Calling into Question the Definition of Cancer

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Calling into Question the Definition of Cancer

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Has anyone ever questioned the premise that cancer is caused from a fault in the cell's DNA? I am not aware of any challenges ever being brought forward that have even questioned this. It has always been taken as a ‘given'. This premise would appear to be the central point from which all studies into the disease stem from. But what if this is wrong? What if we made a mistake right out of the gate? The last 125 years have been spent looking exclusively at our DNA as the culprit for this unwanted tissue growth, with questionable progress and frustrating statistics.

There are two distinct methods from which a living cell can be reproduced.   Since the procedures that are capable of creating a living cell are limited to just two methods, a flaw in the generation of unwanted cells must therefore be limited to one of these two methods. That is to say that cancer, which is defined as the growth of unwanted tissues, must either be the result of a defect in our DNA, or a defect in our repair aspect of our immune system, the only other way in which a cell can come into being. A third scenario does not exist that is capable of creating a living cell, therefore a third scenario cannot exist that could be a possible explanation for when something goes wrong. Thus far only one of the two methods has been considered as the culprit for when something goes wrong with the orderly generation of cells. Only the DNA method (the much studied process in which the cell's DNA instructs the cell to divide as outlined in the internal code of the cell) has been considered as the root cause of cancer.

Because the DNA method of cell regeneration has never been called into question, it has never required a label. For the purposes of this dissertation, I will be using the term ‘DNA model' to refer to a sporadic mutation flaw that is currently believed to be the root cause of cancer. Cancer has only been considered as a defect at the cellular level and as a result a solution to the problem of cancer has only been looked at from the cellular level. Perhaps now it will be possible to turn the page and look at our immune system,... the only remaining viable explanation that could also account for this activity.

The second and only other process that exists that is capable of generating a living cell, is this much less studied, and less understood method whereby the body's own immune system is sent to a region immediately following some form of trauma; initially to stimulate the neighbouring cells into rapidly reproducing themselves in an endeavour to seal over a wound to hinder any blood loss, as well as prohibiting the entrance into the body of foreign contaminants. We refer to this process as the formation of scar tissue, and it is a function of our complex immune system. Scar tissue is principally associated with our skin tissue. However any cell in the body is capable of being stimulated by the immune system into generating scar tissue. Broken bones or torn cartilage are repaired with the controlled formation of scar tissue.

 Many of the intricacies are not yet known as to how this process is set into motion. However it is intuitively obvious that there must be a start mechanism. When the body experiences a trauma, it springs into action and sends this repair mechanism to the damaged site. It must then follow that there need be a mechanism in place to tell the immune system when the healing process is complete. With the same certainty that we know there is a ‘start mechanism'; obviously there must also be a 'stop mechanism'. Without fully understanding the intricacies of how these mechanisms work, we can know for certain that they do exist. It doesn't require too much imagination to predict what a defect in one or both of these start and stop mechanisms would result in. A defect in the 'start mechanism' would set the immune system into motion as if it had experienced some form of trauma, and the body would begin doing repairs to tissues without first being given a need too. Similarly, a defect in the ‘stop mechanism' would result in the inability for this repair process to know when to shut off this process. Either one of these two scenarios would result in the manufacturing of unwanted tissues. This event then would meet the definition of, and be indistinguishable from, what we presently refer to as 'cancer'. Instead of viewing cancer as a defect in the p53 tumor suppressor gene, we could view it as a defect in our immune system which is carrying out repairs on tissues that do not first need repairing, and/or repairing cells and then not receiving a signal as to when to stop. There must be a stop code. I will be using the term ‘Scare tissue model' to refer to the premise that the unwanted tissue we call cancer is a result of a defect in the immune system that is carrying out work on tissues that do not require work, or failing to receive the signal telling the body to stop this elevated level of activity.

All of what we presently know about cancer can be viewed from and accounted for using this model for cancer. When further examined, all of the anomalies that currently surround the disease can be explained away. All of which has a tendency to add support to this new framework for understanding cancer, and simultaneously call into question the original premise of the DNA model.

The cancer cell is distinguishable from the normal cell because it was manufactured by a different process than normal cell replacement. But the DNA method of cell regeneration is not different and not distinguishable from the original. No explanation has been put forward to explain why this underlying characteristic would change just because the controlled order of cell replacement went haywire. If the DNA model were to be true, then tumors would be clusters of cells indistinguishable from the host cells around them. A defect in the P53 gene should result in the formation of a wart, or a small polyp that could only grow to a size that could be supported by the existing blood supply.  But we are still faced with the fact that the tumors are distinguishable from the surrounding tissue, and often accompanied by their own modified blood supply.

A close examination of tumor tissues reveals that there are similarities between the formation of scar tissue (with its accompanying inflammation that is necessary to support and maintain the existence of this newly generated cell) and cancerous activity. This relationship is most easily observed by comparing skin surface scars with skin cancer. Because scar tissue was manufactured rapidly, and by a different process than that of normal tissue replacement (normal cell division as outlined in the cell DNA), it has different characteristics. Scar tissue made from skin cells has a distinct appearance with a smoother surface, firmer density, (described as a waxy appearance) and a different pigment from that of the surrounding tissue. The following quote can be found at www.google.com final report on Grant GR/K71394 Mathematical Model of Scar Tissue

"Scar tissue formation is a ubiquitous feature of adult wound healing, with
the resulting repair both functionally and cosmetically inferior to normal
skin. At microscopic level, the main difference between scar and normal
tissue is in the alignment pattern of the collagen fibers of which they are
composed." 

‘Functionally and cosmetically inferior' are characteristics shared by cells thought to be manufactured by cancer cells, and cells known to be manufactured by our immune system. And yet ‘functionally and cosmetically inferior' characteristics are not attributed to cells known to be manufactured by the normal DNA method in cases other than cancer.

