cancer & quantum biology

7/27/2019 Cancer & Quantum Biology

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Number of

Cancers

Radiation Exposure

Number of

Cancers

A.

Number of Cancers

Radiation Exposure

As the population was studied over the years, another study was done which found that a higher percentage of the peopleexposed did get cancer. Thus in diagram B, we can see that the supposition was that perhaps a straight-line function was what theexposure of radiation would look like.

B.

From diagram B, we may still surmise that there might be a safe level at which radiation is harmless.More years passed. Recent studies have shown that diagram C is a truer example of what happened at Hiroshima and Nagasaki.

Radiation Exposure

C.



As we can see, there is probably only a very small range in which radiation is safe.The results of Hiroshima and Nagasaki were devastating, not only in the short term, but also in the long term. Any entity on the

planet willing to use atomic weaponry is making a grave mistake.From our research in hormesis we have found that very small levels of radiation might have stimulatory effects on the human

body. So there might indeed be a safe level of radiation, but this level would be very, very minute (a homeopathic).It is known that one ionizing ray striking one cell could produce a mutation. It would be up to the body to neutral ize this

mutation; up to the immune

With this in mind, we must reevaluate the radiation statistics and the approach of the radiation industry in America. TheOccupational Safety and Health Association (OSHA) needs to look at a more quantic idea of what ionizing radiation could do. Industrystandards have not come close to really providing safety in the work area.

In our second factor of toxicity we find that the epigenetic and genetic information is attempted to be maintained through the process of metabolism.

Metabolism_ ))))))))))))))))))))))))))

G _ Detoxe _ En _ Pe _ It _ Gi _ E

c _ N _ ESIS

The emergent metabolic processes work through the incremental negative resistance factor, as displayed with electronics inour chapter on incremental negative resistance. Just as cue multipliers can be tuned for electronic circuits, theincremental negative resistance factors can be tuned to certain metabolic processes and certain vibratory sti

As Isaacs points out, there is a time-dependent increase in the probability of epigenetic and geneticinformation degradation in neoplasia. The second factor is that the influence which enhances the rate of the time-dependent information loss by alteration of the emergent metabolic process maintains the fidelity of the geneticand epigenetic information transport process. Thus this sense of a cycle, where information loss contributes toinformation loss, does so across a time-dependent factor.

Metabolism_ ))))))))))))))))))))))))))

G _ Detoxe _ En _ Pe _ It _ G

i _ Ec _ N

_ ETIC

Revici found that there were anaerobic vs. aerobic cancers, and there were many different types of cancers, including types thatwere acid-responsive or alkaline-responsive. In Revici's work they were classified by their shift in dualism, through the differentenvironments of the lipid control.

Thus in fatty acid deficiency states, where there are excess sterols, cancer might be developed because of the porousness of thecellular membrane, which is made up largely of fatty acids in calcium. In fatty acid deficiency states the membrane becomes porous andallows too many toxins and chemicals in and out of the cell, which can be cause for an alteration of the information process, and thus thetype of cancer.

This fatty acid deficiency was coupled with the change toward acidity in the human being, which he measured through changesin urine and blood pH, as well as changes in specific gravity of the urine, which would be toward quite thick ranges of one thousandthirty specific gravities. This variable of high specific gravity and low pH were found to be conducive of the type of cancer Revicilabeled as the acid-dependent or A type. This is somewhere between seventy and eighty percent of the types of cancers presenting in theUnited States, as we are in an over-increasing acid forming society.

The other type of condition would produce alkalinity, or high pH readings, correlated with low specific gravity readings of the



An Excerpt from the Advanced Treatise in QUANTUM BIOLOGY

The unhealthy frequencies were then sent through an invertor. The result of the inversion as well as the amplification wasamplification of healthy waves, and inverting or canceling out of the frequencies associated with the cancer cells.

Morra therapy has been largely utilized by only alternative practitioners in Europe and America. It was not until 1988 that Dr.

Nelson, this author, looked at radiation and found ways to perfect the Morra radiation. There were other bands outside the frequenciesreported by Dr. Morrel which also could cause and aggravate cancer.

Thus a true Mora unit had to be developed, which patients could carry with them to help cancel the frequencies in the long term.Such a unit has been under study by Dr. Nelson for several years, with outstanding results in the cancer field. This unit is now marketedas the Quantum Med C.I. in Hungary and is legal for import elsewhere.

The two big groups of neoplasms are carcinomas and sarcomas. They involve epigenetically differentiated tissues in which theemergent metabolic processes of information transfer have been dis rupted. Varied cells such as these cannot undergo proper sexualconjugation, and in some cases cannot undergo mitotic division, so they are not able to conserve their information. If the bad informationis passed on, we may have the process of carcinogenesis.

