, the production of DDT, BHC, Lead, Arsenic, Polio vaccinations and the author’s theory that chemical poisoning, vaccination, and lifestyle and dietary choices are a more likely causes for the symptoms of Polio, neurological diseases, Cancer, HIV/AIDS and now Zika.

THE POSSIBLE CAUSE OF POLIO, POST-POLIO, CNS, PVIPD, LEGIONNAIRES, AIDS and the CANCER EPIDEMIC – MASS ACIDIC CHEMICAL POISONING?

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Tom Brady’s pH Alkaline Lifestyle and Diet

New England Patriots quarterback Tom Brady — a five-time Super Bowl Champion and three-time NFL MVP — is widely considered to be one of the greatest athletes of all time. Lately, however, Brady has been following an alkaline lifestyle and diet.

In September 2017, Brady released his book, The TB12 Method: How to Achieve a Lifetime of Sustained Peak Performance. In this book, Brady detailed exactly what he eats every day. One main feature of his diet is liberal amounts of alkaline foods and liquids.

 

In the mornings, Brady doesn’t eat a full meal. When he wakes up at 6:00 am, he drinks 20 ounces of alkaline water infused with electrolytes, including sodium, potassium, magnesium and calcium. He then drinks a smoothie and/or juices containing alkalizing grasses, vegetables, fruit, nuts and seeds. Two hours later, he has another glass of alkaline electrolyte-infused water, and a post-workout protein shake. Brady claims to drink somewhere between 12 and 25 glasses of alkaline water per day.

 

He also heavily encourages snacking. He usually snacks at around 11:00 am, just before lunch. For lunch, Brady will usually have a piece of fatty fish like salmon and a lot of green vegetables. In the afternoon, he may have another protein shake or protein bar, and around 6:00 pm, Brady eats dinner, which, again, consists of mostly green vegetables.

His book provides recipes for green juices, green soups, green salads, and a few carbohydrate recipes such as his pasta dish — which is odd, considering that he supposedly rarely eats carbs. But even Brady treats himself sometimes. He doesn’t often eat dessert, but he does give a recipe for his famous alkaline avocado ice cream.

 

His book also contains several alkalizing rules for eating. Brady won’t eat carbohydrates and protein together. He recommends eating carbs or protein with green vegetables instead, as he knows that this is better for assimilation and elimination.

Brady’s chef Allen Campbell says that 80 per cent of his diet is green vegetables and the rest of his diet is grass-fed organic steak and wild salmon.

Brady follows what he refers to as an alkaline lifestyle and diet created by Robert O. Young PhD, in order to minimize muscle inflammation caused by the buildup of lactic acid in the interstitial fluids of the Interstitium (see illustration below). This entails limiting ‘acidifying foods,’ which mostly includes starchy foods like potato, pasta, bread and ALL dairy products.

What is even more interesting is the list of acidic foods that Brady doesn’t eat. For Brady, caffeine, white sugar, white flour, dairy, and some nightshade vegetables —  eggplant and mushrooms — are completely off the table. He also won’t consume olive oil if it’s used in cooking — but he’ll have it raw. And he won’t eat high sugar fruit, unless it’s in a smoothie.

Since there are profound benefits with Brady’s pH alkaline diet, and it is clearly sustaining his play on the field, there a 100’s of specific health and fitness benefits of the pH alkaline lifestyle and diet which are backed by published scientific evidence.

 

He claims that limiting acidic foods helps control the body’s pH balance. What one eats, drinks, breaths and thinks has a huge effect on the body fluids, including the blood plasma, interstitial and intracellular fluid pH which is ideal at 7.365.

Brady also knows that the alkaline lifestyle and diet can decrease the lactic acids that causes inflammation in the body, leading to ALL sickness and disease, including connective tissue disorders that can end an athlete’s career.

 

At 41 years young, which is considered ancient in football years, Brady says he wants to play at least another five years. While he is certainly capable, his pH Miracle lifestyle and diet will be a major reason he WILL achieve HIS goal.

To learn more about the pH alkaline lifestyle and diet read The pH Miracle revised and updated – http://www.phoreveryoung.com

To learn more about the lifestyle and attend a pH Miracle Retreat in Marbella, Spain or Sardenia, Italy, go to: http://www.phmiracleretreat.com

SHOCKING STUDY IN 2016: Chemo Kills up to 51% of Patients within 30 days

cause of death

For decades now, many scientists have been raising red flags that chemotherapy can oftentimes do more harm than good, and in a surprisingly large number of cases, it simply does not work.

Dr. Hardin B. Jones, a former Professor of Medical Physics and Physiology at Berkeley, California, studied the impact of chemotherapy, radiation, and surgery on the survival rates of cancer patients, and found that instead of prolonging lives, these treatments actually make the patients die almost four times sooner. This was found more than 40 years ago, and yet not much has changed in the way the hospitals treat cancer.

For terminal patients as well, a 2016 study in the peer-reviewed journal of the American Cancer Society CANCER found that living at home instead of being treated at the hospital prolonged their lives by about 45%.

And now, a new study was just published earlier this month that analyzed 30-day mortality rates caused by the treatment itself: chemotherapy and chemotherapy plus radiation.

Cancer Study: Early Mortality Rate Caused by Chemotherapy

The study, published in The Lancet’s Oncology, looked at 23,228 breast and 9,634 lung cancer patients in England.

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The results showed high death rates linked to the treatment, increased use of SACTs (systematic anticancer therapies – cytotoxic chemotherapy). The researchers stated it was due “poor clinical decision making.”

“Patients dying within 30 days after beginning treatment with SACT are unlikely to have gained the survival or palliative benefits of the treatment, and in view of the side-effects sometimes caused by SACT, are more likely to have suffered harm,” states the study.

The researchers write that while there a few patients who may have benefited from SACTs, there were too many who were harmed by it, or even killed by the treatment.

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In 2014 , the year the study was researched, almost 1,400 patients in England died within 30 days of their first chemotherapy treatment. In some hospitals, the mortality rate was significantly higher than in the others: up to 51% of breast cancer patients died in Milton Keynes (although the number of total patients was small), and up to 29% of lung cancer patients died in Lancashire Teaching Hospitals.

“Simply reducing doses of or avoiding SACT altogether would reduce or eliminate instances of treatment-related early mortality.”

The study was done after noticing a clear lack of data analyzing the risk versus gain of using chemotherapy and mortality rates caused by it in the first 30 days of treatment. As the researchers state, this is the first time this topic has been brought up and investigated at a national level.

The “million dollar questions” (or perhaps “billion dollar” since this is the cancer treatment industry we’re talking about) raised by the researchers included: is chemotherapy use still advocated based on small clinical studies — most sponsored by the pharmaceutical industry?

And it has never been fully studied how well it works in a real hospital setting?

Do Most Hospitals Know What They Are Even Doing?

The study points out two problems. One is that mortality rate is high due to poor clinical decisions. Perhaps because in most hospitals chemotherapy is given in a one-size-fits all manner or a fixed-dose with no consideration to a patient’s health history, and characteristics such as weight and age.

In England’s database, it was found that for many patients, the doctors did not include why the chemotherapy was given, and the overall health of the patient and the severity of their cancers was never recorded.

Both of these factors, as the study points out, could significantly change the outcome for these patients.

In America, another study found that doctors gave palliative chemotherapy to terminal cancer patients, and in at least two-third of cases, the patient did not know that the treatment could not cure them, but it only alleviated some symptoms, such as pain.

Knowing that the treatment could not help them in the end, would they have searched for alternative options that may have worked better?

Death Rates from Chemotherapy Are Rarely Properly Documented

The second issue the study found is that mortality rates are hard to analyze because they are not well or properly recorded.

In England’s case, many dates of deaths were simply missing from the national database. Some were documented twice, and the two dates did not match.

 

800px-Death_certificate_of_John_Otto_Siegel,_front_view

In America, the national statistic of cancer mortality comes from the death certificates. This is what the National Center for Health Statistics (NCHS) along with the doctors use to see how many people are die from cancer, and how many people die from the treatment. Unfortunately, the National Cancer Institute reports “cancer” as the cause of death for almost all cancer patients, regardless of what actually caused it, as pointed out in a 2002 article.

This article raised concern that “cancer death rates are systematically underestimated, in that many patients who die as a result of cancer treatment do not have cancer recorded as the underlying cause of death.”

For example, they studied patients who died within one month after a cancer-surgery between 1994 and 1998, and 41% of these deaths were not properly recorded. The authors write that cancer treatment was the likely cause of death.

“…Many deaths subsequent to 1 month after cancer-directed surgery may be similarly miscoded.”

Unfortunately, even though the study points out that many death certificates quote some condition other than cancer as the cause of death (such as liver failure), they want the cause of death to be just “cancer.” That would lead to further incorrect data as many patients do die from cancer treatments, and liver failure that would not happen from cancer, is often caused by the toxic chemo drugs. But what this study does show us, is that because of a 1999 revision in the International Statistical Classification of Diseases and Related Health Problems (ICD), instead of a cancer or cancer-related death, death certificates now have to show the “underlying” cause of each death, such as: thromboembolism (blood vessel obstruction), infections, organ failures, and hemorrhage (excessive bleeding).This leads to improper classification and underestimated cancer death rates and statistics.

How many patients die from the treatment instead of cancer?

That is hard to say until every doctor and hospital begins classifying the causes of deaths correctly. Until then, it is important to keep studies like this in mind when considering pros and cons of starting a chemotherapy treatment.

There are more and more alternative options out there – and for many, they do work. (Just look up testimonials from the Nutritional Oncology Research Institute, or even studies on carotenoids antioxidants derived from natural sources, and even IV curcumin and sodium bicarbonate).

“I think it’s important to make patients aware that there are potentially life threatening downsides to chemotherapy. And doctors should be more careful about who they treat with chemotherapy,” writes one of the study’s co-authors, Professor David Dodwell, Institute of Oncology, St James Hospital, Leeds, UK.

This article is for informational purposes only. Consult a doctor before beginning any treatment. See our full disclaimer here. 

Want to learn more about the most effective ways to prevent and reverse cancer?  Read The pH Miracle revised and updated and The pH Miracle for Cancer –

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References

1) https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(16)30383-7/abstract?code=lancet-site

2) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360753/

3) https://althealthworks.com/8088/berkeley-scientist-cancer-patients-live-4x-longer-by-refusing-chemotherapyyelena/

4) https://academic.oup.com/jnci/article/94/14/1044/2519814

5) Alkalizing Nutritional Therapy in the Prevention and Treatment of Any Cancerous Condition – https://www.amazon.com/Alkalizing-Nutritional-Prevention-Treatment-Cancerous-ebook/dp/B01JKCXJRY/ref=la_B001ILKCSU_1_14?s=books&ie=UTF8&qid=1528429047&sr=1-14&refinements=p_82%3AB001ILKCSU

6) The pH Miracle for Cancer: Discover the Truth about the Cause, Prevention, Treatments, and Reversal of ALL Types of Cancers – https://www.amazon.com/PH-Miracle-Cancer-Prevention-Treatments-ebook/dp/B01JJX1Q8S/ref=la_B001ILKCSU_1_6?s=books&ie=UTF8&qid=1528428158&sr=1-6&refinements=p_82%3AB001ILKCSU

7) Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of All Sickness and Disease – https://www.amazon.com/Potassium-Bicarbonates-Prevention-Treatment-Sickness-ebook/dp/B01JLHJ1Y8/ref=la_B001ILKCSU_1_30?s=books&ie=UTF8&qid=1528429161&sr=1-30&refinements=p_82%3AB001ILKCSU

A Finger on the Magic of Life-Antoine Bechamp, 19th Century Genius (1816 – 1908)

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The Magic Eraser

There have been several notable occasions in history when persons offering invaluable contributions to the advancement of human understanding have been ignored, ridiculed and even persecuted in their time. In most cases, however, their work has subsequently been given a deserved measure of recognition. Some great ones, though, have not enjoyed such rejuvenation and have “suffered the slings” of obscurity.

So it is with Antoine Bechamp. Had the profound voice of his science not been silenced, much of humankind may have been spared the worst aspects of the infectious stresses of the 20th century. Since the case can be made that the approved but improper and dangerous treatment of infectious “diseases” over the last century has in large part given rise io the present epidemic wave of degenerative “disease,” including cancer and AIDSyndroine, we might have been spared these miseries as well. At the least, we would have understood much more clearly why we have them. Fortunately, however, Bechamp’s work has been kept alive by small, successive bands of truth-seekers.

The adoption by science of Louis Pasteur’s germ theory as the whole truth, without regard to the subtleties and deep insight of Bechamp’s microzymian principle, represents one paraphrased: “There is no medical doctrine so potentially dangerous as a partial truth implemented as whole truth.” Any medical professional, bioscientist, health care practitioner, or lay person for that matter, who wishes to gain insight into the origins and nature of infectious and chronic illness, against the backdrop of a marvelous view of the life process, must consider Bechamp. And they must entertain one of the most important concepts to come out of his illustrious career-microbiological pleomorphism as it relates to disease and its symptoms.

There are four books written about him of which this writer is aware (although there are very likely more) and many works published by him. Of the ones by him, all except one are in the original French. Fortunately, his last book, The Blood and Its Third Anatomical Element, was translated into English in 1911 by Montague R. Leverson, M.D., Ph.D., M.A., although it has been difficult to obtain. Of the two major books about him, one is in French and the other (E. Douglas Hume’s Bechamp or Pasteur?) is also rare. The other two books about Bechamp are by R.B. Pearson. The Hume book, one Pearson book, and The Blood are once again available as reproductions in the U.S. after a hiatus of several years.

Bechamp considered The Blood his crowning work, and therein he describes an amazing microanatomical entity and its participation in the clotting process. He also includes details of his work and his experiences with the plagiarisms and “pettifogging ratiocinations” of Louis Pasteur. The French book about him, which author Christopher Bird praised highly to this writer, is by Marie Nonclercq, entitled Antoine Bechamp, 1816- 1908: L’Homme et le Savant, Originalite et Fecondite de Son Oeuvre. The latter part means, The Man and the Scientist, the Originality and Productivity of His Work. According to Bird, in an account given at a 1991 facts that did not set well with reigning theory, many questions arose … as I read essays and books, of a heretical nature, one could say, written by researchers whose names I never heard mentioned in my classes.  

Twenty years ago, the World Health Organization proudly declared recently the discovery that the single greatest factor in heart disease is a vitamin E deficiency.

Also perversely awe-inspiring is the fact that a person of Bechamp’s extraordinary accomplishments has been written out of history books, textbooks and all encyclopedias. It is sobering to consider the required degree of authoritarian control over key academic elements in our culture. It is not my intention to belabor the politics, but as the wonders of Bechamp’s work unfold to the mind, the question simply arises, “Why is this not common knowledge?” Yet, we must be grateful that his “erasure” was far from complete.

It is difficult to do full justice to Bechamp without recourse to a book. His work was incessant and prodigious, and his observations prolific. I will attempt to convey some essentials of his biological work-only a part of the picture, as the total output includes chemistry, medicine and pharmacy. He left a remarkable legacy of scientific insight that borders on the spiritual, yet died in relative obscurity with virtually no recognition by peers or the public. Having outlived his wife, his beloved associate Professor Estor, and his four children, he had to endure those hard lessons of life in addition to the one of professional anonymity. However, in keeping with his extraordinary mind, he never lost conviction that the truth would come to light, as would his role in its revelation.

I’m not sure why, when his life touched mine through E. Bechamp is known among a coterie of modern and contemporary admirers, and his work has been followed up, knowingly or not, by perhaps a total of 50 scientists. This group includes such names as Gunther Enderlein; Wilhelm Reich; Royal Raymond Rife; the courageous Australian team of Glen Dettman, Ph.D. and Archie Kalokerinos, M.D. (who for many years published information in the Toorak Times, an Australian newspaper); and Gaston Naessen, including myself, who have brought the Bechampian locomotive to a full head of steam.