 If cancer was a disease of the cell losing the ability to replicate itself in a controlled manor, then we could expect to see uniformity between the cancer tumor and the parent cell that had lost this ability to replicate itself in a controlled manner. However; there would be no reason to expect to see uniformity between the various cancers themselves( if this uniformity did not first exist between the parenting cells). But the Nobel laureate Otto Warburg, while studying the metabolism of tumors, noted that "cancers of various species and tissue origins reveal a high uniformity from tumor to tumor." Warburg, O.: Stoffwechsel d. Tumore, Springer, Berlin, 1926. Engl. edn., The Metabolism of Tumors, tr. F. Dickens, London, 1930.

 In fact there have been numerous studies all of which point to a number of parallelisms between cancer tumors of all types. There are a series of "common denominators" that are shared between all cancerous tissues that do not have this shared characteristic with the host cells, which becomes an anomaly under the present DNA model for explaining cancer. The following 4 quotes with references point this relationship out.

i)  "Correlatively, the Coris find the lactic acid and sugar content of the various exhibitions of cancer to be highly uniform. Williams and his co-workers report a pronounced degree of uniformity in the concentration of eight B vitamins in a great variety of animal and human tumours, regardless of the tissue of origin or the manner of their induction." Cori, C.F., and Cori, C.J.:J. Biol. Chem., 64:11, 1925

ii) "Shack describes an almost complete uniformity in cytochrome oxidase content in a number                                                                                                     of mouse tumors." Shack, J.: J. Natl. Cancer Inst. 3:389, 1943

iii) "Maver and Barrett describe substantial evidence for an immunological uniformity among malignant tumors. Greenstein reports an impressive degree of uniformity in enzyme concentration among malignant tissues, regardless of their means of induction, tissue of origin or species of origin." Greenstein, J.P.: Symposium on Cancer, A.A.A.S. Research Conference on Cancer, ed. F.R.Moulton, Am. Assoc. Advancement of Science, Washington, D.C., 1945, p. 192

iv) "The uniformity of various exhibitions of cancer in respiratory properties, lactic acid production, vitamin content, enzyme content, action on a given substrate, effect on liver catalase, cytochrome oxidase content immunological properties, and many other characteristics is correlative to an uniformity of malignant tumors in the ability to metastasize, in their amenability to heterotransplantability, and in their autonomy, invasiveness and erosiveness. Indeed, there is no known basic property unique to any single exhibition of cancer---the only variation being a morphological one partially conditioned by admixed benign or somatic components." Cancer and the Immune System The Vital Connection

After considering all the above quotations, a fair question to be asked is, ‘Why is there such uniformity between cancer tissues from tumor to tumor?' Another question would be, ‘If a fault in the DNA is causing this tissue growth, why then is the daughter cell even distinguishable from the normal cell?' If we grant that a flaw in the p52 gene is allowing for the orderly manufacture of cells to going astray, this by itself does not give licence to the cells that are spontaneously being generated to be any different from the host cell.

All of this uniformity seems to point to the credible scenario that there is one common theme in all cancers, which implies a single source of manufacture. It is impossible for the present DNA model to account for this anomaly of uniformity. Yet ‘uniformity' is an obvious inference if the cancers were all being formed from a single source (i.e. the ‘repair' arm of our immune system). A pattern of uniformity would be necessary if the immune system were responsible for the manufacture of all of these tissues and a pattern of uniformity is what is being observed. To account for this uniformity under the present definition of the DNA model of cancer, it is said that the original cancer has metastasized to another part of the body. The word ‘metastasized' imparts the belief that the new cancer has similar characteristics to the original cancer. The patient is never considered to have come down with two bouts of cancer, but rather one which has managed to have cells 'break away' and commence their havoc at a new site. The model for explaining how cancer can ‘spread' like this under the DNA framework is troubling. The belief is that some cancer cells have broken away from the original site, and migrated to a new location and began work there (metastasized). But the original cancer is thought to have been caused by some antigen entering the body and attacking the DNA gene that is responsible for the orderly generation of cell replacement. The secondary site is never thought to be a new antigen that has managed to enter this same patient, and started a new defect in the patients DNA. This ‘metastasize' model allows for the similarities in the various cancer tumors to be understood and accounted for within the dogmatic confines of the current DNA model. The new cancer is described as a continuation of the original cancer at a new location. But this model requires a host of special abilities being granted to these ‘cancer cells'. They are given the ability to recruit allies, and ‘cloak' themselves in the endeavour to explain how they can travel undetected and unharmed by the immune system as they journey to this new site.

Since there are only two ways in which a cell can be manufactured, and only one of the two methods can account for this ‘uniformity', and in conjunction, account for why the new cell is distinguishable from the parent cell, then it would be prudent to entertain the possibility that the ‘repair' aspect of our immune system (the only other way in which a living cell can come into existence) could be responsible for this non requested cell growth we call ‘cancer‘.  

There still remains many ‘mysteries' surrounding the immune system, and much is remaining to be learned. At present, the term ‘immune system' is used to describe a complex series of body functions that is in actuality three distinct systems with three distinct responsibilities. The term ‘immune system' is currently used to describe all three of these functions; it is the responsibility of the immune system to

i)  Identify foreign antigens that are deemed to be enemies of the body.

ii)  Destroy these enemies of the body; and

iii) Repair any damage that may have occurred during this onslaught.

( Enveloped within the repair aspect, is the immune system's ability to ‘inflame' the site with increased blood flow, a natural and vital component necessary to sustain the life of these newly generated cells by supplying oxygen and nutrients, as well as waste removal to these newly generated cells. The DNA model can adequately account for the generation of new tissues, but an entirely distinct explanation must be employed that is thought to be happening simultaneously to account for the accompanying blood supply necessary to maintain the existence of the newly generated cells from the framework of the DNA model).