Some of the more wild and growing neoplasms come from organs in which the epigenetic information transfer ability is not lost, but enhanced , and thus the cell system starts feeding energy into reproduction, and the cell starts splitting at a wildly fast rate.

In more primitive species, where the cells have not developed sophisticated epigenetic conditions, we see much less cancer,much less neoplasia. These less sophisticated plant machineries have smaller numbers of hormones, as we have linked hormones to theepigenetic process. Thus, by having less epigenesis , we find that there is less chance of cancer. This also helps to show why somecancers are hormone-dependent, where the existence of the epigenetic phenomenon can help stimulate their growth into wildly developed

cycles.

Outline of the Metabolic Morphogen Cycle. A brief outline of the hypothesis we have presented inthis chapter follows.

1. The chromatin of the nucleus is the only molecule in the cell capable of self-reproduction. It consists of

nucleoprotein, which in turn is composed of a desoxyribonucleic acid and various protein

moietics containing the cytomorphogen determinants for the cell structure.

2. The reproduction of this chromatin is necessary for cell division, and also occurs constantly together with the dynamic state of

living proteins, as a part of the vital energy cycle of the cell.

3. The energy cycle is connected with phosphatase hydrolysis of the dipotassium salt of creatine-hexose phosphoric acid; the

synthesis of nucleic acids, and their change from ribo- to desoxyribo- forms; and possibly the radioactivity of potassium in the morphogen molecule and its influence on the stability of the biological colloids.

4. The morphogens that have participated in this constant energy reaction are broken-down or split and are eliminated into the

cytoplasm of each division, or at a slower rate in non-dividing cells. (The fact that after division ceases, aging

still proceeds with eventual lysis, proves that morphogens are still being "shed" by the nucleus.)

5. These split morphogens must not be confused with the cytomorphogens and protomorphogens that are secreted by the nucleus

into the cytoplasm at intervals to exert their histogenetic determinant effects.

6. The split morphogens in the cytoplasm are prevented from exerting lethal effects by a fatty or lecithin envelope, and are

further discharged into the surrounding media.

7. The split protomorphogens in the media are available as determinants for cytoplasm protein synthesis at the cell wall; in thismanner they are necessary to, and stimulate, growth. (In this effect they are not species-specific for they are

simplified to the point where their complexity no longer allows it. If the cytomorphogens and protomorphogens

present in the cytoplasm for determinant activity are experimentally extracted, they will also stimulate this

protein synthesis, but will retain the species specificity as a consequence of their complexity.)

8. The split protomorphogens are now back in the cytoplasm as a part of cytoplasmic protein. (Other mineral elements are also

present in the cytoplasmic protein that were supplied by the nutritive media.)

9. These protomorphogens, along with mineral elements and protein from the media, are now utilized at the nuclear wall for the

synthesis of new cytomorphogen and chromatin material. The dynamic state of cytoplasmic protein insures a

constant supply of protomorphogens at this point for chromatin synthesis.

10. Due to the fact that nuclear cytomorphogen synthesis utilizes many minerals associated with cytoplasmic protein but notnecessarily as morphogen linkages, the split protomorphogens in the media accumulate if the media is stagnant.




11. The increase in cytoplasmic and media concentration of polymerized protomorphogens causes a gradual breakdown of the

integrity of the surface boundary of the cell and consequently of the nuclear membrane. (The primary lethal

effect of split protomorphogens is exerted by the concentrat ion in the cytoplasm. The toxic effect of the

concentration in the media is simply due to its influence in preventing further discharge from the cytoplasm.)

13. This degeneration of the membrane results in a lowering of the electrical potential between the protoplasm and the media, and

between the cytoplasm and the nucleus.

14. Concomitant lowering of pH values in the cytoplasm and nucleus inhibits the constructive phase of the protoplasmic enzymes,

prevents repair and facilitates a general lowering of cell vitality.

15. As a consequence of lowered vitality and inhibition of protein synthesis, the synthesis of chromatin is impaired and mitosis

ceases.

16. Eventually the vitality and cell potential drop to the point where the integrity of the cell can no longer be maintained against

the physical forces of the environment; the cell "dies" and undergoes lysis.

17. This cycle may be broken by removal or dilution of the accumulating morphogens from the stagnant media, preventing the

development of lethal concentrations.

18. When cells are transferred to new cultures, they exhibit a time lag before commencing mitosis. This is the time necessary for

the cytoplasmic protomorphogens to be eliminated into the media in sufficient amounts to restore the catalytic

balance of intra- and extracellular protomorphogens necessary for commencement of mitosis. If the cell

contains depolymerized protomorphogen at the peak of its diffusibility, this time is negligible.