It is at once unbelievable and understandable that the superficial dogma of Louis Pasteur could have prevailed over Bechamp’s insights in the 19th century French Academy of Science. Unbelievable because of the meticulous documentation and presentation Bechamp made of his prolific work. Understandable because Pasteur stole enough of the truth to make it pass, while having on his side upper class connections and a doctrine that more suited the cultural (especially religious) moods of the time. Abetting, if not creating, an atmosphere repressive to truth was a mood of impassioned ignorance among ecclesiastic authorities at the University of Lille, where Bechamp had moved in 1875 to teach. In a manner similar to that which devastated Galileo, they vigorously opposed the “heresy” of the microzymian view. Heightening the poignancy of this tragedy was the depth of that ignorance, which was unable to realize that the view was not heretical at all. In fact, Bechamp was a devout Christian who felt his inquiries merely to be revealing the Creator’s modus. But it is perversely awe-inspiring to see such bias having persisted for a century, supported by the structure of authority in bioscience, so that Bechamp’s principles have not yet (2015) been given fair examination in the mainstream.

Things may soon change-for a number of reasons, not the least of which is that research in the medical literature is now burning a raging blaze below the lofty suite in which the few powerful controllers lurk. They will soon have to surrender themselves at the window, or be consumed by the flames. Of course, one way in which they surrender is to rediscover the truth, that is, claim credit for making scientific “discoveries” about matters long ignored or repressed by them and long held as principle in alternative venues. For example, “science” has just discovered that antioxidants are good for asthma, especially vitamins C and E. And after the tireless, definitive work on vitamin E by the Shute brothers probably 20 years ago, the World Health Organization proudly declared recently the discovery that the single greatest factor in heart disease is a vitamin E deficiency.

Also perversely awe-inspiring is the fact that a person of Bechamp’s extraordinary accomplishments has been written out of history books, textbooks and all encyclopedias. It is sobering to consider the required degree of authoritarian control over key academic elements in our culture. It is not my intention to belabor the politics, but as the wonders of Bechamp’s work unfold to the mind, the question simply arises, “Why is this not common knowledge?” Yet, we must be grateful that his “erasure” was far from complete.

It is difficult to do full justice to Bechamp without recourse to a book. His work was incessant and prodigious, and his observations prolific. I will attempt to convey some essentials of his biological work-only a part of the picture, as the total output includes chemistry, medicine and pharmacy. He left a remarkable legacy of scientific insight that borders on the spiritual, yet died in relative obscurity with virtually no recognition by peers or the public. Having outlived his wife, his beloved associate Professor Estor, and his four children, he had to endure those hard lessons of life in addition to the one of professional anonymity. However, in keeping with his extraordinary mind, he never lost conviction that the truth would come to light, as would his role in its revelation.

I’m not sure why, when his life touched mine through E. Douglas Hume’s historical biography, such a strong feeling arose in me-the need to “exonerate” him, to bring his name and work to their deserved place of honor in history. Part of it, I’m sure, as with M. Nonclercq, is realizing the health benefits society might reap from understanding him, not to mention the inspiring, if not magical, insight into life and being that his views represent. But I’m still not quite sure why I want to be able to say (if in some way my various expositions about him over the last decade, added to the voices of others who have seen with his eyes, contribute to open re-evaluation of his science), “There, Antoine! Rest in peace, my friend.”

Principles of Micromorphology

While some of the ideas Bechamp addressed predated him, they had not been so clearly described, fully developed, or strongly supported by experimentation. It is said there is nothing new under the sun. If true, it may be because all things, or situations, exist at once in the Creation. It is a matter of perspective, much like looking at a tapestry. Bechamp’s perspective allows us to step back from tight focus and see the loose threads of the germ theory amidst a harmonious and astounding pattern of the life process. He had his “finger” on the magic of life. According to Hume, the essence of what he brought to us was as follows:

First, he demonstrated that the air is filled with microscopic organisms capable of fermenting any suitable medium on which they happen to land. He showed that the chemical change is carried out by a soluble ferment produced by the organism, and this ferment is analogous to the digestive juices of the stomach. Thus, he identified fermentation as a digestive process. (Dr. Young theorizes that all decomposition, even the rusting of steel, is mediated by ferments. It is known, for example that bacteria decompose rock into soil. Microorganisms are at or near the foundation of all life and life processes on Earth. For example, fungal forms are indispensable parts of the roots of most plants, including the largest trees.)

Secondly, the most profound conclusion to which Bechamp’s untiring and painstaking research led him is that there is an independently living microanatomical element in the cells and fluids of all organisms. This element precedes life at the cellular level, even the genetic level, and is the foundation of all biological organization. What originally piqued Antoine’s procreative curiosity was the discovery, somewhat by accident, that pure chalk from geological deposits at least 11 million years old would liquefy starch and ferment sugar solutions, while man-made chalk would not. After years of work tracking down the cause (fermentation was not understood at the time), he attributed the action to the living remains of organisms long dead. He called this tiny living element a “microzyma,” or small ferment.

Thirdly, he claimed that microzymas routinely become forms normally referred to as bacteria, and that bacteria can revert or devolve to the microzymian state. (This is the principle of pleomorphism, which is central to understanding the appearance of “infectious” and degenerative disease symptoms in the body.)

Fourthly, he explained that atmospheric germs are not fundamental species, but are either microzymas, or their evolutionary forms, set free from their former vegetable or animal habitat by the death of that “medium.”

Bechamp explained: “The microzyma is at the beginning and end of all organization. It is the fundamental anatomical element whereby the cellules, the tissues, the organs, the whole of an organism are constituted.” He referred to microzymas as the builders and destroyers of cells. The quotation emphasizes the constructive aspect of microzymian activity and purpose, but it is the destructive aspect, or the “end of all organization,” which concerns us in disease. He always found microzymas remaining after the complete decomposition of a dead organism, and concluded that they are the only non-transitory biological elements. In addition, they carry out the vital function of decomposition, or they are the precursors of beings (bacteria, yeasts and fungi) which do so. Thus, he clearly presented the idea that the physical life of higher biological forms arises from, is dependent upon, and is recycled by, microscopic beings. Simple, immediate proof of dependence is the indispensable bacterial population in the human GI tract. And it adds piquancy to the whole matter to consider that our digestive and metabolic associates are plants.

The crucial “catabolic” aspect of microzymian behavior enters the picture when the body becomes diseased, for, according to Bechamp:

In a state of health, the microzymas act harmoniously and our life is, in every meaning of the word, a regular fermentation. … In a condition of disease, the microzymas which have become morbid, determine in the organism special changes . . . which lead alike to the disorganization of the tissues, to the destruction of the cellules and to their vibrionien evolution during life.

The microzyma is an organized (insoluble) ferment: a living element. Controlled fermentation is a vital physiological process. For example, it is utilized as a means of breaking down toxins in intercellular fluid and the lymphatics. Also, some commercial dietary fiber products contain acacia and slippery elm. These soluble fibers ferment in the gut, resulting in short-chain fatty acids such as butyrate and acetate, which are highly beneficial to the colon wall. Bechamp published a paper (still in French) about the role of microzymas in the production of salivary diastase (ptyalin). Since there are microzymas in every cell, in the blood and intercellular milieu, it is likely that many vital substances, mostly enzymes, are produced by them or by their complexes.

Bechamp said that the process of cellular breakdown is mediated by microzymian fermentation-even in a healthy body. Though there is renewal happening as well, breakdown fermentation (aging) eventually takes over, greatly increasing in intensity upon death. When oxidative metabolism ceases and a body dies, negative surface charges are lost and the terrain goes acid. Microzymas respond to biochemical signals, the most important being pH. The condition of disease is a milieu which presents to the microzymas a premature biochemical signal that the organism is dead. They consequently change their function and evolve into forms capable of more vigorous fermentative breakdown-forms that reflect disease-what Bechamp called “morbidly evolved microzymas.” If the host pays no attention while it is still feasible to adjust, s/he will be recycled sooner than would otherwise be the case.

And further:

“… In disease, it is the elementary tissues or cellules that are affected….

It should result therefrom that tissue and cellular pathology are in reality microzymian pathology. In disease, the cellules have been seen to change, be altered and destroyed, and these facts have been noted. But if the cellule were the vital unit living per se, it would know neither destruction nor death, but only change. If then the cellule can be destroyed and die, while the microzyma can only change, it is because the microzyma is really living per se, and physiologically imperishable, even in its own evolutions, for, physiologically nothing is the prey of death; on the contrary, experience daily proves that everything is the prey of life, that is to say, of what can be nourished and can consume.”

Further Conclusions by BeChamp

“That there is produced in the organisms of all living beings, including man, in some part and at a given moment, alcohol, acetic acid, and other compounds that are the natural products of the activity of organized ferments, and that there is no other natural cause of this production than the microzymas of the organism. [Emphasis added. Here is where, in a compromised terrain, the culminate forms described by Dr. Young in the main text of his book Sick and Tired, could play a role. As described by Bechamp-i.e., in an apparently healthy organism-it would likely be the initial development phase.] The presence of alcohol, acetic acid, etc. in tissues reveals one of the causes, independent of the phenomenon of oxidation, of the disappearance of sugar in the organism, and of the disappearance of the gluco-genic matters and that which Dumas called the respiratory foods.”

“That, without the concurrence of any outside influence except that of a suitable temperature, fermentation will go on in a part withdrawn from an animal, such as the egg, milk, liver, muscle, etc., or, in the case of plants, in a germinating seed, or in a fruit which ripens when detached from the tree, etc. The fermentable matter that disappears earliest in an organ after death is the glucose, gluco-genic matter or some other of the compounds called carbohydrate, that is to say respiratory food. And the new compounds that appear are the same as produced in the alcoholic, lactic acid and butyric fermentations of the laboratory; or, during life, alcohol, acetic acid, lactic or sarcolactic acid, etc.”

“That the microzymas, after or before their evolution into bacteria, attack albuminoid or gelatinous matters only after the destruction of the … carbohydrates.”

“That the microzymas and bacteria, having effected the transformations before mentioned, do not die in a closed apparatus in the absence of oxygen; they go into a state of rest, as does the beer yeast in an environment of the products of the decomposition of the sugar, which products it formed.”

“That . . . the necessary destruction of the organic matter of an organism is not left to the chance of causes foreign to that organism, and that when everything else has disappeared, bacteria-and finally the microzymas resulting from their reversion-remain as evidence that there was nothing primarily living except themselves in the perished organism. And these microzymas, which appear to us as the residuum of what lived, still possess some activity of the specific kind that they possessed during the life of the destroyed being.”

Microzymas Unique to Each Organism and Organ

The microzymas were too minute to differentiate with the microscope (even for today’s equipment), and Bechamp knew he was not going to see them in detail. His brilliance shows again, however: “The naturalist will not be able to distinguish them by description, but the chemist and also the physiologist will characterize them by their function.” Having masterful skill in chemistry, he utilized that ability, accompanied by ingenious use of the polarimeter, to draw many of his conclusions. He was led to conclude that an organism’s microzymas are unique to it, and are not interchangeable with those of another. He went further to say that even within a single organism, each organ and tissue has functionally unique microzymas, and that, for example, those of the kidney do not belong in the liver. What, therefore, did he have to say about inoculation?

The most serious, even fatal, disorders may be provoked by the injection of living organisms into the blood; organisms which, existing in the organs proper to them, fulfill necessary and beneficial functions-chemical and physiological-but injected into the blood, into a medium not intended for them, provoke redoubtable manifestations of the gravest morbid phenomena.

“. . . Microzymas, morphologically identical, may differ functionally, and those proper to one species cannot be introduced into an animal of another species, nor even into another center of activity in the same animal, without serious danger.”

How much more foolhardy is it then, when vaccinal microzymas are not only from another species, but are already morbidly evolved and are accompanied by preservatives, formaldehyde, and other chemicals? There is no sanity whatever to this practice. The best that can be said about it is that it may prevent, against the odds, the appearance of varying sets of symptoms. But this is at the price of weakening the immune system, toxifying the body, and possibly setting the stage for degenerative symptoms later in life-all the while doing absolutely nothing for, except perhaps worsening, the underlying disease condition.

As indicated in the above quotation concerning “granulations of the protoplasm,” it would seem that microzymas are also closely related to, and perhaps precursors of, genetic molecules. In an August 8, 1977 address to the (now defunct) International Academy of Preventive Medicine, Drs. Dettman and Kalokerinos had the following to say:

“It became increasingly apparent to us that the problems relating to infection and immunization were, to say the least, oversimplified by organized medicine. Perhaps Bechamp was thinking in advance of our modern molecular biologists who refer to genes controlling enzymes! We wondered whether Bechamp’s writing anticipated, in some respects, the discovery of RNA and DNA? It now appears to us that the experimental data described in Bechamp’s work has, in part, been independently and unknowingly repeated by Professor Bayev of the USSR Academy of Sciences.”

In a personal communication with Prof. Bayev (1974) concerning the common factors of his and Bechamp’s work, Bayev states:

“Self-restoration of the molecule from its parts was obtained with pure transfer RNA from baker’s yeast. It is a rather simple organic substance of molecular weight 30,00 daltons. Its chemical structure is now identified exactly. I think the microzyma by Bechamp has a more complex chemical nature than a simple organic molecule, but our experiments with transfer RNA molecules prove that self-restoration is possible already at the molecular level.” [Emphasis added.]

Finally, might we not ask ourselves how much our uncritical acceptance of Pasteur’s work has retarded the development of medical science to this day? In our own work we found that when we became aware of Bechamp’s arguments we were better able to understand some of the puzzles of ourfindings with Aboriginal infant death in Australia, which initially led us into conflict with the prevailing medical models of disease and immunization. We feel that we have gone too far to turn back, and that we need the help of all health care professionals who dare to think for themselves in working through the tangled web of relationships that govern disease-immunization- nutrition interactions.

Bechamp and Pasteur

Bechamp never denied that the so-called germs of the air or other causes may be contributory, either to decomposition or illness, but only that these have not been expressly created, nor are they needed, for these purposes. As noted, the germs of the air are nothing other than microzymas or their evolved forms from fermentatively destroyed organisms. Their destructive or morbid influence may be added to that already faced by the organism’s endogenous microzymas, which may or may not have initiated morbid evolution. This is a crucial departure from germ theory. That is, without the predisposition of inherent microzymas-which condition is engendered primarily by a faulty internal environment-the germs of the air, or those of other sick bodies, will not produce illness in a person. One can see how this holistic view confers responsibility and power on the individual, as opposed to making him a victim to be saved (by a medical science powerless to do so). In addition to microzymas in the atmosphere, “The spores of the entire microscopic flora may intrude, as well as all the molds that may be born of these spores.”

In the earlier phase of his career, as Professor of Medical Chemistry and Pharmacy at the Faculty of Medicine at Montpellier University, Bechamp and his tireless colleague Professor Estor had many opportunities to test microzymian theory in practice. Examination of an amputated arm and many examinations of frozen plants during a particularly cold winter, convinced them that upon injury, bacteria developed internally without any outside influence. Bruising an apple without breaking the skin is an example; the broken cells will autoferment. This is one basis for the surgical cleaning of wounds.

Pasteur, on the other hand, a non-physician and proponent of the germ theory, seems to have lacked a certain understanding of living systems. He considered the body to be a collection of inert chemicals, and therefore after death he expected nothing living in it. When life would inevitably appear in dead organisms, he had to draw the conclusion that it resulted from invasion from without by the beings whose existence had been taught to him and the world by Bechamp. Either he saw but would not admit, or he simply could not fathom, that microorganisms are already inherent to humans and every other organized medium on the planet, all of which contain, are composed of, and have developed from, microzymas. Unfortunately, the persuasiveness of Pasteur’s superficial conclusions held sway over the deeper, rather elusive, complex, profound, even mystical workings of life and pathology.