It has been observed and acknowledged that there is a corresponding activity in the lymphatic system in episodes of cancer. Often it is observed that the cancer has spread to the adjacent lymph nodes, and a study of the individual's lymph nodes is used to determine if the cancer has spread (metastasized). Yet the purpose of the lymph nodes is to serve as the center for production of phagocytes, which engulf bacteria and poisonous substances. Lymph nodes are a vital component of the immune system, and are always associated with immune system activity. In other words, with every non-cancerous situation, the enlarged lymph nodes indicates that the immune system is active and fulfilling its function. However; we are told in episodes of cancer, although it is acknowledged that the lymph nodes are active, the immune system is thought to remain inactive, and they are not fulfilling their function. Under the DNA model, it is not yet understood why the immune system would sit idle while events that it is designed to prevent, takes place. No explanation is provided to account for how or even why the cancer employs the lymph nodes in the spread of the disease. From the framework of the scar tissue model, the lymph nodes would obviously be enlarged as the immune system was carrying out this work.  But the present definition of cancer has this activity taking place without arousing an immune system response. If the cancer is to be defined as a defect at the cellular level as outlined in the DNA model, it is a necessary maxim to hold that the immune system is permitting the existence of these newly generated cells because it is unaware of their existence. From the framework of the DNA model the evidence supports that the immune system does not make any attempt to prevent this cancerous activity from taking place. The explanation for how these cancer cells do this requires that the cancer cells are bestowed a number of special abilities that are unique only to the cancer cells, all of which exceeds my level of gullibility.  These special abilities are attributed to the cancer cells to help explain away why this event is being observed. This anomaly has never been adequately addressed and remains as a major conundrum of the present DNA model of cancer. It defies reason to accept that the immune system is doing nothing, and simultaneously accept that the lymph nodes are enlarged, but for a reason other than an immune system activity. A more credible explanation for this phenomenon is that the immune system is doing everything.  If cancer were found to be a function of a defective immune system then this conundrum becomes a logical inference. The immune system will not attack the cancer because the immune system sent the cancer. I suspect that ‘cancer' will one day be shown to be a maverick arm of the immune system, i.e. the patient has a defective ‘repair arm' of his or her immune system which has lost the ability to know when not to commence work on damaged tissues, and/or lacks the ability to know when to shut off this work once it has commenced.) .

Al l of the anomalies that surround this disease would suddenly vanish if cancer were to be viewed as a product of a defective immune system. We would not have to address how the cancer causing antigens enter the bodies of some individuals, and not others. These ‘antigens'  are the genesis point and mark the birth of cancer from the DNA model yet still remains to be unobserved at the cancer site. We would not have to address how cancer can move undetected throughout the body and take up residence at a new location without being detected, or encountering any form of resistance along the way. The study of cancer would then become an analysis of the way in which various cultures treat their immune systems, which then paves the way for this malfunction to take hold. Cancer becomes much less mysterious if we simply take the point of view that the immune system is causing the lawless proliferation of growth, (since it is its job to do so,) and the immune system is also supplying the essential blood supply to support this newly generated growth, by way of inflammation (again, because it is its job to do so). To read the present accounting of how the cancer cells manage to build the infrastructure of a blood supply system to support the existence of these newly generated cells requires an unrealistic level of trust. The cancer cells are attributed with a host of special abilities unique to them alone, all of which are necessary to account for this event taking place within the confines of the DNA model. Yet at the same time, the philosophy in treating cancer patients with radiation and chemotherapy is from the belief that these are the weakest cells and will be the first ones to die. Why would these cancer cells which are deemed invincible, immortal, perpetual cells be expected to be the first ones to die?

 Mark Twain is quoted as having said "What gets us into trouble is not what we don't know... It's what we know for sure, that just ain't so."

Cancer could be viewed as the fulfillment of a two part equation. First, the individual must be in possession of a faulty immune system that is capable of generating cells without there being a need, and/or generating cells and not receiving the stop code. Secondly, this individual must then have their defective immune system directed toward and perform this non requested work on a specific group of tissues.

Statistical connections have been difficult to extract using the DNA framework because the scientific community is only looking at half the equation, i.e. why the cancer cells are attacking a specific tissue. Currently, scientists are only looking at the hierarchy of cell types to come under attack, which produces only ‘links' to lifestyle choices or environmental exposures, etc.. If we factor into this how an individual treats their immune system, then perhaps some concrete relationships could be observed, and the global mapping of cancers would have significance. From the framework of this new model for cancer, the global mappings can be understood, and they do tend to have significance.

Immunosuppressant medications were developed to intentionally decrease the effect of the immune system in organ transplant patents, for the purpose of preventing the body's defence mechanism from attacking (rejecting) the foreign tissues of the transplant operation. If the patient survives the operation, and overcomes the rejection, they will live longer lives then they would have, had they not had the operation. Unfortunately, the statistical evidence shows that the transplant patient will ultimately succumb to a bout with cancer. This phenomenon has scientists struggling for an explanation:

"Scientists believe transplant recipients were already at risk
for cancer because their weakened immune system could not
keep healthy cells from becoming malignant".

"The use of immunosuppressants(cyclosporine) increases the
chance cancer cells will divide and invade surrounding tissue.
However it is not clear if cyclosporine can change normal cells
into cancer cells researchers say"
web search for ‘organ transplants'
Organ Transplant Drug Increases Cancer Risk
Friday, Feb.12, 1999\

By using this new model for explaining cancer, we would predict that by creating a defective immune system, we increase the likelihood that some form of cancer will result. We would then have satisfied the first part of the two part equation. We have an individual with a weakened immune system that is capable of generating non requested tissues. All the other ‘links' and ‘markers' merely help to ascertain which of the numerous types of cancer the patient is apt to acquire. That is to say, the numerous lifestyle links, dietary links, and environmental links (physical carcinogens, chemical carcinogens and biological carcinogens.), all have a tendency to either promote any given tissue in the body towards cancerous activity, or to demote specific tissues away from cancerous activity. If the immune system is the root cause of cancer, then obviously it will be difficult to discover a cure so long as our efforts are focused on employing the immune system to attack itself. The immune system is designed to recognize and not attack itself. Perhaps this explains why there are presently only treatments for cancer, and not yet any cures.