Virus as a Cause of Cancer

Many Decades ago, doctor called Vilhelm Ellerman and a vet called Olaf Bang were working together on chicken leukaemia.Leukaemia in th ose da ys was not e ven recognized to be a form of cancer. The two doctors soon discovered that they could transmi t the diseaseto healthy chickens using filtered blood taken from a diseased chicken. This discovery is the earliest evidence linking the viruses with cancer, bu t when it was publi shed in 1908 it received li ttle a ttent ion . A similar d iscovery was announced in 1911 by Peyton Rous of America, bu t thistime it concerned a recognized solid cancer of chicke ns. Rout cut out the cance rous t issue from diseas ed chicken breast s, added it to mineralsolution and then gr ound it up with san d. The resulting cell debris was then removed by centrifugation and the remaining fluid portion passedthrough a filter. The filtered fluid was completely free of cancer cells and yet when it was injected into healthy chickens they often went on todevelop cancer. Rous did not realize that the infectious agent responsible for transmitting the cancer was a virus. This fact slowly becameapparent over the coming years. A British doctor called William Gye was so impressed by this discovery that he wrote a book "The Cause of Cancer" declaring his belief that canc er was essentially a viral disease . Gye's belief that the mystery of cancer had been solved was somewhat

accurate but still premature.Rous and other scientists, in the mid-1930s, had proven that quite a few animal cancers were transmissible using filtrates of virus-

infected tissue ; but skepticism and disinterest remained the most common res pons e to t he emerging "virus t heory" of cancer. Much of the earlyreluctance to believe in the viruses as a cause of cancer probably stemmed from a simplistic Reductionistic desire to find just on e caus e of al l cancers. If viruses were to be accepted as that cause then cancer would need to behave like a typical virus infection. This was obviously not thecase, especially considering the lack of any excessively obvious pattern of person-to-person transmission.

John Bittner demonstrated for the first time thatnaturally transmitted viral infections could also caus e cancer. He found in 1936 that br east cancer could be pas se d on to newborn mice by an infec tious ag ent carried in their mother's milk. The infect ion was eventual ly identi fiedas a retr ovirus and is no w known as mouse mammary tumor virus (MMTV). The discovery of MMTV peaked interest in the possibility thatsimilar viruses might be involved in human breast cancer. Retroviruses have indeed since been occasionally involved in tha t disease . I n onestu dy, a retrovirus was fou nd in the milk of 60 per cent o f women who se families ha d a history of breas t cancer, but in only 4 per cent of womenwith no family history of the disease. Evidence was also obtained suggesting t hat a retroviral genome is often present wit hin breast cancer cellsthemselves. Such results, however, certainly do not prove that a retrovirus actuallycauses human breast cancer. In most people's opinion thequestion of whether or not viruses really are involved in causing human breas t cancer is still open . No-one wants to investiga te a theory thatsuggests that the cancer can be transmitted by breast- feeding in a similar way to t he disease in mice.

Bittner's early work demonstrated a problem. Seeking out a viral cause of any cancer, without taking other cofactors into

consideration, might be a drastically oversimplified approac h. He made the crucial observation that the involvement of MMTV in cancer i s nota simple story of infection followed by the inevitable development of cancer. Instead, the end result of an i nfection is dependent on at least twoother factors - the genetic make-up of the infected mouse and the prevailing levels o f various hormones. The virus will only cause cancer if the




overall constitution of an infected mouse is "right".After Bittner's discoveries, the viruses as carcinogens theory became accepted and research into t he ph enomenon began to accelerate

up to its present accelerated pace. A wide range of both retroviruses and DNA viruses are no w known to be undoubte d causes of cancer in

many types of animal including birds, cats, rodents, monkeys, cattle and humans. But the prospect of human viral relation to cancer was notaccepted in the 1940s. A few years ago, the talk was of "possible" or "suspected" links between viruses and human cancer; but the level of confidence has recently increased sufficiently for Professor Ant hony W ater son of London's Royal Postgraduate Medical School to declare "Atleast some human cancers are caused by viruses" although he quickly added "but not all - and perhaps not even more than a small minorit y

Proving allopathically that viruses are a factor in human cancer requires the ultimate test. Can the cancer virus demonstrate that itreally can cause cancer when healthy individuals are infected on purpose. This is possible when laboratory animals are the subjects but isclearly unethical even for Allopaths if performed on humans.