Bechamp:

Long before Davaine considered the inside of the organism to be a medium for the development of inoculated bacteria, Raspail said,

“The organism does not engender disease: it receives it from without..

. . Disease is an effect of which the active cause is external to the organism.” In spite of this, the great physicians affirm, in Pidoux’ happy words, “Disease is born of us and in us.”

But M. Pasteur, following Raspail . . . maintains that physicians are in error: the active cause for our maladies resides in disease-germs created at the origin of all things, which, having gained an invisible entry into us, there develop into parasites. For M. Pasteur, as for Raspail, there is no spontaneous disease; without microbes there would be no sickness, no matter what we do, despite our imprudences, miseries or vices! The system, neither new nor original, is ingenious, very simple in its subtlety, and, in consequence, easy to understand and to propagate. The most illiterate of human beings to whom one has shown the connection between the acarus and the itch understands that the itch is the disease of the acarus. Thus it comes about that it has seduced many people who give unthinking triumph to it. Above all, men of the world are carried away by a specious, easy doctrine, all the more applicable to generalities and vague explanations in that it is badly based upon proved and tried scientific demonstrations.

Much of Pasteur’s refusal to accept microzymian theory may have arisen from pure rivalry which came into focus when Bechamp solved, right under the Pasteur’s nose, a disease crisis threatening the French silkworm industry. Since the two must have known each other previously, we must be open-minded enough to allow that Bechamp, though concerned for his country’s important industry, may have indulged himself in a little one- upmanship in his embarrassment of Pasteur, who gained more privilege from social connection than from earned merit (thus, in most books, Pasteur is given credit for solving the crisis). If so, it may have cost Bechamp dearly, because it earned him the eternal resentment of the volatile chemist, who took every future opportunity to oppose his tormentor. And it was primarily the “specious easiness” of germ theory that allowed Pasteur to get away with it, because few scientists of the time were sufficiently skilled to probe deeply enough beneath the superficialities. Few possessed enough knowledge or insight to understand the elusive complexities. And Bechamp warned against facile judgments when he wrote in 1869:

“In typhoid fever, in gangrene, in anthrax, the existence has been proved of bacteria in tissue and in the blood, and one was very much disposed to take them for granted as cases of ordinary parasitism. It is evident, after what we have said, that instead of maintaining that the affection has had as its origin and cause the introduction into the organism of foreign germs with their consequent action, one should affirm that it only has to do with an alteration of the function of the microzymas, an alteration indicated by the change that has taken place in their form.”

Again:

“An egg contains nothing organized except microzymas; everything in the egg, from the chemical point of view, will be necessary for the work of the microzymas; if in this egg its ordered procedure should be disturbed by a violent shaking, what happens? The albuminoid substances and the bodies of fat remain unchanged, the sugar and the glycogen disappear, and in their place are found alcohol, acetic acid and butyric acid; a perfectly characterized fermentation has taken place there. That is the work of the microzymas, the minute ferments, which are the agents and the cause of all observed phenomena. And when the bird’s egg has accomplished its function, which is to produce a bird, have the microzymas disappeared? No, they may be traced in all the histological elements; they pre-exist-one finds them again during the functioning and the life of the elements; one will find them yet again after death; it is by them that the tissues are made alive.”

“The part of organized beings essentially active and living, according to the physiologists, is the granular protoplasm. We went a step farther and said it is the granulations of the protoplasm, and though for their perception a sort of spiritual insight is required, we have based our conclusions upon experimental proofs of the most varied and positive nature. Bichat looked upon the tissues as the elements of the bodies of higher animals. With the help of the microscope, very definite particles, cells, were discovered, and were regarded in their turn as elementary parts, as the last term of the analysis. . . . We have said in our turn: The cell is an aggregate of a number of minute beings having an independent life, a separate natural history. Of this natural history we have made a complete description.”

Bechamp apparently had a good sense of place in the scientific pursuit (“in our turn”) of the ever-retreating Ultimate Secret. He realized that the truth of empiricism is for the time, or is in the process of evolving. No doubt he would willingly have given up microzymian theory in face of right evidence of a newer observation. I am presenting science with a newer, though highly correlative, observation. For, as Bechamp attributed all fermentation in the body to microzymas, we now are able to see that it is also carried out by higher evolutionary forms-yeast and fungus. He would have been open to the idea that bacteria also evolve, and that there may even be a step or two between microzymas and bacteria, e.g., viruses. However, as I have suggested,  functionally the virus form is very likely something other than what it is thought to be in the mist-ified Pasteurian version of bioscience.

In this article the distinction has repeatedly been made between the disease condition and its symptoms. This idea is inherent in microzymian principle, and it is interesting that Bechamp alludes to the source of the disease condition as “imprudences, miseries or vices.” This is a close approximation in different terms of the holistic gamut of precursors to physiological ill-being: improper diet, emotional upheaval and various self­destructive behaviors. Yet it is a testimony to the power and skill of the propagandists of mainstream medicine and the Pasteurian decalogue itself that serious illness remains such a mystery in the mind of the masses.

Cosmic Microzymas

It is also interesting to hear the scientist speak of “spiritual insight.” And it is interesting as well to consider microzymas in terms of Eastern modes of spiritual thought, such as yoga, in which it is felt that our creation is an ongoing process. That is, life was not put here and simply proceeds, but it, and we, are coming into being in the moment. Thus, there is constant “turnover,” or renewal and healing. In this scenario, the microzyma may be seen as an early, if not the primary, transmutation from the fine vibrations of the Cosmic Life Force into a denser form or pattern of life-something not explainable by biochemistry, certainly. Due to the colloidal nature of these nascent elements, they carry high levels of energy and may also be receptive to frequencies of light and radiation asactivating or informational signals. During formation, or once formed, they may be stimulated by cosmic energy, which comes directly into our being, which provides energy that cannot be accounted for in the Krebs cycle, which is ionizing, and which has been interpreted as carrying part of the holographic human archetypal information. Is the microzyma Colloidal Intelligence, or a modus of the Creative Intelligence-a living transducer for the Idea in Consciousness, which it translates into the cellular anatomy? It was said earlier that microzymas respond to the pH of the surrounding medium, reforming when appropriate. However, the chemical aspect may be just an obvious way for us to qualify the situation. Perhaps the change in pH alters vibrations or resonant frequencies, changing the microzymian quality of reception, transmittal or transduction of the Life Force and cosmic rays. 

Bechamp said the microzyma is imperishable. Canadian microscopist Gaston Naessens says his analogous somatid particles have survived carbonizing temperatures, 50,000 rems of radiation, and all acids. If these claims are true, could such imperishability stem from being at the interface of energy/matter and Consciousness, i.e., from the imperishability and constant materialization of life itself? It may therefore be that only the Mystery of life stands prior to the microzymian patterns.

Elaborate Colonies

An interesting corollary to microzymian principle is the idea presented by Lynn Margulis and Dorion Sagan in their book Micro-Cosmos-that all higher forms of life are elaborate colonies of microforms that have undergone a natural assimilation into the more complex whole, thus becoming cells or cooperative parts of cells. Some forms have not, or not yet, become assimilated into tissue, and so appear as separate symbionts. The intestinal bacteria are an excellent example. Based on this theory, an entertaining conjecture is that since the primordial, colonizing forms are plant life, animals don’t exist per se, so that humans are complex, mobile, talking vegetation.

Unfortunately, Micro-Cosmos lacks the insight microzymian principle might bring to it. It fails to recognize life prior to the cell, and therefore cannot consider what may be the primary orchestrative tools of the colonization process. It discusses DNA repair enzymes with no suggestion as to their origin.

This article also does not take into account the rapid functional changes of microforms in response to terrain imbalance, and is mystified by cancer:

“It is as if the uneasy alliances of the symbiotic partnerships that maintain the cells disintegrate. The symbionts fall out of line, once again asserting their independent tendencies. . . . The reasons, of course, are not all that clear, but cancer seems more an untimely regression than a disease.”  Here is what seems a struggle with the bonds of the Pasteurian decalogue. The symbionts falling out of line might easily have been expressed, “The microzymas change their function.” 

Confirmation of Bechamp

There have been many modern and contemporary confirmations of various aspects of Bechamp’s work. One of the earliest and most piquant was reported in an article in The Times, a London newspaper, on April 8, 1914. A French bacteriologist, Mme. Henri, had succeeded in transforming an anthrax bacillus into a coccus form having entirely different functional properties. It could easily have been explained by Professor Bechamp, who sat virtually unrecognized at the London Medical Congress in 1881, where plagiarist Pasteur appeared amidst outbursts of cheering as his country’s representative, and where, as reported in The Times, August 8, 1881, he categorically denied the pleomorphism of B. anthracis.

Pasteur also jumped to the conclusion that each kind of germ produces one specific fermentation, while Bechamp proved that a microorganism might vary its fermentation effect in conformity with the surrounding medium. Bechamp’s assertion that these microforms, under varying conditions, might even change their shape was proved conclusively by F. Loehnis and N.R. Smith of the U.S. Department of Agriculture in 1916 {Journal of Agricultural Research, July 31,1919, p. 675).

And, for evidence that the biological terrain is the determinant factor over the mere presence of a symptogenic microform, we may return to Kalokerinos and Dettman:  

It should come as no surprise to discover that almost every pathogen may be isolated from the majority of so-called “healthy” people: Candida is such an example, and here we quote from the Manual of Clinical Mycology (Conant, Smith, Baker & Calloway, 1971): “Since pathogenic strains of C. albicans can be isolated from (1) normal skin, (2) normal oral and vaginal mucous membranes and (3) stools of normal individuals, it is obvious that most infections have an endogenous source, and the determination of the source of the infection is as difficult as it is with Staphylococcus aureus infections.

This revelation also highlights a recent example of the false conclusions to which one is led by germ theory: The news in research on atherosclerosis is that scientists have isolated a chlamydia-type organism in the plaque, and have concluded that it is the cause of this symptom. The plan is to use antibiotics to combat this “pathogen.” There is only one guarantee in this folly: at the very best they may achieve atherosclerosis without the chlamydia. At worst, they will exacerbate the mounting crisis in health caused by a half-century of antibiotic abuse.

R.R. Rife

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Perhaps the most profound confirmation of pleomorphism was executed by another nearly obliterated genius, this time an American microscopist with the alliterative name of Royal Raymond Rife. His story was told in an impressive piece of work called “The Rife Report” by investigative reporter Barry Lynes. It has been published in book form as The Cancer Cure That Worked!, which is highly recommended from several standpoints-for its revelations about Rife’s research and technology, which would be astounding for these times, never mind for the late 1920s to mid-30s; for a wonderful background on many pioneering figures in biology; for anyone interested in a deeper understanding of where medicine has gone in the United States; and not least, for a wonderful Foreword by John W. Mattingly of Colorado State University, whose writing has always been an inspiration whenever encountered.

Rife’s extraordinary microscope (with 31,000 diameters resolution), reported on in great detail in the Feb. 1944 Journal of the Franklin Institute (Vol. 237, No. 2), was capable of detail and clarity surpassing the newly emerging electron microscopes. Its use of prismatically dispersed natural light frequencies, rather than electron beams and acid stains, allowed clear views of living subjects. Weighing 200 pounds, standing 2 feet high, and consisting of 5,682 (!) parts, the Rife Universal Microscope was an unsung wonder of the world, and the world has thus far been robbed of this absolutely elegant design.

In 1920 Rife began doing research in the electronic treatment of “disease,” specifically to find a way to destroy the tubercle bacillus by means of radio frequency (r.f.) radiation. Attempts to do so were trial and error because the organism’s resonant frequency was unknown. Lynes tells us that when the frequency was finally found and the bacteria killed, the subjects (poor guinea pigs!) died of toxicity. Rife reasoned that there was a viral form in the bacteria that survived the beam because it had a different frequency. But the virus was beyond the reach of his current microscope, which relied on chemical stains. Through an intuitive flash, he “conceived first the idea and then the method of staining the virus with light.’’’’ The idea was based on the principle of resonant frequency. Each microorganism has its own fundamental frequency of light, something Bechainp apparently took advantage of with his polarimeter. Rife arrived at the conclusion that light could be used, instead of fatal chemicals, to “stain” the subject. This was brilliant. Equally brilliant was its execution. A brief, partial description of the instrument, taken from the Journal’s review, is irresistible:

The entire optical system-lenses and prisms, as well as the illuminating units-are made of block-crystal quartz. The illuminating unit used for examining the filterable forms of disease organisms contains fourteen lenses and prisms, three of which are in the high-intensity incandescent lamp, four in the Risley prism, and seven in the achromatic condenser, which incidentally has an aperture of 1.40. Between the source of light and the specimen are subtended two circular, wedge-shaped, block-crystal quartz prisms for the purpose of polarizing the light passing through the specimen, polarization being the practical application of the theory that light waves vibrate in all planes perpendicular to the direction in which they are propagated. When light comes into contact with a polarizing prism, it is split into two beams, one of which is refracted to such an extent that it is reflected to the side of the prism, without, of course, passing through the prism, while the second ray, bent considerably less, is enabled to pass through the prism to illuminate the specimen. When the quartz prisms on the Universal Microscope, which may be rotated with vernier control through 360 degrees, are rotated in opposite directions, they serve to bend the transmitted beams at variable angles of incidence while, at the same time, since only a part of a band of color is visible at one time, a small portion of the spectrum is projected up into the axis of the microscope. It is possible to proceed this way from one end of the spectrum to the other-infra-red to ultra-violet. Now, when that portion of the spectrum is reached in which both the organism and the color band vibrate in exact accord with one another, a definite, characteristic wavelength is emitted by the organism. In the case of the filter­passing form of the Bacillus typhosus, for instance, a blue light is emitted, and the plane of polarization is deviated plus 4.8 degrees. … A monochromatic beam of light corresponding exactly to the frequency of the organism is then sent up through the specimen and the direct, transmitted light, enabling the observer to view the organism stained in its true chemical color and revealing its own structure in a field which is brilliant with light.

Recall that Bechamp said the chemist would identify microzymas by their function. Their evolved forms would also have a chemical function, or in this case, a signature. Thus, we evolved scientifically from analysis based on light polarizations to that based on the emission of light frequencies, which Rife referred to as the organism’s “true chemical refractive index.”

The Journal then explains that instead of light rays from the specimen passing through the objective and converging, they pass through a series of special prisms which keep the rays parallel:

It is this principle of parallel rays in the Universal Microscope, and the shortening of projection distance between the prisms, plus the fact that three matched pairs of ten-millimeter, seven-millimeter and four-millimeter objectives in short mounts are substituted for oculars, which make possible not only the unusually high magnification and resolution, but which serve to eliminate all distortion as well as all chromatic and spherical aberration….The coarse adjustment, a block thread screw with forty threads to the inch, slides in a one and one-half inch dovetail which gibs directly onto the pillar post. The weight of the quadruple nosepiece and the objective system is taken care of by the intermediate adjustment at the top of the body tube. The stage, in conjunction with a hydraulic lift, acts as a lever in operating the fine adjustment. A six-gauge screw having a hundred threads to the inch is worked through a gland into a hollow glycerine-filled post, the glycerine being displaced and replaced as the screw is turned, allowing a five to one ratio on the lead screw. This, accordingly, assures complete absence of drag and inertia. The fine adjustment being seven hundred times more sensitive than that of ordinary microscopes, the length of time required to focus ranges up to one hour and a half.

A major upshot of Rife’s work was his ability, through several pleomorphic stages, to transform a virus he found in cancer tissue into a fungus, plant the fungus in an asparagus- based medium, and produce a bacillus E. coli, the type of microform indigenous to the human intestine. This was repeated hundreds of times. By this accomplishment, Rife showed that the pleomorphic capacity of microforms goes beyond the bacterial level to the fungal level. Dr. Young has observed this cycle, and is suggesting that its progression to the last stage-mold-is critical. And he includes in this cycle the very important stages intermediate to microzymas and bacteria, the protein complexes usually referred to as viruses, and their immediate descendants, the cell-wall deficient forms detailed by Lida Mattman, Ph.D.