 If a weakened immune system has been shown to causes cancer, would it not therefore follow that a strengthened immune system, should overcome, or at least prevent cancer? There is a paradox with immunosuppressant medications which clearly establishes that there is a cause-effect relationship between cancer and a weakened immune system. It should be anticipated that a concrete cause/effect relationship between cancer and a substance would be the Holy Grail in the cancer research world. This is the one thing that I would expect everyone would have been searching for. But no one seems to be able to recognise this because it doesn't fit with the DNA model.  The DNA model is focused exclusively on the inner workings of the cell for the answer as to why it is reproducing itself relentlessly. When the malfunctioning immune system generates this relentless cell production from outside the cell itself, it is dismissed as an unexplained anomaly because it cannot be accounted for within the confines of the dogmatic view that cancer is happening at the cellular level.

 Cold-Hot; Inactive-active; benign-malignant. These are the differences between non life threatening benign tumours, and life threatening malignant tumours, specifically one is active (cancerous) and one is benign (scar tissue). In all likelihood, I suspect that it will one day turn out that the fundamental difference between a benign tumor and a cancerous tumor is in the timing of when they are being observed. If you discover a benign tumor (or perhaps we could call it a tumor ‘‘after-the-fact''), the body has stopped, and there is a mass of fibrous scar tissue that is currently not undergoing any development. If however, you were to stumble upon this very same tumor as it was being manufactured, it would be deemed to be a cancerous tumor. If your body is capable of producing a benign tumor, it is capable of producing a cancerous tumor. In the benign tumor, the immune system began a repair process that may or may not have been required, but evidently it did eventually receive the ‘stop code'. In a cancerous tumor, either the cells do not receive the ‘stop code', or you are observing it before it has received the ‘stop code'. I have never heard of an Oncologist saying to a patient "You've got some sort of tumor being produced, but let's leave it be, and see if it doesn't stop and become benign on its own". If that same tissue were to be observed when it was inactive, it would simply be dismissed as a benign tumor that had previously been produced at some time in the past. The benign scar tissue has already been manufactured by the immune system, and is now dormant. It is dismissed as scarring, and is of no immediate concern, because it is of no immediate danger to the patient. Everyone freely accepts that the inactive scar tissue was manufactured by the repair arm of the immune system. It should therefore be an easy inference to accept that cancer, or active scar tissue, or perhaps ‘runaway scar tissue', is currently being manufactured by this same arm of the immune system, though be it a defective one.

When medical professionals discover an active tumor being produced, they may opt to surgically remove the tumor and the offending cancer cells that made it (excision biopsy). As this radical surgery has not yielded the desired success rates, the medical profession has expanded the scope of the surgery to include the surrounding tissues (margin), believing that these tissues might contain some stray cancer cells. They test this removed tissue and may confirm that it too was cancerous. They then close up the wound and hope that they have managed to remove all of the cancerous tissue. Now they must wait until the immune system has had time to heal up the surgical wound before testing the area, because the activity of the inflammatory nature of the healing process will read as ‘hot'. We then have the defective immune system, which may turn out to have caused the tumor to begin with, being invited back to the site, and being expected to heal up this surgical cut. Healing is what the immune system does. Therefore, this is an exercise for it. Often, the immune system heals over the surgery and then stops. The surgery was a success. Sometimes, however; the immune system doesn't stop. The immune system continues to produce scar tissue, and rapidly divide the adjoining tissues without receiving the message that the task has been completed. The poor surgeon is mystified that he or she could have missed some of the cancer cells, and now they appear to have merely taken up where they left off. If the DNA model were to be true, that some carcinogen ventured to the site and caused a defect in the cell DNA, then this patient, now rid of the offending tissues, should mathematically be given the same bill of health as a non patient (i.e. someone who has never had cancer). But the statistics do not support this optimistic expectation. Quite often, the cancer patients who undergo surgery have recurrences at the original site. If the cancer returns but at another location, then the surgery would be statistically labeled as a success. Even with this clemency being granted, the statistics for the surgery are not too favorable. The apparent failure of the surgery has given birth to the suspicions that exposing the cancerous tissue to the air helps it to spread. Or exposing the cancer to the light of the Operating Room, perhaps, is what causes it to flourish. Exposing the cancer to the light and air is merely a necessary by-product of the fact that these cells have been operated on, and as a result, the immune system is re-invited back to the region to repair the surgical wound. The suppositions that the light or air has anything to do with any reoccurrence can be dismissed because surgeries that are preformed on patients, who have not been diagnosed with cancer, are not subject to similar incidences of tumors, despite also being subjected to the light and air. These patients do not have the first prerequisite, namely the faulty immune system that is incapable of generating the "stop code". Even the supporters of the DNA model, acknowledge that cancer cells are in all of us (because the ‘spontaneous existence of matter' is a hard concept to ‘sell' and an absurd proposition). If we were to attribute this reaction to the light and/or air as yet another mystical feature enjoyed only by cancer cells, we would still need to account for why every surgery was not subject to the same level of reoccurrence. From the point of view of this new model, this anomaly would be addressed as follows; the non cancerous patient has a properly functioning immune system which still has the ability of knowing when to stop the healing process. In cancer patients, the immune system has already shown to be defective, therefore it should not be surprising to find out that sometimes it does turn out to be relentlessly continuing the healing process and in so doing, inflict the area with a new cluster of cancerous activity, despite how diligent and careful the surgeon had preformed.