The application of the postulates of Robert Koch are so reductionistic that they are often inappropriate and simplistic at best . The four points are 1. The in fec tious ag ent must be present in the di seased tis sue. ( the fact tha t an agent might ca us e a metabolic error and leave escape dKoch) 2. The infectious agen t should be cultureable from the di seased tissue (some viruses being impossible to culture) 3. The culture should beable to cau se the dise ase in other organisms(ignoring the idea of co-factors. 4. Then the infection should be reculturable from the infected tiss ue.All of these postulates are simplistic and reductionistic and speak nothing of immunity, cofactors, toxicity, mental factors etc.

To develop a more modern day approach , we must consider some more non-linear thinking. The incidence of the particular type of cancer in question should obviously correlate with the incidence of infection by the susp ect virus. One important piece of evidence pointing tosuc h a correlation would be t he pr esence of antibodies directed agains t the virus more often, or in greater amounts in patients suffering from thecancer, than in healthy people. Infection with the virus should be seen to precede the onse t of cancer, rather than following on from and per haps

being a result o f carc inogenesis . The virus or some part of the virus (i ts genet ic mater ial for example) should be consi stent ly found inside thecancer ells. Next, virus purifi ed from the cancer cells should either cause cancer in laboratory animals, or else convert cultured human cells intocancer-like cells. A final and very convincing link implicating a virus in human cancer would be the demonstration that vaccinating peopleagainst the virus actually reduced their chances of suffering from the cancer.

One cancer that has responded to anti-viral homeopathic vaccination is liver cancer, or "primary hepatocellular carcinoma". This isthe cance r found in 80 to 90 per cent of all cases of "liver cancer" and when I speak of liver cancer in the discussion that follows, I am referringspecifically to primary hepatocellular carcinoma - by far the mos t common form of the disease. It is one of the top ten cancers world-wide andin much of the Third World it accounts for up to 30 per cent of all cases of cancer. As recently as the early 1970s most medical textbooks madeno mention of any possible viral involvement in liver cancer, a situation tha t has been rapidly transformed into the current view that hepatitis Bvirus infection is responsible f or (or at least crucially involved) mos t cases of the disease . This is despite the fact that hepatitis B virus infectionhas never be en cultivated in cell cultures, making even the direct demonstration that it causes cancer in animals or cultured human cellsimpossible. So the incrimination of hepatitis B in liver cancer provides an excellent example of the indirect methods forced upon virologists intheir quest for links between viruses and human cancer.The hepatitis B virus was found t o have a str ong correlation between the incidence of hepatitis B infection and liver cancer. In the first place,deaths from liver cancer are extremely common in t hos e parts of t he world (such as Africa and Asia) in which hepatitis B infection is alsocommon. Secondly, people who died of liver cancer are much more likely than the rest of the population to have suf fered from hepatitis B

infection in early life, or to be carriers of the disease.In 1975 and 1978 R. Palmer Beasley of Washington University identified over 3000 male Taiwanese civil servants who were carriers

of hepatitis B and over 19,000 who were non-carriers. In co-operation with Taiwanese scientists Beasely enrolled both groups into a research program to examine their future chances of live r cancer. The result s were impress ive. By the end of 1980, 41 men in the s tud y had contractedand died of liver cancer and all but one of thes e men came from the hepatitis B carrier group. Even suc h stro ng resul ts do not pro ve that thevirus actually causes the cancer, but having established that a correlation does exist, virologists then followed the case further.Man y studies have found a considerable excess of bot h hepatitis B virus antig ens a nd anti-viral antibodies in liver cancer patients, compared tothe amounts of these mater ials in healthy peopl e. Examining the actual cancer cells has proved even more interesting. In 1977, Larry Lutwick and William Robinson of Stanford were able to isolate hepatitis B virus DNA from liver cancer cells, and then a few years later it was shownthat the viral DNA was actually integrated into the cancer cells' own chromosomes. The hepatitis B virus genome had apparently become a permanent par t of the genet ic information carried by mo st of the cancer cells examined. Car riers of hepat itis B viru s were always found to haveviral DNA somewhere in their liver cells and the longer a person had been a carrier, the more likely it was that integra tion of the DNA wouldhave occurred. In some cases viral DNA was also found to be integrated into non-cancerous cells taken from a cancer patient's liver. The usualinterpretation of all thes e results is that integration of the viral genes takes place before a liver cell become cancerous, and tha t it is the activityor presence of the integrated genes that actually causes the cancer.

W e can see many of the criteria required to incriminate hepatitis B virus as a cause of human liver cancer. The virus has been linkedto the canc er on epidemiological and geographical groun ds; viral proteins and anti bodies against these proteins are more prevalent in cancer pat ients than the populat ion at large; viral genetic material is present within the ca ncer cells and there is good evidence to sugg es t that infectionwith the virus does precede the onset of cancer.