What’s more, Rife identified 10 families in the whole spectrum of microlife. Within each family, any form/member could become any other. Also, the fact that organisms have resonant frequencies allowed Rife to further develop his r.f. “beam ray,” which helped rid the body of cancer symptoms.

Apparently, Rife was not aware of Bechamp. Had he been (he was about 20 years old when Bechamp died on the other side of the Atlantic), a light of another frequency might have been thrown on his research,  What a marvelous and beneficial revelations might have arisen with Rife’s technology guided by Bechamp’s vision?  However, even though saddled i the beginning with a germ-theory mindset, he managed to rise above its worst effects.  Demonstrating an instinctive understanding of the disease process, Rife made the following statement: ” We do not wish at this time to claim that we have cured cancer, or any disease, for that matter.  But we can say that  these waves, or this ray, as the frequencies might be called, have been shown to possess the power of devitalizing disease organisms, or ‘killing’ them when tuned to an exact wavelength, or frequency, for each different organism.”  And again: “In reality, it is not the bacteria themselves that produce the disease, but the chemical constituents of these microorganisms enacting upon the unbalanced cell metabolism of the human body that in actuality produce the disease.  We also believe if the metabolism .  . . is perfectly balance or poised, it is susceptible to no disease.”

While he was making the classic error (perhaps a semantic one) of referring to symptoms as the disease, he seemed aware that disease-associated microorganisms do not originally produce the condition which has supported their morbid evolution in the animal or human body.  This fine, but critical, distinction is missing in the views of all the researchers reported on in Lynes’ book.  Even as they stood opposed to the orthodoxy, they still pursed these morbidly evolved symptoms with the intent of curing the visible, or diagnosed “disease.”

When Rife first destroyed the tubercle bacillus, the guinea pigs died of toxic poisoning. Could that poison have been bacterial debris, including endotoxin, and the death a severe Herxheimer reaction? Rife went on to search for a virus he assumed was released when the bacteria died, but if he had understood what Bechamp explained and what I am emphasizing now, he would have known that the organism’s microzymas were thus set free in the medium. And we can now understand that there was no virus per se, but only variously complexed microzymas.

As a poignant insight into the passion of a man of brilliance whose revelations were denied to the world by avarice, Lynes presents a report given in 1958 by one of Rife’s co­workers, who had known him from the early days of his career:

“He finally got to a point where from years of isolation and clarification and purification of these filterable forms, he could produce cancer in the guinea pigs in two weeks. He tried it on rats, guinea pigs and rabbits, but he found finally that he could confine his efforts to guinea pigs and white rats, because every doggone one was his pet. And he performed on them . . . the most meticulous operations you ever want to see in all your born days. No doctor could ever come near to it.

“He had to wear a big powerful magnifying glass. He performed the most wonderful operations you ever saw. Completely eradicating every tentacle out from the intestines, and sewed the thing up and it got well and didn’t know anything about it at all. Did it not once but hundreds of times. This is a thing that again and again I wish was published. I wish with all my heart that all the detailed information that he developed could be published because the man deserves it.”

“He finally got these cultures on the slide. He could look through this thing and you could see them swimming around absolutely motile and active.”

Then he’d say, ‘Watch that.’ He’d go turn on the frequency lamps. When it got to a certain frequency, he’d release the whole doggone flood of power into the room. The doggone little things would die instantly.’

“He built the microscopes himself. He built the micro-manipulator himself. And the micro-dissector and a lot of other stuff.”

“I’ve seen Roy sit in that doggone seat without moving, watching the changes in the frequency, watching when the time would come when the virus in the slide would be destroyed. Twenty-four hours was nothing for him. Forty-eight hours. He had done it many times. Sat there without moving. He wouldn’t touch anything except a little water. His nerves were just like cold steel. He never moved. His hands never quivered.

“Of course he would train beforehand and go through a very careful workout afterward to build himself up again. But that is what I would call one of the most magnificent sights of human control and endurance I’d ever seen.

“I’ve seen the cancer virus. I have seen the polio virus. I’ve seen the TB virus. Here was a man showing people, showing doctors, these viruses of many different kinds of diseases, especially those three deadly ones-TB, polio and cancer.

“Time and time again since that time some of these medical men have made the proud discovery that they had isolated we will say one of the viruses of cancer, had isolated one of the viruses of polio. Why, that was one of the most ridiculous things in the world. Thirty-five years ago Roy Rife showed them these things.

“These machines demonstrate that you could cure cancer- all crazy notions of usurping the rights of the AMA notwithstanding. They definitely could take a leaf out of Roy Rife’s book and do an awful lot of good to this world for sickness and disease. As a consequence, we have lost millions of people that could have been healed by Rife’s machines.”

“I like Roy Rife. I’ll always remember Roy as my Ideal. He had a tremendous capacity for knowledge and a tremendous capacity for remembering what he had learned. He definitely was my Ideal. Outside of old Teddy Roosevelt, I don’t know of any man any smarter than him and I’ll bank him up against a hundred doctors because he did know his stuff with his scientific knowledge in so many lines. He had so many wrinkles that he could have cashed in and made millions out of it if he had wanted to and I do mean millions of dollars. Which would have benefited the human race, irrespective of this tremendous thing that he built which we call the Rife ray machine.”

“In my estimation Roy was one of the most gentle, genteel, self-effacing, moral men I ever met. Not once in all the years I was going over there to the lab, and that was approximately 30 years, did I ever hear him say one word out of place.”

“All the doctors used to beat a path to Rife’s lab door and that was a beautiful lab at one time. It was beautifully arranged inside. The equipment was just exactly right; his study was just wonderful. It was a place of relics and the atmosphere could not be duplicated anywhere.”

(It is noteworthy that even though Rife entered the realm of vivisection, he at least showed the compassion to fix the damaged animals.)

More Cosmic Tones

For some time there have been “Rife instruments” on the market, using his frequencies in an electrode-pad configuration, and sold for research purposes. But that r.f. beam ray, that was the “magic,” technologically speaking, at least. And now an instrument has appeared claiming to be a re-creation of the original (see “Revival and Caution” below). Rife would probably have been the first to question whether the beam deals with the underlying disease condition. In this respect, I would like to suggest a consideration of the beam in terms of both the microzyma and the yogic principle of the chakras.

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In yoga, the chakras (“wheels” or vortices of energy) are said to be the “organs” of the subtle body (the energy blueprint of the being). They are tuned to light frequencies corresponding to the colors of the rainbow. One’s personality, physical and physiological qualities, and even the health of the individual are said to arise from their infinitely complex configurations and their interactions with other fields. They are also spiral vortices through which the meridians of acupuncture flow. By way of the neurolymphatic reflexes and neurovascular points of the body, these flowing energies are intimate with the systems, organs, cells and chemistry of the physiology.

In terms of what was suggested earlier about the cosmic microzyma, consider what Christopher Hills, yogi and physicist, has written:

“… (It is) very likely that the chromosome, when exerting its biochemical effects in replication is NOT an indivisible unit with all its many constituents, in a precise, unchanging hereditary chemical pattern existing from one generation to the next. It is, of course, subject to evolutionary CHANGE. Yet in their function, these chromosomes have to be capable of precise replication, so they must spontaneously aggregate into patterns of LIFE (consciousness of form), which is characterized by the chemical environment in the nucleus of the cell. Any change in this immediate environment, such as a change in the specific frequency of a sharply selected energy, of radiation, of light, of electromagnetic waves or of sound, may alter not only the structural relationship of the molecules in the cell nucleus, but also their biochemical and genetic activity.”

(Taken from pp. 813-814 of Nuclear Evolution, a work on the physics of Consciousness published in 1977, almost one century after Bechamp created the name “microzyma.”)

“Consequently, what if the Rife beam, in addition to its resonant effect on microforms, was influencing the frequency balance of the chakras or the balance and freedom of flow in the meridians, perhaps doing what might be called R.F. Acupuncture, and perhaps ultimately “tuning” the microzymas? This might constitute a sufficient rebalancing of the being, or an altering of its vibrational condition, to be considered curative; and it might be maintained if the individual were subsequently to nurture their psychobiological terrain, which includes “the chemical environment in the nucleus of the cell.”

Leading the Horse to Water

What more could the scientific world have been waiting for than what Rife showed it? Significantly, he was not working in a vacuum but had the attention and support of respected biomedical scientists and doctors, including Dr. Edward C. Rosenow of the Mayo Clinic; Dr. Arthur I. Kendall, Director of Medical Research at Northwestern U. Medical School; and Dr. Milbank Johnson, member of the board of directors at Pasadena Hospital in California. As Lynes informs us, newspapers reported on Rife’s work, including significant clinical success. And as noted, no less a prestigious organization than the Franklin Institute did a detailed report on him. But, not only did the medical establishment (AMA) turn its back on Rife and his safe, effective means of eradicating cancer symptoms, but it systematically conspired to destroy him-which it did not once, but twice. Thus, Bechamp and then his unwitting supporter, Rife, geniuses of the caliber of Copernicus, Galileo and Lavoisier, were rubbed into obscurity. (While on this note, we might remember another genius pleomorphist, Wilhelm Reich, who died miserably in an American prison for attempting to bring truth to light.)

It didn’t take much to see that if Pasteur’s noxious poisons could garner even a semblance of success, the monetary potential would be stupendous. Thus, his greatest claim to fame ought to have been the inauguration of the “calamitous prostitution of science and medicine to commercialism” (Hume). Research facilities modeled after the one opened in 1888 in Paris, and used for brutal experimentation on living animals, as well as the production and sale of vaccine drawn from sickened bodies, came into existence all over the world. Bechamp’s brilliant expositions took second place to the dawning of a “new” era. It was the era of stone-hearted torture of fellow creatures and cruelty to our own species. It was the era in which bacterial disease symptoms were supplanted over time with a second wave of modern chronic fungal “infection.” Surfing this wave of degenerative mycotic infestation-officially unacknowledged as such-partially comprising heart disease, cancer, diabetes, so-called autoimmune disease and AIDSyndrome, were the profiteers, supported by arrogant, single-minded adherence to a scientifically and philosophically flawed, superficially plausible, and financially exploitable model of life and health.

Lynes tells us that Rife found himself in the path of Morris Fishbein, the Hitlerian ruler who headed the AMA from the mid-1920s until 1949, when he was forced from his position by a revolt among doctors. In Chicago, Fishbein had gotten wind of a clinic in San Diego using Rife’s beam-ray method of eliminating cancer symptoms. When refused a buy-in, he used his influence to bring the manufacturing company down in court for operating without a license. This blow to medicine in the late 1930s was a major step in suppressing the knowledge of pleomorphism, the mind-boggling Rife Universal Microscope, and the amazing radio frequency beam instrument used in the clinical setting.

In the second wave of suppression, the establishment (FDA) “Elliot-Nessed” a factory established in the 1950s by Rife and associate John Crane to manufacture the beam ray instrument. Everything was destroyed, records confiscated, and every practitioner possessing a unit was pursued and forced to surrender it as illegal.

Many other courageous individuals have been a part of the process of bringing the hidden truth about microorganisms and their symptogenic properties to light. One of the most significant is Dr. Virginia Livingston-Wheeler. Though she is discussed in the main text, she deserves another mention as a key figure who also faced suppression-the stress of being made invisible-by the sciomeds (power structure of scientific medicine). She published a book in 1983, The Conquest of Cancer, and, according to Lynes, wrote many articles and made presentations to science societies, including the New York Academy of Science, and international conferences. Lynes reports that she once returned from a presentation at an international symposium in Rome to find that her research funds with a major hospital had been canceled and the laboratory closed. During the four or five decades following the first establishment backlash at Rife, several other scientists, including Dr. Eleanor Alexander-Jackson, Dr. Irene Cory Diller, and Lida Mattman, Ph.D. (cell-wall deficient forms), stood in the face of intimidation to continue the valiant, yet feeble, tradition of unbiased biomedical science.

Revival and Caution

There is now afoot, as recently shown on the television show “Strange Universe” (March, 1997), a movement to revive the Rife beam-tube technology. Equipment was shown, as were moving pictures of the lysis of several unidentified microorganisms implied to be culprits in disease. Testimonies were given by a few people saying that they, or people they knew, have been helped by this beam ray. While this is an interesting and promising development, a note of caution is very much in order, so that folks do not end up like Rife’s guinea pigs, being put to death by a violent Herxheimer reaction. I believe the approach I recommended by is safer-more holistic and harmonically based in that we make the environment dissatisfactory to these symptoms of disease, so that instead of exploding on the spot and spewing poisons, they simply “pack their bags and leave.” That is, they will, of themselves, devolve into stages of the pleomorphic cycle consistent with the frequencies natural to a harmonious terrain; or will become so devitalized that the immune system can easily trash them.

It is hoped that this overview has given a provocative taste of what lies obscured in the history of biology. The reader is encouraged to explore the Hume and Lynes books especially, as well as that of the beacon of 19th-century bioscience, Antoine Bechamp: The Blood and Its Third Anatomical Element. 

A Note of Emphasis:

In this writer’s opinion, it is a poverty of compassion, the utmost arrogance, faultiness of perspective, and an error of science to inflict self-generated human miseries on innocent animal species in research laboratory experiments. Each year some 100 million animals are killed. Though many such experiments are used as references in this book, this is not a sanction. It is done to show the kind of results being ignored by “authorities” who believe in these methods, to accommodate professionals who live by them, to appease reductionist minds, and to suggest that enough is enough.  Human development and quality of life are unlikely to improve in any way by this torture of fellow creatures, unless such change occurs in the heart to make such practice unthinkable. The benefit to science and society is highly speculative and frequently negative. Let the experiments be done on human volunteers, whose physiology at least lends some logic to the process. Thalidomide was animal tested. Aspirin will kill a cat. Sheep can eat arsenic.

The habitual basis for vivisection is not founded in true science, but in profound alienation from nature and detachment from the nature of being. It continues out of species prejudice and an egocentric machismo that feeds on conquering nature via destructive analysis. It continues out of a merry-go-round intent to keep laboratories busy, researchers working, and to keep the research supply industry rolling in money. And it continues out of the habitual ignore-ance of the principles of wellness, which have long been in place in many forms. The fault for our rampant “diseases” may be ascribed to such ignorance and not laid at the feet of helpless animals, who play no part except to suffer for us and to die by the hundreds of millions. This is an insult to the Creation, not to mention an ecological disaster from the disposal of bodies. And to make matters worse, much of the research is based upon biased and erroneous science.

But the bottom line is, though we have the power over these creatures to inflict our cruelty on them, to do so may have dire consequences, given a Universe that operates on balance. Individuals of compassion and conscience may wish to consider opposing, through words and actions, this Frankensteinian madness. 

General References 

[1]  Bechamp, Pierre Jacques Antoine. The Blood and Its Third Anatomical Element .(Montague R. Leverson, translator). London: John Ouseley Limited, 1912.

[2]  Bird, Christopher. Gaston Naessens. Tiburon, Cal.: H.J. Kramer, Inc., 1991.

[3]  Bird, Christopher. To Be or Not to Be?. A paper presented in an address to L’Orthobiologie Somatidienne Symposium 1991, Sherbrooke, Quebec, hosted by Gaston Naessens.

[4]  Hills, Christopher. Nuclear Evolution. Boulder Creek, Cal.: University of the Trees Press, 1977 (out of print).

[5]  Hume, E. Douglas. Bechamp or Pasteur? Ashingdon, Rochford, Essex, England: The C.W. Daniel Co. Ltd., 1923.

[6]  Kalokerinos, A. and Dettman, G. Second Thoughts About Disease/ A Controversy and Bechamp Revisited. Warburton, Victoria, Australia: Biological Research Institute [booklet published from an article in Journal of the International Academy of Preventive Medicine-, July 1977; 4(1)].