 It is reasonable to expect from what we know about cancer, that there should be some occurrences of ‘heart cancer'. The heart is a vital organ with access to an unlimited blood supply, just as the liver, pancreas, lung etc. Yet we never hear the term ‘heart cancer'. Hardening of the arteries could be accounted for by the immune system repairing the cells of the artery walls with the formation of scar tissue. Scaring can be observed in many of the heart attack victims. Post-mortems and biopsies of heart attack victims have shown that there are both fat and fibrosis (scar tissue) replacing the muscle cells in the heart. Often a patient can be identified as having suffered a heart attack by observing scaring of the heart tissue, even if the patient is not aware that he or she has had a heart attack. A long drawn out fight with the disease is unlikely because any blockage or restrictions caused by the scar tissue will have immediate and severe consequences. Perhaps this is why we have not needed the term "heart cancer". When we compare the similarities between the two diseases, we could deduce that the same element exist in heart disease, as in cancer. Both diseases were relatively scarce as recent as a century ago. According to the U.S. Bureau of Census, heart attacks caused less than three thousand deaths in the United States as late as the year 1930. The lifetime risk for North Americans of developing heart disease now is one in two if you are male and one in three if you are female, which coincidentally is identical to the lifetime risk of developing cancer. Cancer statistics have had an equally poignant escalation in numbers over the same period. It is also of interest to note the resemblance between global cancer events, and global heart disease. The latest available data from the World Health Organization (WHO) MONICA Project indicate that the coronary event rate (per 100,000) in men was highest in Finland (North Karelia,835) and lowest in China (Beijing, 81). A global map of coronary events show that you are more than ten times as likely to have heart disease if you are raised in Finland as opposed to being raised in China. These WHO global maps of cancer clusters show that you are four times more likely to acquire cancer from being raised in Denmark, as compared to being raised in Thailand. Both of these diseases have been attributed the term ‘modern disease', and as a result, the goal of finding the cause has been confined to ‘modern' practices (modern food additives, modern lifestyles, etc.) Practically every aspect of our modern lives have been studied and considered as a possible cause. But the one thing that has avoided being studied, and is most definitely a modern phenomenon, is our treatment of the immune system itself. This modern tendency to supply the body with these immunity enhancing pharmaceuticals is the one thing that has escaped being studied, primarily because such studies into the causation of diseases are conducted and financed to a large degree by the pharmaceutical industry itself. If it were to be true that we were doing harm to ourselves with this modern tendency to be reliant on pharmaceuticals, how would we ever come to know it? It is absurd for us to expect the pharmaceutical industry to bring this to our attention?

At present, the three most promising treatments for cancer are Chemotherapy, Radiation Therapy, and Surgery.  All other treatments are aimed at invigorating, boosting, stimulating, enhancing etc. the immune system into attacking the cancer. Paradoxically, the three most successful treatments make no attempt at employing the immune system in the fight against cancer. These three protocols have two things in common. They go after the cancer cells themselves, and all three make no attempt at employing the immune system in their attack.  The second thing these three protocols have in common is that they inadvertently cause stress to the immune system. In all of these three most successful cases, the immune system must come onto the scene to repair the damage that has been inflicted against the tissues at the cancer site. This ‘stress' places a workload on the immune system which provides a workout, or exercise for it. Thus the three most successful treatments for cancer could be viewed as benefiting the cancer patient by increasing the workload and responsibilities of his or her immune system. The remaining less successful treatments all tend to actually "demote" the immune system by taking responsibility away from it. Any substance that claims to assist, invigorate, enhance etc. the immune system actually  takes the workload away from it and , may inadvertently be causing the immune system to become weaker. From this new vantage point of understanding cancer, we can see why treatments that do not attempt to involve the immune system would be the most effective treatments in the fight against cancer. If the immune system were found to be ultimately responsible for this non requested tissue growth we call cancer, it would be absurd to expect it to attack itself. The fact that the list of the most effective tools to date in the fight against cancer all happen to be the ones that do not involve the immune system directly, adds support to the hypothesis that the immune system is responsible for this event.

If we make this simple adjustment in our model for explaining cancer, [by taking the blame away from the individual cell's DNA, (chromosome p53) and placing the blame on the immune system as a whole, or more specifically, the repair aspect of our immune system,] then we simplify things immensely. This phenomenon then becomes a candidate to apply Occam's razor. Why employ a complex set of beliefs when a simple explanation already exists? Unexplainable events become, for the first time, explainable. As to why the immune system leave the cancer cells alone would become straightforwardly explained if the cancer were a function of the immune system. Similarly we would be able to account for how the cancer can travel throughout the body undetected and take up residence in another part of the body without being detected or encountering resistance along the way. We would not require the use of imaginary antigens that set this mystery disease in motion, yet cannot be observed either at the site, or journeying to the site.

It has for some time been observed and recognized that people who are pet owners live longer lives than those who do not own pets. It was asserted that the satisfying feeling of well being as a nurturing caregiver to these pets was a stress release, and this ‘stress release' is what was responsible for this longevity. It has more recently been proposed that the germs and bacteria that the caregivers are exposed to from their pets is more likely what is responsible for the difference. Pet owners have immune systems that get more of a workout relative to the non pet owners, and this ‘exercised immune system‘is actually what is responsible for the increased health benefits.

Cancer is not limited to the human species. Farm animals and pets also have been diagnosed with cancer. But observe however, that the animals that are diagnosed with cancer all tend to be animals that routinely receive treatments from veterinarians, or care giving owners, who attempt to improve the animal's health with enriched or fortified feed, medicines, vaccines and booster shots designed to assist the immune system. Animals such as raccoons, bats, foxes and skunks have all been diagnosed with rabies, but it is extremely rare to learn of these animals, which are outside of the domestic category (wild animals, who receive no treatment of any kind) being diagnosed with cancer. On the other hand, horses, cats, and dogs, have nearly the same rates of cancer as humans have. (There will always be exceptions. Just as an animal can be born with a defective heart, or defective liver, it is conceivable that there might also be cases in which an animal could be born with a defective immune system, but I would expect that such a defect would be self correcting, i.e. the animal would perish prior to passing this defect on to its offspring).

There have been studies undertaken to attempt to find out why squirrels don't get cancer. They have a long lifespan and live amongst us, therefore are exposed to the same carcinogens as we are, yet they do not get cancer. Scientists are astute enough as to wonder why this is, but they are locked into the dogmatic restraints of looking inside the cell. They believe "that cells of long-lived, small-bodied rodents are hypersensitive to cues from the surrounding tissue. If the cells sense that conditions are inappropriate for growth, they slow down cell division. Such a mechanism would arrest tumor growth and prevent metastases." quoted from article http://www.scientificblogging.com/news_releases/squirrels_know_a_cure_for_cancer

The fact that squirrels don't go to the medicine cabinet when they feel they are coming down with something, might also be a factor.

The following paragraph is an interesting excerpt from an article titled Buffaloes Don't Get Cancer.