The evidence sugg esti ng that hepatitis B virus infection can ca use cancer now seems to be substantiable, with most researchers now being more interested in how the virus can give us cancer than in whether or not it really does . With the case against hepatitis B virusconsidered as proven (being blamed specifically for up to 80 per cent of all cases of primary hepatocellular carcinoma) the virus now standssecond only to cigarette smoking in the league table of known human carcinogens.

The discovery that hepatitis B virus "ca uses " primary hepatocellular carcinoma certainly does not mean either that it is t he so le cause,or that it can pr oduce canc er regardless of other aspects of the overall constitution of its victims. Remember the MMTV virus, which certainlycan c aus e brea st cancer in mice, but only if the genetic make-up and hormonal state of an infected mouse allows. Similarly, the consensus aboutmost liver cancers is that they are the cumulative result of several interacting factors, only one of which is hepatitis B infection. Some other factors sus pect ed of involvement are the victim's overall genetic make-up and st ate o f health, the condition o f the immune system, th e levels of various hormones an d exposure t o chemical toxins and carcinogens. In some cases, these other factors might unite to produce cancer withoutthe participation of hepatitis B virus, accounting for those cases of liver cancer that show no evidence of viral involvement. The co-factor Fractal research needs to be expanded to understand cancer better.

So liver cancer might be largely preventable, if only anti-hepatitis B homeopathic vaccines can prove to be successful. Severaldifferent hepatitis B vaccines are now available and at least one homeopathic vaccine developed by New Vistas in Denver. The initial stepstowards a possible gl obal effort t o eradicate the virus are currently under way. The evidence against some of the ot her suspected human cancer




For example, new genes become active within the nucleus of a transformed cell and new proteins appear within the cytoplasm. The chemicalcomposition of the cell surface chan ges, with some new proteins a nd carbohydrates appearing while others disappear. The rate at which somespecific materials are tr ansported i nto and o ut o f the cell becomes altered. The task faced by cancer researchers is to explain how carcinogens,

including some viruses, can bring about such drastic changes in a previously healthy and well-regulated cell.Many viruses can produce cancer, both those with a DNA genome and those whose genetic material is made of RNA. Butinterestingly, all of the RNA-containing cancer viruses are retroviruses. The retroviruses make a DNA copy of their genome which thenintegrates into the chromosomes of the infected cell. That the ret roviruses are t he only RNA viruse s known to cause cancer should assumeincreased significance when I tell you that mo st cells transformed into cancer cells by DNA-containing viruses also carry th e viral genes in anintegrated form. We have already seen, for example, that liver cancer cells often contain integrated hepatit is B virus DNA.

A general theory from studies of viral carcinogenesis is that when viruses transform cultured cells or produce real cancers, the viral gene s must us ua ll y b ec om e int egra te d int o the cancer cell DN A. Of course, by no means all of the viruses capable of transforming cells have been fully invest igated, an d there is evidence sugge st in g that in isola ted cases integra tion is no t an absol ute requirement for carcinogenesis. Butfrom the results so far, we can certainly say that at the very least, integration must make it much easier for a virus to cause cancer.

One theory is that t he actual act of integration is somehow responsible for producing the cancer. For example, the viral genes mightintegrate into the middle of, and therefore dest roy or cha nge, genes that are important for keeping the ho st cells healthy. Alternatively, simply by integra ting nearby important cellular gene s the viral genome might increase or decr ease the activity of thes e ge ne s, again leading to cancer .It is certainly well known that the activity of genes c an be strongly influenced by nearby sections of DNA, so the idea that neighboring viralgenes might disturb normal gene activity makes good sense.

Integration might simply serve to ensure that t he viral genes responsible for encoding suc h "cance r proteins" become a permanent part

of the cance r cells' genetic material. After all, a cancer i s a mass of rapidly dividing cells and if the viral genes did not become integrated , thentheir effect might quickly be diluted. The speed of cell division might prevent sufficient viruses from being produce d to keep all the new cellscancerous. Only integration of the viral genes would ensure that each new cell contained a copy of these genes to keep it cancerous.

Cancer may sometimes be pr oduced by viral proteins, sometimes result from integration of viral DNA at a sensiti ve site, withintegration in both circumstances serving to pa ss on t he viral genes to every cell in a rapidly expanding cancer cell population. Ma ny cance r viruses certainly do produce "c ancer proteins" t hat are directly responsible for transforming healthy cells into cancerous ones . And o f cours ecancer proteins must be encoded by genes - "cancer genes".