[7]  Lynes, Barry. The Cancer Cure That Worked! Fifty Years of Suppression. Queensville, Ontario, Canada: Marcus Books, 1987.

[8]  Margulis, Lynn and Sagan, Dorion. Micro-Cosmos. New York: Summit Books, 1986.

[9]  R.O. Young, Sick and Tired, Reclaim Your Inner Terrain.  Woodland Publishing, Orem, Utah, 1999.

[10]  R.O. Young, S.R. Young, The pH Miracle, Hachette Publishing, New York, New York, 2010.

 

 

Pathological Blood Coagulation and the Mycotoxic Oxidative Stress Test

 Robert Young PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa and Universal Medical Imaging Group

Abstract

Historical analysis suggests that conventional understandings of Disseminated Intravascular Coagulation (DIC) may be misguided; further examination may be necessary.  Here, a theoretical analysis provides an alternative explanation for DIC pathology; it is suggested that the cause and mechanics of DIC are largely due to the proliferation of several intravascular microforms and their associated metabolic toxic acidic waste products — Mycrozymian Acidic Toxins (MAT) and Exotoxic-Mycotoxic-Producing Microorganisms (EMPO).  The Mycotoxic Oxidative Stress Test (MOST) is presented here as an easy, inexpensive and non-invasive alternative to conventional measurements for the detection of intravascular  acidic toxins, DIC  and oxidative stress.

Introduction and Historical Perspective

More than 150 years ago, British physician T. W. Jones asked the question, “Why does the blood circulating in the vessels not coagulate?”[1]  though a general answer to this question is now obvious, the biochemical mechanisms involved in how the blood coagulates (clots) are complex and varied, and all the intricacies have not yet been explained. A. Trousseau, recognized that the blood of cancer patients is in a hyper-coagulable state in the process of coagulation, even while confined in the blood vessels.[2]  The name given to this discovery is still in use today, as “Trousseau’s Syndrome.”[2]  Early in his career, Rudolph Virchow, the Father of Pathology, was interested in thrombosis and embolism.  He speculated that intravascular blood could be altered so it would clot as a result of a stimulus too weak to clot normal blood.[3]  In 1856 Virchow delivered a lecture setting forth this concept.

Although the concept of partial clotting within vessels reaches back to the beginnings of modern medicine, much of the discovery of its biochemical mechanisms – the activation of clotting factors – has been left to chance.  The admission of a patient to the hospital with an unceplained bleeding disorder challenged researchers to discover the cause of hemorrhaging.  Analysis of blood from normal persons helped in the study of the patient with the blood disorder. A new clotting factor was hereby discovered which was missing from the  patient’s blood.  For this reason, several clotting factors have been named after the individuals in which they were missing: e.g., Christmas factor (factor IX)[4], Hageman factor (factor XII)[4].

In this article, the causes of pathological (intravascular) clotting will be described, as will various methods of detecting this condition, especially a blood test I call the Mycotoxin Oxidative Stress Test (MOST).

The Mechanics of Blood Coagulation

Blood clotting is a highly detailed chemical-mechanism involving many distinct components.  The problem for the hematologist hs been to understand it at the biochemical level.  Undoubtedly, efforts to fully understand blood clotting will continue for many more years.

Recalling Antione Bechamp’s[8] and Gunther Enderlein’s[9] research into the sub cellular living elements and combining this with what is known of colloidal flocculation[6], it is suggested that the clotting of blood begins with the end-linking (polymerizing) of the fundamental protein unit called by Bechamp the microzyma[8].  A chain of these living units constitutes fibrinogen, which is still dispersed 9micro-hetergenous0 in the blood, and it may or may not be further processed.  If processing continues, it will be either by continued end-linking or by cross-linking.  End-linked fibrinogen is referred to here as fibrin monomer, which I have suggested is a repair protein also dispersed in the blood. Due to a number of blood clotting factors, the process may continue until the excess fibrin monomer and/or until fibrin becomes excessively end-linked.

Cross-linking the polymerized strands to form a three-dimensional network results in what is called the hard clot (fibrin – the major protein of clotting blood).  Factor XIII, which instigates the forming of these blood networks. is always present but latent in the blood, and must be activated before the formation can occur.  Persons who are producing fibrin monomer or excessively linked fibrinogen are said to be in a hyper-coagulable state, while those having diminished  ability to form clots are in a hypo-coagulated state.  It is the activation of the colloidal clotting factors which is so complex.  Blood clotting may occur through many pathways and be initiated by many different stimuli.  Regardless of initiation factors, the process is a sequence of events in which the activation of one factor triggers another, until, after a series of discrete steps, fibrin is formed.

When blood is clotted prematurely, and the factors involved are consumed (incorporated into) the body recognizes a deficiency of clotting agents and generates more.  Thus, people with a tendency to clot excessively will alternate between a hyper coagulable state and a hypo-coagulatable state.  When in the hypo coagulated state, such people hemorrhage until the deficient clotting factors are replaced.[4]  When only fibrin monomer or excessively linked fibrinogen is formed (no cross-linking), it is quite subtle and may go undetected.  It may be detected by a change in blood viscosity (sedimentation rate), by the Mycotoxic Oxidative Stress Test (described later), or by other more subtle means.  If strands of fibrinogen are cross-linked, however, a suggicient amount of insoluble precipitate of fires may result, and these can be detected microscopically using a phase contrast and dark-field microscopy in prepared slides of fresh tissue or blood.  An excessive formation of fibrin leads to  an impairment in circulation, and eventual organ failure usually results.[5]

With this background, we are in a position to consider a standard medical term: disseminated intravascular coagultion (DIC).[6]  This term encompasses the hyper coagulable state, i refer to as pathological blood coagulation which consists of both insoluble and excess dispersed polymers of colloidal proteins.

Key Ingredients of Pathological Blood Coagulation

Before discussing DIC in more detail, it si necessary to introduce its fur important ingredients according to this view – mycotoxins, endotoxins, exotoxins, and tissue factor.  Any of these elements, or any combination of them, can play a major role in initiating unwanted DIC.[6]  However, mycotoxins or the acids from yeast have been found to be the underlying element which instigates and intensifies the participation of the other three.[6]  Each will now be described in turn and brought into the clotting picture.

(Micrograph 1: left, shows normal hyper-coagulated blood in a healthy blood clot sample and right, hypo coagulated blood in an unhealthy blood clot sample)

Mycotoxins and Metabolism by Fermentation

As discussed in the main text of my published book, Sick and Tired book[7 ]. acidification of blood and body tissues and organs and the accompanying lack of oxygen lead to pathological metabolic fermentation, which is carried out primarily by yeast and mold.  Such pathological microorganisms, or their precursors, ar inherent to the human body and to all higher organisms.  Their precursors according to Bechamp, the microzymas, carry on a nominal and homeostatic fermentation themselves. under healthy conditions.[8]  The primary function of yeast and mold is to decompose the body upon the death of the animal or human organism.  Their premature overgrowth indicates a biochemical environment akin to death.  During pathological metabolic fermentation, high concentrations of several acidic substances called mycotoxins are created.  They are highly damaging, always acidic, metabolic products.  If not immediately buffered by specific antioxidants, such as hydrogen peroxide and the hydroxyl free-radical, mycotoxins can seriously disrupt the physiology by disrupting normal metabolism and by penetrating blood and body cells and poisoning them.  As will be seen, they interact with many of the mechanisms for DIC in various pathological symptomologies.

In my published article called The Finger on the Magic of Life: Antoine Bechamp, 19th Century Genius (1816-1908),  I discuss pleomorphism in some detail.[7] Understanding this phenomenon – the rapid evolution of microorganisms across traditional taxonomic  lines is helpful in getting a complete picture of DIC.  Briefly stated, collodial living microzymas evolve intracellularly into more complex forms (microorganisms), beginning with a healthy primitive stage comprising of repair proteins.  As the disease condition worsens, morbid intermediate forms (filterable bacteria or viruses, cell-wall deficient forms and full bacteria) develop from repair proteins, or directly from microzymas.  A third macrostage comprises the commonly recognized culminate microorganisms which are yeast, fungus to mold.  In terms of pleomorphism, all of these microorganisms represent a single family of variously functioning forms.[8]  The culminate forms produce the lions share of acids, which are mycotoxins and the primary focus of my research.[7][8][9]  For convenience, bacteria, yeast, fungus and mold that produce acidic metabolic wastes and protein cellular fragments called exotoins, endotoxins and mycotoxins will here be referred to collectively ash EMPO, or exotoxic, mycotoxic-producing microorganisms.

What follows is a shortened description or the description and origin of several exotoxins and mycotoxins, referred to collectively microzymian acidic toxins of MAT, which are involved in the processes leading to DIC.  The bio-effects, or the pathology of cellular fermentation, of these toxic metabolites are know as mycotic illness, mycotoxicosis, or mycotoxic stress as seen in the MOST and described and published by Dr. Bolin in the 1940’s.[10]

One such metabolic product is acetyl aldehyde, which is formed by  cellular breakdown of food, especially carbohydrate and the birth of  EMPO.  Acetyl aldehyde can also break down into a secondary substance know as ethyl alcohol.  Although acetyl aldehyde presents an immediate hazard to health and well-being, nature has provided a means of buffering of neutralizing this acidic by-product of cellular digestion and fermentation almost as soon as it is created.[11] The controls of acetyl aldehyde (and ethyl alcohol) are the sulfur amino acids, cysteine, taurine, methionine and the peptide glutathione which is found in red blood cells and almost all cells utilizing oxygen.[12]  In an attempt to buffer or neutralize MAT, the body will also bind or chelate both fats and minerals to them.[12]

Another member of the MAT family is uric acid, which is formed by the digestion of protein and the creation of EMPO.[13]  Uric acid can also break down into secondary substance, on of which is alloxan.[14] This has been shown to damage the insulin-producing pancreatic beta cells leading to diabetes [Refer to Tables 1 and 2]

A shortage of alkalizing nutrients or an excess of MAT initi­ates an immune response in which a special class of free radicals which I call microzymian oxidative buffering species (MOBS) are released.[15] These oxygen metabolites carry unpaired electrons and are intended to disrupt bacteria, yeast, fungus and mold, and buffer exotoxins, endotoxins, and mycotoxins. Current medical savants believe that they can disrupt just about any­thing they contact, including healthy cells and tissue: this is not accurate. The fact is that MOBS carriers a nega­tive surface-charge and repel healthy cells, which also have a negative surface-charge. [16] It is the positively surface-charged bacteria, yeast/fungus, mold, exotoxins, endotoxins, and myco­toxins that MOBS bind too.[17]  This aspect gives some insight into autoimmune phenomena, which are not, as is often maintained, the result of an overburdened immune system. They result either as a side-effect of the immune system’s attempt to remove foreign or toxic ele­ments, or as a direct attempt by the immune system to remove cells or tissue rendered useless or disturb­ing to the body by MAT.

In every degenerative symptomatology I have studied, I have found excessive MAT and MOBS (see Tables 1-3). Some of these degenerative symptoms and their underlying disease conditions, including cancer are described in my recently published paper on a deficiency on alkaline nutrition and cancer. [15] But the fact that myco­toxins cause harm to humans and other animals is purely a secondary effect, since, as noted, the prima­ry function of the microorganism is not to cause illness. We know from the fossil record that pleomorphic microforms existed long before animals.[19] In fact, humans and animals developed in terms of micro­organisms.[20] The reverse, however, is not true. Since micro­organisms appeared first in the developmental sequence, they are not physiologically aware of humans and animals. There is much evidence that human and animal physiologies are highly aware of, and respond to MAT – these acidic compounds signaling the presence of bacteria, yeast, fungi and/or mold or  EMPO.[21].

Endotoxins

Also involved in the process leading to DIC are endotoxins, substances endogenous to symptogenic (i.e., “pathogenic” in orthodox terms) bacteria. Endotoxins are a family of related substances having certain common characteristics, but differing from one bacterial form (or strain) to another. Endotoxins are lipopolysaccharides (LPS). LPS form a widely diversified group because of (1) the number of long- chain fatty acids composing lipids; (2) the number of individual sugars as well as their modes of linkage to one another; (3) the branching of sugar chains; and (4) the number of possible arrangements of these units. Endotoxins also contain proteins, further com­pounding the structural diversity.[22]

One theory on endotoxin states that its purpose is to act as a semi-permeable membrane for the bac­terium, limiting and regulating substances entering the organism.[22] Endotoxin resides solely on or near the interior surface of the cell membrane and is shed into the surrounding medium only upon the death of the bacterium. Thus, as these microforms die off, or are lysed by bodily activity, endotoxin is released. (This fact may well be an explanation for the Herxheimer reaction, in which a patient becomes worse following the administration of toxic drugs or other forms of treatment that drastically alter the associated organ­ism.[23]) Another endotoxin theory states that LPS are a constituent of the membrane, and as the organism grows, endotoxin fragments are repeatedly sloughed off into the medium. This phenomenon has been observed in the digestive tract.[24] Since bacterial translocation into the blood is not only possible but common where epithelial hyperpermeability exists, one can assume that the process will continue there. Both theories may be correct if we think of the first one as true of “adult” forms, and the second as true of newly developed and expanding ones.

Basic to the structure of an endotoxin is the lipid common to all forms, designated lipid A, to which is attached a “core” polysaccharide, identical for large groups of bacteria. To the core polysaccharide is attached the O-antigen, consisting of various lengths of polysaccharide chains which are chemically unique for each type of organism and LPS. These chains pro­vide endotoxin specificity.[25] Experiments conducted over many years indicate that most, if not all, of the toxic effects of an endotoxin may be attributed to the lipid portion, and it is sometimes used per se in experiments rather than the entire molecule.[26] An important additional feature of lipid A is its phos­phate content. Each phosphate group carries a nega­tive charge, and since lipid A is a rather large mole­cule, it provides, essentially, a negatively charged sur­face. The importance of this will be seen shortly.

Exotoxins

These are the metabolic excretions of bacteria. While endotoxin’s ongoing effect is, in a manner of speaking, in the background, exotoxins, like myco­toxins, present a double-edged sword. Not only do they initiate DIC, but they produce, or influence the body to produce, the various and numerous infec­tious symptomatologies, such as typhoid fever, diph­theria, etc. (See “Vaccination Reconsidered” in Section 4 of the Appendix of Sick and Tired for details on the action of diphtheria toxin.)[7] By comparison, mycotoxins not only initiate DIC, but there is much evidence to sug­gest that they produce, or influence the body to pro­duce, degenerative symptomatologies, such as arthri­tis, diabetes, etc., and cancer and AIDS as well.

Tissue Factor

Crucial to the understanding of DIC is recogni­tion of the role of tissue factor (TF), formerly known as thromboplastin. This transmembrane lipoprotein exists on the surface of platelets, vas­cular endothelial cells, leukocytes, monocytes, and most cells producing EMPO.[27] It plays a major role in several biochemical mechanisms leading to DIC.

TF is the primary cell-bound initiator of the blood coagulation cascade. Its gene is activated in wound healing and other conditions. By itself it is capable of initiating clotting, but also becomes active when complexed with factor VII or activated factor VII (Vila).[28] TF has been described as the receptor for factor VII because of the close association between the two proteins and because it causes a shape change (conformational) in factor VII, allowing it to attain activity. Both factor Vila and the TF/VII com­plex activate factors IX and X, which initiate the clotting cascade and the formation of thrombin.[29]

Development of Disseminated
Intravascular Coagulation
(DIC)

DIC Induced by MAT and Tissue Factor

An infusion of toxins into the blood has a direct effect on TF gene expression in leukocytes. Contact of MAT, endotoxins (lipid A), or exotoxins with leukocytes, activates proteins that bind to DNA nucleotide sequences, thereby activating the TF gene.[30] (See Tables 4-6.)