Buffaloes Don't Get Cancer. An edition of The New York Times Sunday Magazine featured a story on the growing popularity of buffalo meat and its economic potential for cattlemen in the American Southwest. It also inadvertently shed light on the nature of diet, health, and natural resistance. The author pointed out that buffaloes are so hardy that ranchers don't need to add hormones, artificial growth stimulants or antibiotics to their feed. A spokesman for the Bison Association (I don't think bison are allowed to join) said that, "Bison are not susceptible to cancer... they're the only mammal that isn't. We don't know why yet; the research has not been done."

When the research is finally done, it will no doubt shed light on the connection between the absence of immune enhancing concoctions and the absence of cancer itself. The Bison fall under the category of semi domestic animals. Like squirrels, they have beckoned scientists to ask the question as to why they do not get cancer. Domestic animals receive health care from owners. Semi domestic and wild animals do not. Domestic animals get cancer. Semi domestic and wild animals do not. It can't get any more obvious than this. It is difficult to imagine that there could be some antigen in our society that is affecting the DNA of domestic animals and avoiding having the same impact on semi domestic animals.

Examine for a moment how we have treated our immune system since the industrial revolution (which preceded the chemical revolution, which gave birth to the medicines that we enjoy today). When we become ill, our immune system requires energy to do its job. Our immune system takes much of the energy normally used to fuel our muscles and heat our body, so we may feel fatigued, run down and chilled while our immune system is preparing itself for the ensuing fight. The stage is set for a classic battle between the immune system, and the offending foreign virus. So what do we do? It is at this point that we (Western Society) start "assisting" our immune system. As the fight progresses, undesirable waste products are produced. The clinical definition refers to T cells secreting cytokines, and lymphokines being secreted by B cells and natural killer cells injecting acidic fluids, etc.. The immune system will employ one or more of the body's orifices to flush out or eject these waste products, but it has become our practice to attempt to stop this. We take medications for nausea and upset stomach, hindering the body's ability to rid itself of the stomach's contents. We take pills or serums for diarrhea if the body attempts to rid itself of the contents of the intestinal tract. We take pills, sprays or ointments for runny noses; watering eyes; coughing; sneezing,... any and every endeavour that the immune system employs to rid itself of the by-products. When you consider that the ears naturally drain into the throat, the immune system has employed each and every orifice that the body has, and we employ medications to stop or hinder the use of every one of them. We medically "handcuff" the immune system from performing its job. Since this tendency of trying to assist our immune systems is a fairly modern phenomenon, it might help us understand why cancer has become classified as a modern epidemic.

One of the most bizarre anomalies in my opinion is in regards to melanoma. Melanoma has been linked to sun damage, and yet it is statistically less prevalent in the tropical regions of the globe. Dark skinned races seldom acquire this or any form of skin cancer, and yet skin cancers are the most prevalent form of cancer. In the rare cases in which a dark skinned person does acquire melanoma, it will be under the fingernails, on the palms of the hand, sole of the feet, or inside the mouth. These areas are tissues that do not possess the darker pigment, and due to the location, these cancer cases could not be attributed to sun damage. Those regions closest to the equator, have people whose skin has evolved or adapted to the more intense sunlight. Their darker skin is a consequence of the human melanin cells having had to develop in order to convert the sunlight's harmful ultraviolet waves, into harmless heat waves. Thus, the people who reside in the tropical regions of the globe, have skin that has already adapted to a harmful attack (ultraviolet waves) and therefore, using this new model, we can view these cells as no longer being the easiest cells for the opportunistic cancer to ‘pick on'. People in the tropical regions who do posses defective immune systems will find that they have cells other than their melanin, which are easier for their (faulty) immune system to stimulate. Or if the cancer does choose to divide the melanin cells, it will be forced to attack the tissues that do not possess this modification (palms of hand, sole of foot, etc.).

Using this model we would predict that similar cultures would produce similar cancer statistics. This fact has eluded no one. We have always been aware that people who share the same culture, same lifestyle, same access to health services and facilities, same documentation methods etc. would have the same life expectancy, and the same mortality rates for diseases. If however, one group of a society were to be immune to one form of cancer, then mathematically, we would expect, (using this new model) that the numbers would have to be made up for in other forms of cancer. We see a prime example of this prediction by observing cancer in African Americans. These people share the same culture as the North American Caucasians, and yet they could be considered to be ‘genetically immune' from acquiring skin cancer. Thus we see African Americans with alarmingly higher rates of lung cancer, for instance. The slight deviation in smoking habits cannot account for the vast deviation in cancer statistics. It has been acknowledged that "African Americans suffer disproportionately from chronic and preventable disease compared to the White Americans." (U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 1998.) Similar anomalies have been observed in American Indians, Hispanics, and Asian/Pacific Island minorities. It has been recognized statistically that these groups all smoke less cigarettes per day then there Caucasian counterparts, yet these groups all have alarmingly higher incidents of lung disease, and lung cancer. No justifiable explanation can be put forth by the present DNA model for this anomaly, although many presumptions are advanced such as "they smoke less, but they inhale deeper". It could be expressed that the North American culture is the common denominator, and as a result, a certain percentage of these people are going to acquire a defective immune system. Since some of these people are going to be ‘exempt' from falling under the category of ‘skin cancer', they will then have to be placed into one of the remaining categories. Thus we see this ‘disproportionate' level of other cancers. If we examine the statistics from the point of view that from the next 100,000 babies born, the American culture is going to produce 225 of which will go on to acquire some form of cancer. If some of these 225 citizens are genetically immune from acquiring the number one type of cancer (skin), then they therefore must fall into one of the other categories of cancer, in this case, the number two category of cancer (lung). From this perspective it can be understood why these groups of individuals can have higher lung cancer statistics then the remaining members of their society, even though they smoke less. It is necessary to view cancer as the fulfillment of two requisites. We must first examine what this society is doing to have 225 of its members go on to develop a faulty immune system that is capable of generating unwanted cells, and then we must examine factors which account for the category of cancer that each of the 225 citizens are ultimately going to be placed. This relationship cannot be understood from the perspective of the DNA model which tries to link the 225 cancer victims to a cause within their society which distinguishes them from the remaining 99,775 non cancerous citizens. Prior to this new model, we were at a loss as to how to account for the vast discrepancies in these numbers. This phenomenon can only be explained when we step outside of the existing DNA framework. I would expect that this phenomenon could be observed by viewing statistics between Australians, and Aborigines as well. Consider the plight of the Australians. Here we have a culture of exiled Europeans. They do not possess the required genetically modified skin to live in this more tropical environment. Thus we now see, as this modern trend of possessing weaker immune systems takes effect, the skin of the Australian and New Zealand Caucasians is coming more and more under heavy attack. If a certain percentage of a culture were to posses the requisite faulty immune system, and they resided in a tropical region without the benefit of the darker melanin, then it would be expected that a disproportionate number of these people are going to acquire skin cancer. This is exactly the plight we are now observing in Australia and New Zealand. This trend can also be observed by studying the cancers of Northern Europe and comparing these with countries closer to the equator in Southern Europe. This explanation accounts for countries nearer to the equator, although their incidence of melanoma is lower, do have a higher incidence of other types of cancer. Liver cancer for instance, is six times more prevalent in Southern Europe (Spain, Portugal, and Italy) than it is in Northern Europe (Denmark, Finland and Norway). This same principal (cancer cells ‘picking on' the easiest target.) can be used to explain childhood cancer, and help to explain why the list for adult cancers and child cancers is so different.