There are an unusual c lass of retroviruses known as the "acute transforming retroviruses". These viruses have been isolated fromvarious animal cancers throughout the world. If artificially administered to healthy animals they can produce cancer very quickly and withimpressive regularit y. One of them is the chi cken cancer virus discovered by Peyton Rous in 1911, which will transform virtually every cell itinfects. Unlike the acute transforming retroviruses, most other viruses linked to cancer can transform cells only infrequently, inducing thecancer-like s tate in only one in every 1000 to 100,000 infected cells. The most significant discove ry abo ut the acu te transforming retroviruses isthat t hey owe their cancer-causing prowe ss to specific genes that d o no t see m to have any other role to play in the life-cycle of the virus. The secancer genes (or "onc ogen es" ) were first detected by st udying mutant viruses that behaved as if a mutation in some gene had r emoved their ability to cause cancer.

New techniques of molecular biology were developed, then it became possible to chop up the v iral geneti c material ( in its double-

stranded DNA form) into gene-sized pieces. These pieces were then artificially introduced into cultured cells, where they would sometimesintegrate into the cell chromosomes and be used to make protein. This sort of experiment revealed that each acute transforming retroviruscarries one gene - the cancer gene - that can on its own transform cultured cells into cancer-like ones.

Something over 20 of these retroviral cancer genes are now known, having been isolated from different viruses that were found inchickens, turkeys, cats, rats, mice and monkeys. The discovery of single genes that can apparently cause cancer obviously aroused greatexcitement. Clearly the next step was to try to work out exactly what the proteins encoded by these cancer genes do . For most of the genes prog ress towards th at goal is stil l ra ther limited, but in mid-1983 two separate research teams c laimed that for the first time, the likely func tionof a viral cancer protein had been identified.

The two teams (one led by Russell Doolittle of the University of California and the other by Michael Waterfield of the British ImperialCancer Research Fund) had discovered that cancer protein produced by a retrovirus found in monkeys was almost identical to a naturallyoccurring human "growth factor". As the name suggests, growth factors are proteins that can stimulate cells to grow and divide. Now sincecancer is essentially unregulated cell growth and division, it makes g ood s en se that viruses should use growth factor, or growth factor-like, proteins to produce cancer. This might be one of the agents that t ip the pr ocess towards growth and away from metabolism.

Research has shown that the product of the viral cancer gene really does ac t very much like a growth f actor and has also uncover edanother retroviral cancer protein whose activities can be fitted into the same general cancer-causing scheme. In this second ca se, the cancer pro tei n is not a gr owth factor, but ins tead appears to resemble part of the cel l-surface receptor tha t binds to extracellular growth factors andcommunicates t he "start growing" mes sage to the re st of the cell. Again, the activity of this cancer protein within the cell presumably stimulatesthe normal cellular processes that lead t o growth and division, this time by mimicking the next step on in the natural seque nce. Thes e cancer genes are altered copies of the crucial cellular genes themselves, "stolen" by retroviruses from the chromosomes of the cells they infect.

Retroviruses can sometimes pick up a cellular gene and incorporate it into the viral genome. The activity of the cellular gene will then be contro lled by the regulatory regions of the vira l genome, which might make it much mor e active that it should be in a hea lthy cel l.Alternatively, the alterations the cellular gene that usually accompany the act o f hijack might make it produce an altered protein, and this altered protein might produce ca ncer rather than cell growth only when requi red . I should poi nt out thatany cellular gene c an probably be picked up bya retrovirus and i ncorporated into its genome, but only if the ge ne is a crucial one involved in the con trol of cell growth will the resulting hybridretrovirus be able to cau se cancer. The acute transforming retroviruses are formed when a retrovirus picks up a normal cellular gene involved incell growth and multiplication. The cell gene will either be crucial ly altered during this process, or else might be expressed at abnormal levels,in both cases leading to the onset of cancer.

Exactly what change in a gene's structure or expression can allow it to become a retroviral cancer gene is still the subject of speculation and further research. But the fact that retroviral cancer genesar e hijacked from the cell in this way seems to be firmly establ ished.The first sugges tion was th at by integrating into, or near, critical cellular gene s, a virus might alter the activity of thes e genes and so give rise tocancer. The study of the acute transforming retroviruses has revealed that there are at least 20 or so suitable genes within normal cellular DNA.

The acute transforming retroviruses alter the activity of the se genes b y actually having them incorporated into the viral genome. Might n ot other viruses alter the activity of the se genes simply by integrating into or next to them? There is a cl ass of cancer-causing ret roviruses known as the sl ow transforming retroviruses that may well be able to transform infected cells and cause cancer in just this way. The slow transforming




retroviruses d o not pick up the cellular genes that ap pear to have t he potential to ca use cancer, but in some cancers the viral gnomes ha ve beenfound integrated next to or actually within these crucial genes.