Endothelial cells damaged in culture by exotoxins, endotoxins, or mycotoxins attract polymorphonuclear leukocytes (PMNs), which adhere to the damaged cells. Once the leukocytes are bound, they can still have their TF gene activated if it hasn’t yet occurred, and they may release MOBS in response to toxins and to organisms of disease, possibly creating further dis­turbances. (Cellular disorganization then releases acti­vating proteins into the blood, which is discussed in more detail later.) Research shows that exotoxic and mycotoxic stress resulting in bound PMNs can be blocked by “antioxidants.”[31] These might better be called anti-exotoxins or antimycotoxins. Both observa­tion and study have led the author to conclude that cellular disorganization is initiated and primarily caused by fermentation pathology, not, as is the cur­rent belief, by the MOBS, or free radicals, generated to destroy toxins and microorganisms. MOBS or free radicals, because of their negative charge, are released to chelate or bind EMPO and MAT. It is suggested by current savants that free radical tissue damage is the secondary, “shotgun” effect of intense immune response to EMPO toxification and MAT-damaged cells. This could not be the case since healthy cells or their membranes carry a negative charge and would resist any electromagnetic attraction because of simi­lar charge. The concentration and instability of MAT generated in a compromised terrain, as opposed to the fleeting existence of free radicals, especially exoge­nous ones, also lead to this conclusion.

Endothelial cells grown in culture can be induced to express tissue factor. In one experiment, no procoagulant activity could be detected in the absence of toxins. However, the addition of mycotoxins from Aspergillus niger or Micrococcus neoformas (Mucor racemosus Fresen) resulted in procoagulant activity which reached a maximum in four to six hours and was dose-dependent. The same experiment was applied using E. coli and Salmonella enteritidis endo­toxin with a similar result.[32] A single intravenous injection of a mycotoxin from Aspergillus niger into experimental animals resulted in circulating endothelial cells within five minutes. In other exper­iments with the mycotoxin, detachment of endothe­lial cells from the basement membrane was noted.[33] (See Table 8.)

Removal of endothelial cells has dire conse­quences from two standpoints: First, the surface of these cells is covered with a specific prostaglandin (PGI2) known as prostacyclin. If blood contacts a surface not covered with PGI2, it will clot. For example, surfaces devoid of this prostaglandin are formed whenever a vessel is cut or punctured. An abrasion or other injury may also expose a surface on which PGI2 is lacking. The removal of endothelial cells by exotoxins or mycotoxins creates a surface devoid of PGI2, leading to blood clotting (see Table 7). Secondly, disorganization of endothelial cells cre­ates increased levels of EMPO and MAT which are attracted to an exposed surface (basement mem­brane) which expresses a negative charge. This also leads to clotting.

DIC Induced by Electrostatic Attraction

It was discovered in 1964 that blood will clot sim­ply from contacting a negatively charged surface.[34] Previously it was believed that the clotting process comprised a cascade of enzyme activity in which one activated the next, etc. The discovery that blood could be clotted simply by contacting a negatively charged surface ruled out the purely enzyme hypoth­esis. Only some of the known clotting factors have been shown to be enzymes.[35] As a result of this sur­prising discovery, detailed research was conducted in an attempt to describe the process. In some experi­ments, the negatively charged surfaces of selected, finely divided, inorganic crystals, including alu­minum oxide, barium sulfate, jeweler’s rouge, quartz, and titanium oxide, were considered.[36]

The clotting factor eventually shown to be activat­ed when whole blood contacted negatively charged surfaces was factor XII, also known as the Hageman factor. This is a positively charged protein migrating in an electric field (electrophoresis) toward the anode.[37] It is believed that factor XII is normally in the shape of a hairpin which binds to the negatively charged sur­face at the bend. Electrostatic attraction forces the two arms to lie flat on the surface, thereby exposing the inner faces and activating the molecule.

It was discovered that if the negatively charged particles were smaller than the clotting factor itself, activation was minimal. Or, if the concentration of clotting factor was too great, there was little or no activation.[38] Both of these observations indicated that the process was one of electrostatic attraction between the negatively charged surface and the clot­ting factor, which is a “basic” protein, that is, posi­tively charged.[39]

Activation of factor XII allows the activation of factor XI, which then activates factor IX. Thus, the blood clotting cascade continues to the formation of fibrin in the normal manner.[40] However, due to a series of activations begun by contact of factor XII with a negatively charged surface, trace amounts of factor Xa also show up in the blood. Factor VII is activated to Vila by factor Xa. Factor Vila then acti­vates factors IX and X, leading to the formation of thrombin. Factor Xa, with co-factor Va, continues the clotting cascade until fibrinogen is activated, leading to fibrin formation.[41] (See Table 5.)

As discussed earlier in terms of prostacyclin, beneath endothelial cells is another surface—the basement membrane. Called the extracellular matrix, it is a thin, continuous net of specialized tis­sue between endothelial cells and the underlying connective tissue. It has four or more main con­stituents, including proteoglycans (protein/polysac- charide).[42] The removal of endothelial cells by’MAT exposes this membrane, which is negatively charged by virtue of its sulfonated polysaccharides in the pro­teoglycans. This brings a reduced negatively charged surface into direct contact with the blood, which activates factor XII and the clotting cascade.[43]The positively charged toxic components of MAT also activate factor XII, as do disturbed disorganized cells, yeast/fungus cells, moldy cells, and the phos­phate groups in the lipid A component of endotoxin. (See Tables 2-5.)

To summarize this section, exotoxic, mycotoxic, and oxidative stress resulting from the overgrowth of bacteria, yeast/fungus, and then mold, has multiple actions, all leading to disseminated intravascular coagulation:

MAT activation of tissue factor gene in leukocytes; subsequent activation of factors VII, IX, and X, resulting in the blood clotting cascade.

MAT activation of tissue factor gene in endothelial cells, again leading to the clotting cascade.

MAT damage to endothelial cells, resulting in neu­trophil attraction, with TF gene activation and generation of MOBS, which, in turn, neutralize MAT, protecting healthy endothelial cells or the basement membrane and supporting the janitorial services of the leukocytes.

Removal of negatively charged endothelial cells by positively charged exotoxins, endotoxins, and mycotoxins, creating a surface devoid of PGI2, also exposes the negatively charged basement membrane, leading to the activation of factor XII and initiation of the clotting cascade. Positively charged components of EMPO, exotoxins and mycotoxins, and several other elements, including the lipid A component of bacterial endotoxin, also activate factor XII and the clotting cascade.

Endothelial Cells as Antithrombotics or Procoagulants

Normal, resting (unstimulated) endothelial cells show antithrombotic activity in several ways: (1) by the inhibition of prostacyclin (platelet adhesion and aggregation); (2) the inhibition of thrombin genera­tion; and (3) the activation of the fibrinolytic system, leading to clot lysis.[45] We will take a brief look at the thrombin aspect.

On the surface of endothelial cells is a protein called thrombomodulin, which acts as a receptor for thrombin. When bound to thrombomodulin, throm­bin can activate protein C. Activated protein C then catalyzes the proteolytic cleavage of factors Va and Vila, thereby destroying their participation in blood clotting. Thus thrombin, which normally activates fib­rinogen, plays an opposite role in this case and inhibits the clotting process.[46,47] (See Table 7.)

On the other side of the coin, the endothelial cell becomes a procoagulant agent when acted on by cer­tain lymphokines, such as interleukin-1. Not only can interleukin-1 induce TF gene expression, but it also suppresses transcription of the thrombomodulin gene in endothelial cells. As in other situations, the lymphokine-activated endothelial cell expresses TF on its surface as a result of TF gene activation. This leads to the production of thrombin and the trigger­ing of the blood clotting cascade.[48] (See Table 5.) Many lymphokines also stimulate adhesion of leuko­cytes to endothelial cells damaged by MAT, resulting in recycling of the cells by MOBS, as described later.

DIC Induced by Intracellular Exotoxic, Mycotoxic, Oxidative Stress by Bacteria, Yeast/Fungus and/or Mold

Any cell which has gone from an oxidative to a fer­mentative state can biochemically cause macrophage production of the lymphokine tumor necrosis factor (TNF). This protein has been shown to activate the gene for TF in fermenting cells, which are so behaved due to morbid evolution of bacteria, yeast/fungus, and then mold.[49,50] In the author’s view, a cell having been switched entirely to fermentation metabolism as a result of a physical or emotional disturbance of that cell, is what constitutes cancer (see Tables 5 and 13). (One might argue that this definition does not fit all “forms” of cancer, such as leukemia, for example. This is because leukemia is not cancer, but an immune response to the rise in EMPO and MAT in the body, and a relatively easy compensation to correct.)

The surface of many disorganizing or fermented cells (cancer cells) is characterized by small projec­tions in the plasma membrane which pinch off, becoming free vesicles containing toxins as well as TF complexed with factor VII. These vesicles can aggre­gate and/or lodge anywhere, ultimately releasing their contents. Also, the presence of excessive amounts of TF/factor VII complexes on the surface of fermented cells allows the formation of a fibrin net around the cell and around the entire mass of cells (tumor). This seems to be an attempt by the body to encapsulate and contain the mass. However, fermented cells do escape from the primary fibrin net, perhaps due to some electromagnetic effect, and become free-float­ing in the circulation. They may thus lodge elsewhere and instigate the fermentation of other cells by fungal penetration or by poisoning them and provoking a morbid evolution of their inherent microzymas.

Because of the surrounding fibrin net, these mobi­lized fermenting cells are protected from collection by the immune system while in transit.[51,52] (See Table 4.) The blockage or dissolution of fibrin net forma­tion by an anticoagulant such as heparin allows freed, fermenting (metastasizing) cells to be dismantled by natural killer cells and other immune cells (see Tables 5, 12 and 13).

DIC Induced by MAT/EMPO and Immune System Response (Release of MOBS)

Unsaturated fatty acids are highly susceptible to EMPO as well as MAT. Linoleic acid, a long-chain fatty acid present in white cells, has 18 carbons and 2 unsaturations. Subjected to MAT, linoleic acid binds the exotoxin, endotoxin, or mycotoxin, there­by forming an epoxide at the first unsaturation.[53] Research has revealed that this compound, named leukotoxin, is highly disturbing to other cells. It caus­es platelet lysis, thereby releasing TF and initiating DIC.[54] (See Table 10.) The fact that MAT result in fermented fats lends further credence to the sugges­tion that the initial and primary degenerative damage to structures and substances in the body is caused by exotoxins and/or mycotoxins, and that damage by MOBS, or by other free radicals, is not possible.

Another mechanism leading to DIC is the release of a special glycoprotein, sialic acid, from the terminal ends of cell-membrane polysaccharides, where it is always found. Polysaccharides play a highly significant role in biochemical processes, with both enzymes and membrane receptors recognizing various groupings of specific sugars linked in highly specific ways.

Immediately preceding the release of sialic acid in the polysaccharide chain is the sugar galactose. The sialic acid/galactose arrangement is utilized as a biolog­ical indicator of cellular and molecular aging. As cells age, sialic acid is naturally expressed from the terminal ends of polysaccharides, thereby exposing galactose. A membrane-bound enzyme from the liver, galactose oxi­dase, recognizes galactose and eventually disorganizes it, disrupting cell function integrity and hastening demise. Aged red blood cells, which have expressed a significant amount of sialic acid, are removed from the blood by this process. (I theorize that the biological ter­rain may be at work in normal cell aging. That is, the rate at which sialic acid is expressed is determined by the levels of corrosive acids in the system and the body’s ability to remove them, although there are no doubt intracellular factors at work as well.)

I suggest from my years of  clinical research  that cellular breakdown is compounded by the fermentation of the galactose by the microzyma. This is a process that begins from within and not necessarily from without. Not only does this action create more sialic acid, it creates other toxic waste products such as acetic aldehyde, alcohol, uric acid, oxalic acid, etc. The increase in cellular disturbances and fermenta­tion of the galactose creates biochemical signals for more galactose oxidase. This leads to greater cellular disorganization and developmental morbidity, espe­cially in the red blood cells, and a rise in the level of detrital serum proteins, which encourages clotting. From this perspective, diabetes, arthritis, atheroscle­rosis and other symptomatologies become more clearly “degenerative” (see Tables 2-5, 12 and 13).

Fibrinogen is a rather elaborate protein having the structure of three beads on a string. Expressed on the end beads is sialic acid, which indicates the beginning of disorganization of the fibrinogen and a declining negative charge to the positive. Prior to the declining charge and the expression of sialic acid on the end beads, fibrinogen, which is negatively charged, will not polymerize the healthy blood due to mutual repulsion. However, fibrinogen will poly­merize to damaged cells, EMPO, MAT and other positively charged areas of the body for repair pur­poses. Thus, as more and more sialic acid is expressed, there will be a significant reduction in the charge of the fibrinogen, acting as the primary requirement for the polymerization of fibrinogen (hypercoagulable state). The resulting polymer, fib­rin monomer, is the protein chain used in the repair of cells and clotting of blood.[55] End-linking will take place after the release of sialic acid (positive charge) by whatever means.

With this background, it is interesting to note that blood taken from persons suffering from anxiety is expressing sialic acid from fibrinogen, and is halfway toward clotting. Hormones released during anxiety states are easily fermented, giving more momentum to MAT and thereby resulting in this important change in fibrinogen. It leads to a clotting pattern characteristic of anxiety stress, and is readily identi­fied in the MOST. As can be seen in this picture, the pattern is a “snowstorm” of protein polymeriza­tions measuring from 2 to 10 microns.

allergiesbefore

 

 

 

 

 

 

 

[Micrograph 2: An Anxiety Profile showing a ‘snowstorm’ of 2 to 10 micron protein polymerizations starting from the center of the clot and moving out towards the edge]

As mentioned earlier, despite the attempt by the body to neutralize EMPO and MAT, an excess will initiate the release of MOBS by immune cells. A major MOBS is superoxide, designated chemically as O 2. It may exist alone or be attached to another ele­ment, such as potassium (KO’2) or sulfur (SO). Again, however, nature has provided a means of pro­tecting healthy cells—their negative charge[1]. Another protection against superoxide is the enzyme superox­ide dismutase (SOD), also found in all healthy cells.

A second member of the MOBS family is hydro­gen peroxide (H202). This molecule is very unstable and tends to react rapidly with other biological mol­ecules, damaging them. The release of hydrogen per­oxide in the body is a response to the overgrowth of decompositional organisms in a declining pH (com­promised biological terrain). The control for healthy cells against hydrogen peroxide is their negative charge and the protective enzyme catalase, one of the most efficient enzymes known.

When leukocytes and other white blood cells are stimulated by the presence of bacteria, yeast/fungus and mold, they treat these organisms as foreign par­ticles to be eliminated. During and prior to phagocy­tosis, the foregoing oxidative cytotoxins, along with the hydroxyl radical (OH’), are generated and released specifically for neutralizing microforms or harmful substances. This release is referred to as an “oxidative burst.” As a result of fermentation and the production of exotoxins and mycotoxins that fer­ment galactose from cells, the immune system is activated. An oxidative burst is released to neutralize the morbid microforms and mycotoxicity.[56] Like other biological processes faced with constantly alarming situations, the continued release of MOBS can get out of control. This may damage endothelial cells, the basement membrane, or other body ele­ments, and this activates fibrinogen to fibrin monomer (repair protein), leading to DIC [see Table 9]. Interestingly, the white blood cells capable of neutralizing MAT through MOBS production are the same ones capable of phagocytosis, the process by which foreign matter, waste products and microor­ganisms are collected and dumped in the liver.[57]

To summarize this section, pathological microforms and their acids create DIC by a number of pathways:

Leukotoxin (linoleic acid bound to mycotoxin) is highly toxic to cells. It causes platelet lysis, there­by releasing TF and initiating DIC.

The expression or release of sialic acid residues from healthy cells that have been disturbed allows for the fermentation of galactose, creating exotox­ins and mycotoxins, biochemically activating galactose oxidase, which further disturbs and dis­organizes healthy cells. This cycle loads the blood with debris.