This principle can be applied across the board in explaining why some types of cancer are rarer then others. The rarer forms of cancer have a cell structure that is more difficult for the immune system to stimulate into scar tissue.

One tissue type that has shown to be amongst the easier tissues to mutate is the mucus membrane tissue. These tissues are located throughout the body, but not arbitrarily throughout the body. Polyps are an abnormal growth from these mucus cells and have been attributed with being a precursor to cancer. Notice that polyps that grow out of the mucus membrane tissue only grow on these specialized tissues which are always located adjacent to a body orifice; Colon polyps, Oesophageal polyps, Endometrial polyps, nasal etc. If the repair arm of our immune system is allowed to roam free and stimulate any tissue into the formation of scar tissue, then there will be a tendency for this activity to take place where the immune system exists in higher concentrations. It is conceivable that the body's immune system would have the mucus membrane tissues surrounding the body orifices heavily fortified with defence cells designed to identify and destroy foreign antigens that tried to enter the body through these portals. A defective immune system, therefore, is most apt to commence work where it happens to be located. When we include the female breast (since it is also a body orifice during child bearing years), this too would have these defence mechanisms in place. Prior to the woman reaching puberty, the breast is not an orifice, and does not require the extra defence strategy from the immune system. Thus the incidence of breast cancer in both men and women are about the same, and very uncommon. Once this portal requires an immune defence, (child bearing years) the statistics for female breast cancer raise alarmingly. But the DNA of the cell does not change. If the root cause of cancer is a flaw in our tumor suppressor gene, why is there any difference at all in the list if childhood cancers versus the list of adult cancers? As far as I can tell there has never been an attempt to account for why there is a difference between adult and childhood cancers. This is simply one more anomaly in a list of anomalies that surround this disease. If however the cancer were to be caused from a defect in our immune system, there would be a viable explanation as to why there was a difference between adult and childhood cancers. This same principal (cancer cells ‘picking on' the easiest target) can be used to explain the entire list of childhood cancer, and help to explain why the list for adult cancers and child cancers is so different. During the initial development of the body, all organs, muscles and bones undergo a growth period which lasts until adulthood. All tissues in the body undergo development during this time. A newborn baby boy starts out at 6 pounds, and 18 years later he weighs 180 pounds. Thus each pound of mass must multiply itself 30 fold. Because of this ongoing development, these tissues are constantly being fabricated and revised. The observed phenomena indicate that these cells are less susceptible to being stimulated by a faulty immune system, due to this elevated activity. That is to say, the defective immune system will not assess these cells as requiring accelerated cell division, because these cells are currently undergoing accelerated cell division, which is a natural part of development of the body during adolescence (a wound that would result in a scare formation on an adult is less likely to form scar tissue when a similar wound is received by a child, due in part to the fact that a portion of the cell generation was performed naturally by the DNA method of cell regeneration, which is not "functionally and cosmetically inferior".). The white blood cells, on the other hand, have previously been manufactured in the bone marrow, and now have left this factory of origin. This circulatory system is best described by using an analogy of a manufacturer with a recycling and maintenance department. Our body continues to manufacture blood throughout our lifetime in this continuous ‘loop' system. Newly repaired or manufactured blood cells leave the factory (bone marrow) and will not be seen by the maintenance department again, until they re-enter the kidney and liver at the other end of the loop. These individual white blood cells commence their journey through the body in the state of decline (no longer being maintained). They have a short life span of between several days, up to two weeks. These cells are not receiving ongoing development, and therefore would become the easiest targets for a defective immune system to divide. Thus leukemia becomes the most common form of childhood cancers. Once the body is fully grown, the organ tissues no longer have this inherent advantage of the ongoing development, and so these organs become susceptible to cancerous activity to the same extent as the rest of the adult population. The observed phenomena supports the hypotheses that developing tissues are less prone to cancerous activity then the matured tissues are.
In the developing years, the human brain undergoes the least amount of mass variance. The brain starts out between 350 and 400 grams and grows to a weight of between 1300 and 1400 grams. Thus, the brain undergoes a mass increase of 3.6 times its original (in contrast to a 30 fold average for all other tissues). This fact denotes that the development of the brain tissue is considerably slower or less intense then the development of all remaining tissue types in the body. This helps us to understand why brain tumors are the principal form of cancer of a solid mass in children. Brain tissue is the ‘low man on the totem-pole' as far as cell activity is concerned. Thus, it becomes the easiest tissue for the defective immune system to ‘pick on'. The combination of leukemia, and brain tumors, represent the majority of all childhood cancers.