The main theory about thes e retroviruses is t hat the y ca use cance r by "switching o n" the activity of genes involved in cell growth and

multiplication simply by integrating near to them on the ho st cell chromosome; or by integrating into a gene t hey might make the gene cod e for an altered protein with an aggressive cancer-causing capability. Cancer brought ab out by t he slow transforming retroviruses is a slower a nd lessinevitable pr ocess than carcinogenesis due to acute transforming retroviruses. An acute transforming retrovirus comes supplied with its owncancer gene , so the transformation of an infected cell may be al most inevitable. When a sl ow transforming retrovirus causes cancer, it m ust firstintegrate next to an appropriate gene in an appropriate way - events which might both be rather unlikely. In rare cases t he very viruses thatnormally behave as slow transforming might be able to pick up one of the crucial cellular genes and so be converted into acute transformingretroviruses.

Retroviruses have at least two paths towards causing cancer available when they infect a cell. They can incorporate genes involved incell growth into the viral genome; changing the virus into an acute transforming retrovirus that will spread thro ughout the host ce lls, causecancer, and probably die along wit the host. Or they can influence the important cellular genes simply by integrating within them or nearby.Most retroviral infections of course, probably follow neither path - most of them are harmless.Apparently, normal healthy cells carry genes that, if abnormally expressed or altered in some way, have the pot ential to produce proteins t hatcan ca use cancer. When these genes become incorporated into the genome of an acute transforming retrovirus, or when they are activated bythe integration of a slow transforming retrovirus, then we can justifiably call them "cancer genes" - si nce i n su ch cas es t hey cl early do ca usecancer. But when the genes are sitting in their normal place within the cell chromosomes and are held in check by the control systems of ahealthy cell, then "potential cancer genes " is their most appropriate label ("proto-oncoge nes" is th e technical term). This label acknowledges the

fact that these genes ca n cau se cancer if they run out of control or are altered in some way, while recognizing that normally they do n ot ca usecancer at all. Indeed, they are believed to play absolutely crucia l roles in the life-cycle of healthy cell s - presumably mediating many of the keyevents during normal cell growth and multiplication (by encoding growth factors or growth factor receptors, for example).Proteins produced by the potential cancer genes only become "can cer proteins" when they are present in excess quantities or altered in someway, in bot h cas es l eading to cancer. Cancer is, of course , caused by many factors othe r than viruses. Far more important than viruses are thechemical carcinogens, radiations and so o n that are the traditionally accep ted causes of cancer. .So both retroviruses and non-viral carcino gensmay well caus e cancer by converting on e or more members of a small set of crucial cellula r genes, the potential cancer genes, int o c ancer genes proper . An appealing simplicity and unity, then, appears to be emerging from research into both viral and non-viral carcinogenesis: The healthy cells of the body contain the potential "seeds of their own destruction" in the form of a small se t of genes that control cell growth and multiplicationwhen working properly, but which can cause cancer when they become altered or forced to run out of control.

The solution of cancer and its cure will lie in the utility of nature' s medicine. As we learn more of the quantic per spect ive of biologyand it's subspace link we will improve our chances of understanding cancer. The lack of medicines acceptance into t he energetic values of medicine, has been a dramatic bottl eneck in ou r understandi ng. The frequencies of the microtubules in a cell can dictate the risk of cancer andits future pathway. Towards this solution this book was written.

MetabolismG ))))))))))))))))))))))))))

eneti Stimulated byc Hormone

Thus we can see the link certain tumors can have with hormones. Certain hormone-dependent or hormone-inhibited tumors can be influenced by changing the amount of hormone in the system, which affects the epigenetic process. Thus in the case of estrogen-dependent tumors, which have high growth rate, if the ovaries are removed and androgen is given to the organism, we can inhibit tumor growth, and if we are lucky, the tumors will degrade their information to such an extent that they will lose the ability to reproduce at a

wild rate, and possibly we might cure the patient and be able to return to the hormone of proper use.Many cancer chemotherapies work by their disruption of the epigenetic process. Since the epigenetic process is more enhancedin these wildly growing tumors, we can see how chemotherapy might be responsible for healing them. Because the chemotherapy agentsinterfere with epigenesis, they will have a more disruptive effect on cells that have over-accentuated epigenesis . He nc e t hechemotherapy agents will interfere more with that accentuated process.