EMPO and MAT disturb fibrinogen, which releas­es sialic acid and reduces the charge, allowing it to polymerize into fibrin monomer and fibrin nets.

The presence of exotoxins, endotoxins, and myco­toxins and their poisoning of cells activates the immune system. White blood cells generate MOBS (e.g., superoxide [0′2] or hydrogen perox­ide [H202]). These substances bind to and neu­tralize EMPO and MAT. MOBS are repelled by healthy endothelial cells and the basement mem­brane because of their negative charge. Cellular disturbances and disorganization stimulate the generation of fibrin monomer for repair purposes, leading to DIC.

Detection of Disseminated Intravascular Coagulation

The Sonodot Analyzer

The Sonoclot Coagulation Analyzer provides a reaction-rate record of fibrin and clot formation with platelet interaction. An axially vibrating probe is immersed to a controlled depth in a 0.4 ml sample of blood. The viscous drag imposed upon the probe by the fluid is sensed by the transducer. The electronic circuitry quantifies the drag as a change in electrical output. The signal is transmitted to a chart recorder which provides a representation of the entire clot for­mation, clot contraction and clot lysis processes. The analyzer is extremely sensitive to minute changes in visco-elasticity and records fibrin formation at a very early stage. The Sonoclot has been evaluated scientif­ically and shown to provide an accurate measurement of the clotting process.[58,59]

One application of the Analyzer has been the development of a test to distinguish non-advanced breast cancer from tumors that are benign. The ratio­nale for the test is the hypercoagulable state seen in cancer patients (Trousseau’s Syndrome), resulting from the generation of TF by leukocytes (mono­cytes).[60] (See Table 4.)

Fibrin Degradation
Products and Fibrin Monomer

DIC can be seen as a two-step process. First, fib­rinogen, which is always present in the blood, is acti­vated by any of several mechanisms. This activation leads to an automatic polymerization (chain forma­tion) resulting in fibrin monomer. This is not apparent in a microscope unless the blood is allowed to clot, as in the MOST.[61,62] The second step is the precipitation or deposition of fibrin (hard clot) by several other mechanisms. One of these is the formation of cross­links through the action of factor XIII. Another such mechanism may be poor circulation in an organ already blocked by deposited fibrin. The deposition of precipitated fibrin may be detected microscopically in tissue sections and diagnosed as DIC.[62]

Because fibrin monomer is not readily detected, a chemical test for it is of immense value in diagnosing DIC. Research has indicated that its detection may be very useful in the early diagnosis of DIC and MAT.[63] There are three fundamental physiologic areas related to blood clotting: (1) the prevention of blood clotting, (2) the clotting of blood, and (3) the removal of clotted blood once it has formed.

Enzymes are present that are capable of removing (lysing) clotted blood, one of which is plasmin. Another enzyme, plasminogen, is always present in the blood, but is inactive as a proteolytic agent. Plasminogen acti­vator converts plasminogen to plasmin, which can degrade deposited fibrin. This process is not specific for fibrin, however, and other proteins may be affected. When fibrin is degraded (fibrinolysis), fibrin monomer, as well as several other products, are formed. Commercial kits are available for the analysis of fibrin degradation. This test is an indirect measure of the pres­ence of DIC and MAT.[64]

Other tests include:

Protamine Sulfate: Protamine sulfate is a heparin binder sometimes used in surgery for excessive bleed­ing. The test, which indicates fibrin strands and fibrin degradation products, is conducted in a test tube, with fibrin monomer and fibrin forming early and polymer­ization of fibrin degradation products occurring later.[65] Ethanol Gelation: A white precipitate is formed by the addition of ethanol to a solution in a test tube containing fibrin monomer as a degradation product of fibrin, indicating DIC and MAT.[66]

The Mycotoxic Oxidative Stress Test (MOST)

Up to now, blood chemistries have been the prima­ry mode of diagnosis or analysis for the presence of pathology. In the view presented here, the bright-field microscope, is used to easily and inexpensively reveal a disease state as reflected by changes in certain aspects of blood composition and clotting ability. DIC is char­acterized by the abnormal presence in the blood of fib­rin monomer. When allowed to clot, blood containing such an abnormal artifact will exhibit distortions of normal patterns. The presence in the blood of soluble fragments of the extracellular matrix and soluble fibronectin, as well as other factors, will also create abnormal blood clotting patterns as described below.

A small amount of blood from a fingertip is con­tacted with a microscope slide. A series of drops is allowed to dry and clot in a normal manner. Under the compound microscope, the pattern seen in healthy subjects is essentially the same—a dense mat of red areas interconnected by dark, irregular lines, completely filling the area of the drop. The blood of people under mycotoxic/oxidative stress exhibits a variety of characteristic patterns which deviate from nor­mal, but with one striking, common abnormality: “clear” or white areas, in which the fibrin net/red blood cell conglomerate is missing.

BowelCancerLive Blood Dried Blood_0166

 

 

 

 

 

 

 

 

[Micrograph 3; An abnormal clot with striking ‘clear’ or white areas or protein polymerization as seen in the hyper coagulated blood of a patient with lower bowel imbalances]

Why the fibrin net is missing may be understood from the following: Two peptides—A and B—in the central protein bead of the fibrinogen structure become bound in the cross-linking process. There are two ways this can be configured: (1) Thrombin is capable of activating peptides A and B, resulting in the formation of a polymer loosely held together only by hydrogen bonds; (2) With peptides A and B acti­vated normally, the resulting hard clot is insoluble, indicating that the peptides are linked by covalent bonds. The difference in bonds results from factor XIII, an enzyme which links the two fibrin strands with a glutamine-lysine peptide bond.

Additional research has shown that the release of sialic acid from fibrinogen inhibits the action of factor XIII, resulting in a soft, white clot. In addition, acetic aldehyde has been shown to inactivate factor XIII directly. The soft clotting, compounded by other polymeric aggregations (described below), results in clear areas in the dry specimens. In the opposite extreme, high serum levels of calcium, for the pur­pose of neutralizing MAT, activates factor XIII, lead­ing to excessive cross-linking of fibrin to form a clot harder than normal. This is reflected in the MOST pattern characteristic of definite hypercalcemia— that of a series of cracks in the clot radiating outward from the center, resembling the spokes of a wheel. High serum calcium is the body’s attempt to com­pensate for the acidity of mycotoxic stress by pulling this alkalizing mineral from bone into the blood. This demand creates endocrine stress in turn, because reabsorption of bone is mediated by parathormone (PTH). Therefore, this clotting pattern indicates cal­cium deficiency and thyroid/parathyroid imbalance.

calciumpattern

 

 

 

 

 

 

 

[Micrograph 4: A mineral deficiency or more specifically a calcium deficiency pattern associated with an imbalance of they thyroid and/or parathyroid}

Advanced research has shown that there are seven carbohydrate chains in fibrinogen (each terminated by sialic acid). A second action of factor XIII is to ferment a large amount of carbohydrate during clot­ting. Because carbohydrate is most often water solu­ble, the loss of this material undoubtedly adds to the insolubility of a clot, while pathological retention contributes to the softness of the abnormal clot.

Clinical experience demonstrates that the MOST is a reliable indicator of exotoxic and mycotoxic stress and, concurrently, of various disorganizing symptoma­tologies associated with fermentative and oxidative processes. As various cellular degradation occurs, the blood-borne phenomena which accompany such symptoms as diabetes, arthritis, heart attack, stroke, atherosclerosis and cancer show up in the MOST, often with sialic acid beads in the clear areas of poly­merized proteins. (Determination of the liberation of sialic acid from carbohydrate has been approved by the U.S. Food and Drug Administration as an accept­ed indicator for cancer, and is clinically available.)

sialicacid

[Micrograph 5: Sialic acid beads are seen inside the protein
polymerization of the hypocoagulated blood as black dots]

The extent and shape of the clear areas are reflec­tive of particular symptomatologies which have arisen from the way in which the disease condition manifests in a given individual. This observation is borne out by having the patient undergo appropriate alkalizing therapy. With success of treatment based on the patient’s freedom from symptoms, sense of well-being, and live blood exams discussed in the main text of Sick and Tired, Reclaim Your Inner Terrain, Appendix C,[7] repeated analysis with the MOST reveals a progressively improving clotting pattern.

[Micrographs 6 and 7: Medically diagnosed cancer patient with large polymerized protein pools (PPP) in the hypo-coagulated blood above. In the picture below PPP’s have significantly reduced in size and the blood is moving to a more hyper-coagulated state as a result of reducing acid loads with an alkaline lifestyle and diet (7, 70)]

Because of its very nature, the MOST is emi­nently suited to reveal and measure the presence in the blood of abnormal substances, clotting factors, and disorganization of cells due to an inverted way of living, eating, and thinking, which gives rise to MAT. The MOST indicates both the direct and indirect activity of MAT on blood clotting, endothelium, and the extracellular matrix (described next), as well as on biochemical pathways, including hormonal ones. The generation of excessive MOBS in response to EMPO and MAT, the inability that accompanies all degenerative symptoms to neutralize or eradicate EMPO and MAT, and the recognized hyper- and hypocoagulable states seen in various symptomatolo­gies, will beyond doubt be revealed in the MOST.

Aspergillusnigercrystal

 

 

 

 

 

[Micrograph 8 and 9: Medically Diagnosed HIV/AIDS micrograph showing above an Aspergullus niger mold crystal using dark field microscopy and below a hypocoagulated blood clot with systemic protein polymerizations measuring in excess of 40 microns using bright field microscopy}

HIV

 

 

 

 

 

 

As mentioned, hormones are easily fermented, and this will show up as a hypocoagulated blood pattern in the MOST. It is my opinion, this hypocoagulated blood appears in the MOST as misty clouds of protein polymerizations throughout the clot, as seen in the accompanying picture.

poorfibrin

[Micrograph 10: Poor fibrin interconnection in the clot associated with endocrine or hormonal imbalance]

The MOST from Solubilized Extracellular Matrix

There is now a clearer picture of the biochemical rationale for correlating abnormal blood clotting patterns with the presence of degenerative symptoms.  A link between symptoms and the distorted clotted blood patterns has been delineated in the MOST.
Another reason for the abnormal clotting patterns accompanying pathological states, in addition to insufficient bonding of fibrinogen peptides as seen in the MOST, is presence in the blood of water-soluble fragments of the extracellular matrix.

Extracellular Matrix Degradation by MAT

The extracellular matrix (EM) is a three-dimen­sional gel, binding cells together and composed of five or more major constituents: collagen (protein), hyaluronic acid (polysaccharide), proteoglycans (pro- tein/polysaccharide), fibronectin and laminin. Also included are glycosaminoglycans and elastin.[67] In every degenerative disease studied by this author, evidence has been found for MAT activity destruc­tive of EM.

One of the proteolytic enzymes activated in response to EMPO and MAT is alpha-1 antitrypsin (capable of neutralizing MAT), normally not active in the presence of the enzyme trypsin. The active por­tion of this anti-exotoxin and antimycotoxin contains the amino acid methionine, which includes a C-S-C linkage. When chelated by the hydroxyl radical (one of the MOBS oxidants), methionine’s central sulfur atom acquires one or two oxygen atoms (forming the sulfone or sulfoxide respectively). The fermentation of methionine is a secondary effect of immune response to an alarming situation, intended to neutral­ize MAT and prevent degradation of the EM. Once alpha-1 antitrypsin is exhausted, MAT will have more access to the EM. If the EM is damaged beyond repair, then the enzyme trypsin is released to disorganize and recycle the cells involved.[68]

A similar scenario holds for the enzymes collage- nase and elastase. Thus, the absence of alpha-1 antitrypsin in the presence of EMPO and MAT activates three enzymes which degrade the extracellular matrix. Degradation of the EM by enzymes and MAT puts into the blood the water-soluble fragments (proteins and glycoproteins) of normally insoluble EM components (see Table 11). The presence of these fragments modifies the normal clotting pattern (described below), as seen in the M/OST, and is therefore an indication of EM degradation, which is always found with degenerative symptoms. (Also present is fibrin monomer, which has been found in the blood of patients suffering from collagen dis­ease.[69] See Table 11.)

Fibronectin is a molecule in EM having several binding sites for various long-chain molecules— heparin (a sulfonated polysaccharide) and collagen, for example. As such, it functions as a cellular glue, bind­ing cells together as well as various components of the EM. A soluble form of fibronectin is normally found free in the blood, and enters into the formation of a blood clot through the action of factor XIII. This form of fibronectin binds to fibrin. Elevated, bound-serum fibronectin results from EM fragmentation by MAT, and accompanies degenerative symptoms such as arthritis and emphysema (collagen diseases).

Water-soluble fragments of the EM bound by fibronectin form a three-dimensional network or gel in the pathologically clotted blood (fibrin and com­ponents of the blood clotting cascade). Since fibronectin binds to both fibrin and collagen, the two polymeric networks are superimposed and intermin­gled, resulting in a modification of the normal clot­ting pattern. Exactly how the pattern is modified depends upon the nature of the collagen abnormally present, the nature and extent of hyaluronate pre­sent, and the degree to which EM fibronectin has been released by MAT.

Conclusion

Thus, it is easily seen that there are many forms which the pattern of clotted blood may take, depending on the individual and the internal terrain that produced the modifying substances. The MOST reveals not only the presence of exotoxic and mycotoxic stress, but indicates as well the nature of the symptom(s) resulting from the stress (see Table 12). Since MAT underlie the entire complex of events which degrade the extracellular matrix, I must conclude that the absence of these exotoxins, endotoxins and mycotoxins would provide substantial improvements in tissue integrity and the overall physiology and functionality of the organism or animal and human.

­

­

References

[1]  Jones, T.W., “Observations on some points in the anatomy, physiology and pathology of the blood.”  British Foreign Medical Review, 1842. 14 : 585.

[2] Trousseau, A., Phlegmasis alba delens. “Clinque Medicale de L’Hotel Dieu de Paris.”, 1865, 3:94

[3]  Virchow, R., “Hypercoagulability: A review of its development, clinical application, and recent progress.”  Gesammelte Abhandlungen our Wussenschaftlichen Medizin, 1856, 26:477.

[4]  Rapaport, S.I., “Blood Coagulation and its Alterations in Hemorrhagic, and Thrombotic Disorders.”  The Western Journal of Medicine, 1993; 158: 153.

[5]  Hamilton, P.J. et al., “Disseminatied Intravascular Coagulation: A Review.”  Journal of Clinical Pathology, 1978, 31: 609

[6] The Harper Collins Illustrated Medical Dictionary, 1994, p.13.

[7] Young, RO, “Sick and Tired, Reclaim Your Inner Terraine,” Woodland Publishing, 1999.

[8] BeChamp, A., “The Blood and Its Third Anatomical Element,”  Hikari Omni Publishing, 1999.

[9]  Schwerdtle, C, Arnoul, F, Enerlein, G, “Introduction to Darkfield Diagnostics”, Semmelweis-Verlag (2006).

[10]  Hawk, BO, Thoma, GE, Inkley, JJ, The Evaluation of the Bolen Test as a Screening Test for Malignancy*, cancerres.aacrjournals.org on December 5, 2015. © 1951 American Association for Cancer Research.

[11]  Uchida, K., “Role of Reactive Aldehyde in Cardiovascular Diseases”,  Labortory of Food and Biodynamics, Nagoya University Graduate School of Bioagricultural Sciences, Nagoya, Japan , Free Radical Biology and MedicineVolume 28, Issue 12, 15 June 2000, Pages 1685–1696

 [12] Chang JCvan der Hoeven LHHaddox CH, “Glutathione reductase in the red blood cells”,  Ann Clin Lab Sci. 1978 Jan-Feb;8(1):23-9.