The eyeball of a newborn is about 75% of the size of an adult's eye. Thus this organ undergoes a mass increase considerably less than the remaining body tissues. Retinoblastoma (eye cancer) is almost exclusively a childhood disease with 90% of all cases being diagnosed before age 4. In all scientific literature there has been mention of only 20 cases of adult (20 years or older) retinoblastoma in a word population of over 6 billion people. Thus the cells of the eye appear to also follow this same principal when attempting to understand why there is a difference between childhood and adulthood cancers.

In 1971, President Richard Nixon symbolically declared war on cancer. The scientific community was caught off guard and had not even settled on a definition for the fundamental root cause of the disease. They hastily came up with a definition of what they were up against, and officially adapted what has come to be the present day DNA model. The "DNA model" label has not been necessary because no opposing models had been introduced, and this DNA theory was taken as a given. 140 years ago, however; there was competing theories for cancer. Only one survived. But the theory that was overstepped was never disproved. The birth of the DNA model was laid our years earlier. The following is an excerpt from Encyclopaedia Britannica 1949

‘Virchow laid great stress upon the importance of chronic irritation in the causation of new growth ...The rival theory put forward by Cohnheim about 1880 that new growth arises from embryological remnants included within the tissue owing to some slight error in development.'

 Here we learn that the first views on cancer (prior to 1880) were thought to be caused by the body repairing cells that were subjected to "chronic irritation". Evidently, this original theory fell out of favor to the ‘new' rival theory (the Cohnheim theory which has evolved into the present day DNA theory because DNA had not been discovered yet).  This chronic irritation would imply the breakdown or continuous damage inflicted on one group of cells, or one tissue type. It had long been observed that betel-nut chewing had been linked to oral cancer. This phenomenon was originally accounted for with the claim that the abrasive quality of these nuts caused an irritation in the cheek tissue of the mouth. When the new theory came along, this phenomenon was attributed to arecoline, one of the properties that could now be scientifically identified to this plant, as being responsible for the oral cancer. Similarly, connections were made between scrotum cancer and soot by observing the high percentage of chimney sweeps that came down with this ailment. As time progressed, it could be isolated that it was benzopyrene, an ingredient in coal tar that was causing the irritation. This new ability to isolate the specific element that was responsible for this ‘cause-effect' relationship coincided with the new proposed theory from Cohnheim (which held that the cancerous growth was caused from "embryological remnants included within the tissue owing to some slight error in development". The newly discovered technique of microscopical staining, lent itself remarkably well to the belief that there was something going on inside the individual cell that was causing it to lawlessly reproduce itself, and this new scientific tool had just become available in 1872. This was a critical time in the fight against the disease, and we found ourselves at a ‘Y' in the road. I can well imagine how this new ability to examine carcinogens at the molecular level, helped this new ‘molecular theory' win favor over the older chronic irritation theory. Nevertheless this does not invalidate the original theory. The original theory was never revoked, or flat out rejected, but rather it was passed over when these new scientific tools came on line. From the ‘Y' in the road, everyone went down the same path (DNA model). It would have been preferable for the supporters of the original theory to concede that it was not the soot that was causing the irritation, (or more specifically the benzopyrene in the soot,) as opposed to overturning the theory altogether. It should have been conceded that it was not the abrasive irritant of the betel nuts that was ‘physically' weakening the tissue, but rather something in the nut that was ‘chemically' weakening the tissue at this location. In either case, the damaged or weakened tissues require a response from the immune system. Then the chronic irritation principal would still remain applicable as a plausible cause for cancer. This adaptation would have allowed the ‘chronic irritation' theory to co-exist with the ‘embryological remnant' theory until more was known about the disease of cancer, and the cells that it attacks. If we concede that it is a ‘chemically' weakened tissue, as opposed to a ‘physically' weakened tissue; what then is the difference between the chronic irritant theory( read: chemically weakened tissue that begins this uncontrolled growth,) and the Cohnheim theory for cancer, which holds that the growth stems from a flaw within the tissue owing to some internal flaw? (Although the model for DNA was only discovered fifty years ago, it had previously been understood that there must have existed some form of ‘gene' that was responsible for passing along the genetic information from parent to offspring.) The major distinction between these two theories is in the role of the immune system. The immune system plays no role in the Cohnheim theory (which places the blame solely on the DNA of the affected tissue cells.). If we re-investigate the chronic irritation theory now, with our new found knowledge of the roles of the immune system, we might conclude that the original theory should not have been so quickly overlooked.

Consider the practice of acupuncture. Thousands of years ago, it was observed that warriors, who were inflicted with non-lethal spear and arrow wounds, would go on to recover from their wounds and then experience superior health to what they had prior to the event. Health practitioners then began to intentionally inflict the body with similar wounds hoping for similar results. They would insert bamboo sprigs and shells into the skin of patients. They got what they were after, and acupuncture has survived through the ages despite being viewed as barbaric and not fitting into the realm of explainable events from the point of view of modern day medicine. Over the years, the practice has been refined and has become less barbaric, with sterilized equipment; however, the immune system must still address the tissue damage inflicted by these needles, thus subjecting it to an ‘exercise".  At the bare minimum the immune system undergoes an exercise of the ‘start' and ‘stop' code productions. The resulting health benefits could therefore be attributed to the exercised immune system.

 Another type of immune system fallibility is with arthritis. I have heard about people treating arthritis with wasp stings. They apply bees or wasps in a jar to the offending joint, and then agitate the jar causing the insects to attack the exposed flesh. The immune system currently being misguided into producing antibodies to attack the joint is given something constructive to do. The arthritis sufferers notice a temporary ‘cure' from their ailment as the immune system must now address the poison from the bee sting. This process must be re-applied as the immune system will eventually revert back to its misguided activity once the bee sting has been addressed. The relief from their arthritis can last several months however.

It would seem foreign, or perhaps even absurd to introduce infectious contaminants into the human body. It would seem ludicrous to do this to someone who is already ill. This inverse line of thinking would help to explain wh

Anonymous

Edited to say:  Nevermind... I just looked at your previous posting from 2010.  I have no comment.