To this ability, we can now turn to Hoxy as a source of different chemotherapy agents. Hoxy's father watched as different farmanimals that had cancer were turned out to pasture. They ate certain types of plants that seemed to help inhibit the tumor growth. Hoxy'sfather took some of these plants, and developed the Hoxy tonic, which utilizes much of the same types of chemotherapy agents used inmodern pharmacology.

The periwinkle plant, the sanguinaria. burdock, and many other plants have been found to have certain chemotherapeutic agents.These chemotherapeutic agents will interfere with epigenesis, and thus have a much more detrimental effect on such cancer cells thanthey do on normal cells. Hoxy found, in developing this formula, that his Hoxy tonic and his Yellow Poultice would work only on cancer cells; they would not have enough potency in the dosages used to disrupt any of the epigenetic processes of normal cells.

In the chemical companys' search for reductionism, these agents were separated from their natural support and concentrated beyond natural levels. Thus a severe sinthetic chemotherapeutic was designed that could affect any cell, even though cancer cells could

be destroyed by chemotherapy. So many patients die not from the disease, but from the cure.Thus nature developed the perfect chemotherapy agent. But the over-reductionistic minds of pharmacology, looking for

sinthetic patentables, tried to synthesize down to the most toxic agent of these chemotherapy agents, and have taken periwinkle and




Perhaps with the types of theories developed in this book, medicine might be able to come out of the wood work, cease to be a pseudo-science, and develop some accuracy through the utilization of scientific homeopathy, naturopathy and behavioral concepts.

NATURAL TREATMENTS

1. Degex 7. Nutritional ImmuneFortifier

2. Degex LiquescenceHerbal Chemotherapy 8. Behavioral Medicine

3. Psychological 9. Humor TherapyVisualization

10. Structural Realignment4. Xenobiotic Detoxifiers

11. Shark Cartilage5. Sarcodal Rebuilding

12. Oriental Herbs6. Anti-Viral Homeopathy

LEGAL ALTERNATIVES TO ALLOPATHIC MEDICINE

1. Homeopathy

2. Naturopathy

3. Chiropractic

4. Osteopathy

5. Acupuncture

These alternative entities are real and legal in the United States. Homeopathy is a viable and real regulated business within thegovernment. This type of medicine is attainable through choice, and with doctors, patients should have the ability to choose their owntypes of therapy.

It has been known statistically that the treatment of cancer is not responding to modern sinthetic medical techniques. We arelosing the battle with cancer; it is time to look for some other ways to help. In finding these ways it would be wrong to over-simplifythem and look for a magic bullet, which then could be manufactured by some sinthetic chemical company in gross. It is the precept of this book that such a magic bullet could not exist. Development of therapy regimes would need to be holistic, complex, and behavioral.Situations of nutritional involvement, psychological involvement, toxicity involvement, viral involvement and immuno-stimulation; andremoving of immuno-suppressants, such as antibiotics, sugar, and other compounds, are needed.

It is not the purpose of this book to try to give an in-depth history of the different types of therapies needed to treat cancer; it ismerely the indication of this book to outline the different theories of a new biology, and a new way to see. In a longer treatise we canattack cancer in a more thorough form, outlining some of the experiences of this researcher and others, in treating cancer by a morenatural means. It is the purpose of this book to try to also outline the threat to personal freedom of choice, which modern sinthetic

chemical medicine has proposed. They seek to remove the freedom of choice in health care.The recent court case that chiropractors had to take against the medical establishment points up how the medical establishment

has plotted behind closed doors to covertly remove chiropractic as a viable choice for people in America. The chiropractors sued, andwon. In the appeal suit the chiropractors won again. Thus we can see, by their stand against the medical establishment, that in the endthe freedom of choice in medicine will win out in America. Now acupuncturists, homeopaths and nutritionists must try to win a similar fight. It is the hope that this book on the highest form of science in biology will also help in this struggle for freedom of choice. It is tothis end that Quantum Biology is written.




SUMMARY

1. CANCER IS TRULY A TOXICITY RELATED DISEASE COMPLICATED BY IMMUNO SUPPRESSION .

2. ANY MEDICAL TREATMENT MUST DEAL WITH CAUSATIVE FACTORS . VIRAL COMPONENTS MUST ALSO BE USED.

3. CHEMOTHERAPY, RADIATION AND SURGERY ARE POOR TREATMENTS FOR CANCER .

4. NATURAL METHODS OF IMMUNE SYSTEM FORTIFICATION ARE THE BEST METHODS OF CANCER TREATMENT .

5. HOMEOPATHY ALREADY HAS DEFEATED MANY CANCERS. IT'S TIME THE ESTABLISHMENT OF MEDICINE LOOKED AT

IT.

cancer & quantum biology

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