[13] Kutzing, MK, Firestein, BL, “Altered Uric Acid Levels and Disease States”, Department of Cell Biology and Neuroscience (M.K.K., B.L.F.), Graduate Program in Biomedical Engineering (M.K.K.), Rutgers University, Piscataway, New Jersey. Address correspondence to: Dr. Bonnie L. Firestein, Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854-8082. E-mail: firestein@biology.rutgers.edu

[14] Claudino, M,. Ceolin,,DS, Alberti, S.,  Cestari, TM,  Spadella, CT, Fischer Rubira-Bullen, IR, Gustavo Pompermaier Garlet, Gerson Francisco de Assis, ” Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats”,  Published: December 19, 2007. DOI: 10.1371/journal.pone.0001320

[15] Young RO (2015), “Alkalizing Nutritional Therapy in the Prevention and Reversal of any Cancerous Condition. Int J Complement Alt Med 2(1): 00046. DOI: 10.15406/ijcam.2015.02.00046

[16] Heloise Pöckel FernandesCarlos Lenz Cesar, and  Maria de Lourdes Barjas-Castro, “Electrical properties of the red blood cell membrane and immunohematological investigation”, Rev Bras Hematol Hemoter. 2011; 33(4): 297–301. doi:  10.5581/1516-8484.20110080 PMCID: PMC3415751

[17] Harris, JO, “The Relationship Between the Surface Charge and the Absorption of Acid Dyes by Bacterial Cells”, Department of Bacteriology, Kansas Agricultural Experiment Station, Manhattan,Kansas, Received for publication March 3, 195.

[18] Young, RO, “Metabolic and Dietary Acids are the Fuel That Lights the Fuse that Ignites Inflammation that Leads to Cancer”. https://www.linkedin.com/pulse/metabolic-dietary-acids-fuse-ignites-inflammation-causes-young. 2015.

[19] Snaders, R, “Did Bacteria Spark Evolution of Multicellular Life?” Berkeley News, Research, Science and Environment,  October 24, 2012.

[20] Wenner, M, “Humans Carry More Bacterial Cells than Human Ones”. Scientific American, November 30th, 2007.

[21} Animals and humans respond to MAT as a poison.

[22]  Morrison, D.C. et al. The effects of bacterial endotox­ins on host mediation systems. American Journal of Pathology, 1978; 93: 526.

[23]  Ibid.

[24]  Ibid.

[25]  Van Deventer, S.J.H. et al. Intestinal Endotoxemia. Gastroenterology, 1988; 94(3): 825-831.

[26]  Morrison, D.C. et al., op. cit.

[27]  Ibid.

[28]  Hu, T. et al. Synthesis of tissue factor messenger RNA and procoagulant activity in breast cancer cells in response to serum stimulation. Thrombosis Research, 1993; 72: 155.

[29]  Rapaport, op. cit. (Ref. 4).

[30]  Ibid.

[31]  Mackman et al. Lipopolysaccharides—mediated tran­scriptional activation of the human tissue factor gene in THP-1 monocytic cells requires both activator protein 1 and nuclear factor kappa B binding sites. Journal of Experimental Medicine, 1991; 174: 1517.

[32]  Yamada, O. et al. Deleterious effects of endotoxins on cultured endothelial cells: An in vitro model of vascular injury. Inflammation, 1981; 5: 115.

[33]  Colucci, M. et al. Cultured human endothelial cells: An in vitro model of vascular injury. Journal of Clinical Investigation, 1983; 71: 1893.

[34]  Cho, T.H. et al. Effects of Escherichia coli toxin on structure and permeability of myocardial capillaries.

[35]  Acta Pathologica Japonica, 1991; 41: 12.

[36]  Rapaport, op. cit. (Ref. 4).

[37]  Ibid.

[38]  Margolis, J. The interrelationship of coagulation of plasma and release of peptides. Annals of the New York Academy of Sciences, 1963; 104: 133.

[39]  23-25. Ibid.

[40]  Morrison, D.C. et al., op. cit.

[41]  Rapaport, op. cit. (Ref. 4).

[42]  Alberts, B. et al, eds. Molecular Biology of the Cell. New York: Garland Publishing, Inc., 1989 (2nd ed.), p. 818.

[43]  Rapaport, op. cit. (Ref. 4).

[44] Bertz, A., et al. Modulation by cytokines of leukocyte endothelial cell interactions. Implications for thrombo­sis. Biorheology, 1990; 27: 455.

[45]  Rapaport, op. cit. (Ref. 4).

[46]  Nachman, R.L. et al. Hypercoagulable states. Annab of Internal Medicine, 1993; 119: 819.

[47]  Ibid.

[48]  Tallman, M.S., et al. New insights into the pathogene­sis of coagulation dysfunction in acute promyelocytic leukemia. Leukemia and Lymphoma, 1993; IT. 27.

[49]  Silberberg, J.M., et al. Identification of tissue factor in two human pancreatic cancer cell lines. Cancer Research, 1989; 49: 5443.

[50]  Grimstad, I.A. et al. Thromboplastin release, but not content, correlates with spontaneous metastasis of can­cer cells. International Journal of Cancer, 1988; 41: 427.

[51]  Gunji, Y. et al. Role of fibrin coagulation in protection of murine tumor cells from destruction by cytotoxic cells. Cancer Research, 1988; 48: 5216.

[52]  Sugiyama, S. et al. The role of leukotoxin (9, 10- epoxy-12-octadecenoate) in the genesis of coagulation abnormalities. Life Sciences, 1988; 43: 221.

[53]  Ibid.

[54]  White, A. et al, eds. Principles of Biochemistry. McGraw-Hill Book Co., New York, 1964, p. 648.

[55]  Mueller, H.E. et al. Increase of microbial neu­raminidase activity by the hydrogen peroxide concen­tration. Experientia, 1972; 23: 397.

[56]  Young, Robert O. Fermentology and oxidology. The study of fungus-produced mycotoxic species and the activation of the immune system and release of microzymian oxidative buffering species (MOBS). Self- published: InnerLight Biological Research Foundation, Alpine, Utah, 1994.

[57]Chandler, WL. et al. Evaluation of a new dynamic vis­cometer for measuring the viscosity of whole blood and plasma. Clinical Chemistry, 1986; 32: 505.

[58]  Saleem, A. et al. Viscoelastic measurement of clot for­mation: A new test of platelet function. Annals of Clinical and Laboratory Science, 1983; 13: 115.

[59]  Spillert, C.R. et al. Altered coagulability: An aid toselective breast biopsy. Journal of the National Medical Association, 1993; 85: 273.

[60]  Bowie, E.J. et al. The clinical pathology of intravascular coagulation. Bibliotheca Haematologica, 1983; 49: 217.

[61]  Muller-Berghaus, G. et al. The role of granulocytes in the activation of intravascular coagulation and the pre­cipitation of soluble fibrin by endotoxin. Blood, 1975; 45: 631.

[62]  Bick, R.L. Disseminated intravascular coagulation. Hematology/Oncology Clinics of North America, 1993; 6: 1259.

[63]  Bredbacka, S. et al. Laboratory methods for detecting disseminated intravascular coagulation (DIC): New aspects. Acta Anaesthesiologica Scandinavica, 1993; 37: 125.

[64]  Sigma Diagnostics, St. Louis, MO 63178; tel: 314- 771-5765.

[65]  Nachman, R.L. et al. Detection of intravascular coag­ulation by a serial-dilution protamine sulfate test. Annals of Internal Medicine, 1971; 75: 895.

[66]  Breen, F.A. et al. Ethanol gelation: A rapid screening test for intravascular coagulation. Annals of Internal Medicine, 1970; 69: 1197.

[67] Hay, E.D., ed. Cell Biology of Extracellular Matrix. New York: Plenum Press, 1981, p. 653.

[68]  Carp, H. et al. In vitro suppression of serum elastase- inhibitory capacity by ROTS generated by phagocytos- ing polymorphonuclear leukocytes. Journal of Clinical Investigation, 1979; 63: 793.

[69]  Wilson, C.L. The alternatively spliced V region con­tributes to the differential incorporation of plasma and cellular fibronectins into fibrin clots. Journal of Cell Biology, 1992; 119: 923.

[70] Young, RO, Young, SR, “The pH Miracle Revised and Updated”, Hachette Publishing, 2010.

Tables

Table 1

Expression of Sialic Acid/Galactose [MAT] from Cell and Protein Degeneration (From All Serum Proteins, RBC/WBC and Other Cell Surfaces)

  1.  Carbohydrate, Proteins, and Fats From Diet, Body Cells or Reserves
  2. As cells breakdown or ferment they give birth to bacteria, yeast, fungus and mold [EMPO] and their associated metabolic acidic waste [MAT]
  3. Exotoxins, Endotoxins, and Mycotoxins [MAT]
  4. Acetyl Aldehyde, Ethyl Alcohol, Uric Acid, Alloxan, Lactic Acid are examples of MAT
  5. MAT  Ferments Other Body Cells and their Extracellular Membranes and Proteins
  6. MAT Modifies Glycoprotein
  7. Binds to liver Galactosidase
  8. Creating an Increase in Cell and Protein Fermentation and Degeneration and Increased Amounts of Exotoxins, Endotoxins and Mycotoxins [MAT]

Table1a

Table 2

Expression of Sialic Acid [MAT] From the Fermentation of Degeneration of Insulin Producing Pancreatic Beta-Cells in Type I, Type II and Type III Diabetes

  1. Pancreatic Insulin producing Beta-Cells with no or minimal Surface Sialic Acid [MAT]A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Diet
  2. Normal regulation of Insulin Production
  3. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choicesdd
  4. Leads to cellular fermentation and degeneration and the birth of EMPO
  5. This lead to increased abnormal amounts of MAT that the immune system, the alkaline buffering system and the elimination organs has to deal with
  6. Fermenting and degenerating Insulin Producing Beta Cells
  7. Giving Rise to Surface Cell Sialic Acid [MAT}
  8. Increased Amounts of Sialic Acid Activates the Immune Response [MOBS] and Sialidase [AB]
  9. Leads to Lowered or No Insulin Production
  10. Symptoms of Type I, Type II or Type III Expressed
  11. The insulin producing beta cells of the Islets of Langerhans express silica acid on their surface as a break down metabolite.  I have suggested that when insulin producing beta cells are physically disturbed by MAT they begin to disorganize and express sialic acid on the surface of the cell.  This indicates the death of the cell and insulin production will stop.

Table2a

Table 3

HIGH BLOOD PRESSURE, ATHEROSCLEROSIS, HEART ATTACKS, STROKES, and CONGESTIVE HEART FAILURE

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the immune system to chelate the MAT.
  4. Increased amounts of MAT will cause endothelial breakdown and the expression of Sialic acid.
  5. Increased Amounts of Sialic Acid and damage to the endothelial will cause a reduction in the negative surface-charge leading to the release of Glycoproteins.
  6. The release of Glycoproteins will cause the activation of Factor XII and the blood clotting cascade.
  7. This cause the creation and formation of fibrin monomers and the increase of Platelet Deposition out of the red blood cells for clotting purposes
  8. The immune system will activate and MOBS will be released as well as sodium bicarbonate, calcium, lipids and other alkaline buffers to reduce metabolic acidity.
  9. The build-up of fibrin monomers in the clotting cascade will lead to fibrin nets and clots causing an increase in blood pressure and the risk of blockages potentially causing a Stroke or Heart Attack.

Table3a

Table 4

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING
FROM INTRACELLULAR DISORGANIZATION OR FERMENTATION WHICH GIVES RISE TO MAT
 AND EMPO

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the Tumor Necrosis Factor (TNF).
  4. Increased amounts of TNF activates the Tissue Factor Gene (TF)
  5. Increased Amounts of TF causes the release of Thromboplastin.
  6. The release of Thromboplastin activates the release of clotting Factors VII (VIIa) and trace amounts of Factor Xa into the blood.
  7. This activates the release of Factors IX and X to IXa and the increase of Factor Xa.
  8. The activation of the blood clotting cascade leads to Disseminated Intravascular coagulation and the clotting or thickening of the blood inside the blood vessels.
  9. The DIC or hyper-coagulation will mask the fermentation of healthy cells to unhealthy cells or cancerous cells.
  10. As the unhealthy cells or cancerous cells increase the body will go into preservation mode and begin forming fibrin nets to encapsulated these unhealthy cells to protect healthy body cells.
  11. As body and blood cells breakdown from MAT this causes an increase of MAT and EMPO leading to systemic latent tissue acidosis and a potential metastatic cancerous condition.

Table4a

 Table 5

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING
IN CELLULAR DISORGANIZATION OR FERMENTATION/OXIDATON AND THE INCREASE OF MAT AND EMPO

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices.
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the Tumor Necrosis Factor (TNF).
  4. Increased amounts of TNF activates the Tissue Factor Gene (TF)
  5. Increased Amounts of TF causes the release of Thromboplastin.
  6. The release of Thromboplastin activates the release of clotting Factors VII and Factor Xa in the blood.
  7. This activates the release of Factors IX and X to IXa and the increase of Factor Xa.
  8. The activated blood clotting cascade leads to Disseminated Intravascular coagulation and the clotting or thickening of the blood inside the blood vessels.
  9. The DIC or hyper-coagulation will mask the fermentation of healthy cells to unhealthy cells or cancerous cells.
  10. As the unhealthy cells or cancerous cells increase the body will go into preservation mode and begin forming fibrin nets to encapsulated the unhealthy cells.
  11. This leads to tumor formation of the unhealthy or cancerous cells.
  12. As the body and blood cells breakdown this causes an increase of MAT and EMPO leading to an increased risk of  systemic metastatic cancer.

Table5aTable 6

ENDOTHEIAl CELL CONVERSION FROM AN
ANTITHROMBOTIC STATE TO A PROCOAGULANT STATE
CELLULAR DISORGANIZING PATHWAY

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This leads to increased abnormal amounts of MAT that damages the protective endothelial cover cells leading to a reduction of PGI2
  4. The absence of PGI2 causes the release of Interleukin-1 and/or Tumor Necrosis Factor (TNF).
  5. In addition the loss of protective endothelial cover cells leads to Tissue Factor Gene Activation and the release of Thrombin causing a pro-coagulate state leading to DIC
  6. Another pathway to DIC would be the loss of protective endothelial cover cells and the absence of PGI2 causes the suppression of Thromomodulin, Protein C leading to procogradulation and DIC.

Talble6

 Table 7

ENDOTHELIAL CELL CONVERSION
FROM AN ANTITHROMBOTIC STATE
(NORMAL PATHWAY)

Table7

Table 8

MECHANISM OF DISSEMINATED INTRAVASCULAR COAGULATION GENERATED BY MAT

Table8Table 9

ACTIVATION OF SIALIDASE AND MICROZYMIAN OXIDATIVE BUFFERING SPECIES (MOBS) BY EMPO AND MAT

Table9

Table 10

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING FROM PHAGOCYTIC OXIDATIVE BURST

Table10

Table 11

MOST BLOOD TEST and DISSEMINATED INTRAVASCULAR COAGULATION WITH SOLUBILIZED EXTRACELLULAR MATRIX

Table11

Table 12

TYPICAL SOURCES OF FERMENTATION INSULT (MAT) IN BIOLOGICAL SYSTEMS INITIATING DIC

Table12

Table 13

POSITIVE CHARGE OF CANCEROUS CELLS AND TUMORS AND THE FORMATION OF FIBRIN NETS AND TREES IN RESPONSE TO MAT

Table13

Acidity is the Cause of ALL Sickness and Disease!

There is only one sickness, one disease and one treatment.  The one sickness and one disease is the over-acidificaiton of the blood and then tissues due to an inverted way of living, eating and thinking.  The one treatment for ALL sickness and disease is to restore the alkaline design of the blood and then tissues with an alkaline lifestyle and diet.

cause-du-cancer

Acidity again and again,… it has not only been doc. Robert O Young crying loudly. The acidity of the blood and then tissues is the common denominator for ALL degenerative disease!

Continue reading Acidity is the Cause of ALL Sickness and Disease!

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