Our definition of Cancer may be wrong. If we change how we define it, everything starts to make sens

 I thought it would be an appropriate starting point to use this quote from Mark Twain. “What gets us into trouble is not what we don't know. It's what we know for sure,… that just ain't so.” This sets up the question, ‘what if we made a mistake right out of the gate?’ What if everyone is pursuing an answer that lies in the opposite direction from where everyone is looking? This certainly would help to explain why the cure for cancer has eluded so many for so long.

 

The term ‘cancer’ refers to a group of diseases. All of these diseases have one thing in common which is the non-required growth of cells.  The last 120 years have been spent looking for a flaw in the cell’s DNA. The medical profession could recognize and identify the disease, but did not know enough about the workings to be efficient at combating it. In 1971, U.S. president Richard Nixon symbolically declared war on cancer. At that point the medical community had not yet adopted an ‘official’ definition of what cancer was and hastily implemented our present definition. This theory has not needed to be labelled as a theory, or even given a title, because it has been universally accepted and has gone uncontested. This is typical in all scientific endeavours. As a starting point there is always some basic idea that is postulated without the need for discussion. This becomes the ‘spinal cord’ from which everything else is hung from; we theorise,  formulize, and connect this central postulate to others. We cannot start from nothing. There needs to be some starting point, but what if the starting point is wrong? What if cancer is caused from something other than a faulty DNA?

I will be referring to our present definition of cancer as ‘the DNA theory‘.  This definition, or ‘root cause of cancer’ has been taken as a ‘given‘, and is the central starting point for all cancer research. It would be expected that as our knowledge improves as to what carcinogens and lifestyles need to be avoided, and what healthy lifestyle choices we need to adapt in order to prevent this disease, the overall statistics for cancer would be steadily going down. Yet the statistics do not point to progress at all.  Admittedly, some advancement has been made in medical science’s ability to keep someone diagnosed with cancer alive for longer periods of time but this has not lead to even one cure for one type of cancer. The tendency towards earlier diagnoses of the disease would also lead to the appearance of longer survival statistics, merely by starting the ‘stop-watch’ sooner. Our new found ability to differentiate between the subtle differences in cancer types that used to be lumped together has permitted new categories of cancer. But this has lead to the appearance that the statistics are going down because a patient cannot simultaneously be labelled with more than one type of cancer. Thus they must be classified as having one of the categories, and since there are now more categories from which to be placed, the statistics of each category have the appearance of getting smaller.

 

But what if the root cause of cancer was not a defect of our DNA?  What if the ‘root cause’ of cancer were something entirely different? 

Back in 1990 scientists set out to produce a complete map of our DNA. It had been anticipated that the completed mapping of the human genome (the entirety of an organism's hereditary information.) would ultimately lead to the cure for cancer, and we anxiously awaited the results. We are now approaching the 10^th anniversary of having the competed map and have been able to pinpoint the gene known to be responsible for the controlled division of cells. As of yet, the cure for the disease has been elusive.

 The ‘root cause’ of the defect that is attributed with the task of controlled cell reproduction has been identified as the p53 gene on the 17^th chromosome. The hope was that if all cancers can be attributed to a single flaw, then perhaps a single solution could be found that cures all cancers.  With over 200 different types of cancer, there could be 200 different solutions, or 200 different approaches or protocols with which to combat the disease, but this would imply that we are 200 times as likely to stumble onto even one of them. If a single solution cannot be found that cures all cancer, then perhaps we should be content with finding one solution for one type of cancer, and then proceed from there. Thus far we have not been able to stumble across any solutions for curing any cancers. The word ’cure’ has been all but removed from the field of cancer research. They seek now to achieve a temporary remission from the disease, and successes are measured by any ability to extend the length of remission. If a type of cancer had the statistics of taking the life of the patient within 6 months of diagnoses, and a protocol was found to extend the patients survival to 8 months, then this protocol would be heralded as increasing the survival rate by 25%, merely by extending the patient’s life by 60 days.

 

   Perhaps we should be open to the possibility that the answer lies somewhere other than where we are looking. All research has been limited to exclusively looking inside the cell. All efforts have be focused on this one approach.  Maybe the answer lies outside of the individual cell. Perhaps instead of looking at the micro level, we should look at the macro level.

 

 There are two distinct ways in which a cell can be manufactured, and only two. The first method is by way of this much studied process in which a cell replicating itself as outlined within that cell's DNA. The only other method that is capable of generating a cell, is the 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 prohibit the entrance into the body of foreign contaminants. We refer to this as the formation of scar tissue, and it is one of the functions of our complex immune system. We often associate scar tissue with our skin; however any cell in the body is capable of being stimulated by the immune system into generating scar tissue. Broken bones and torn ligaments can be mended with this formation of scar tissue. With over 200 different types of cells in the human body, there are correspondingly over 200 different types of scar tissue.(And either ironically, or essentially, there are over 200 different types of cancer.)

 

It is difficult to account for, nevertheless presently held that the immune system sits idle as cancer activity proliferates. Simultaneously it is observed and acknowledged that there is a corresponding activity in the lymphatic system. Often it is observed that the cancer has spread to the adjacent lymph nodes, and the lymph nodes are studied to determine how advanced the cancer has become. 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 an immune system response. In other words, with every non cancerous situation, the enlarged lymph nodes indicates that the immune system is active and fulfilling its duty. 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. It is not yet understood why the immune system would remain inactive while events that it is designed to prevent, takes place. This position is however a necessary stratagem if the DNA theory is to prevail. If cancer is brought on by some defect within the cell, it will be necessary to account for why the immune system does not successfully address the problem. If this defect is attributed to some form of antigen that has journeyed to the cell, it will also be necessary to address why the immune system did not attack the antigen itself as it journeyed to the site where the activity would ultimately take place. In both cases, the explanation is that the cancer cell has the unique ability to ‘disguise itself’, but this unique ability must further be extended to the antigen itself, that has journeyed to the cell to cause this defect. This anomaly has never been adequately addressed.

It defies reason to accept that the immune system is doing nothing. A more credible explanation for this phenomenon is that the immune system is doing everything. This is not as bizarre as it sounds since all of the characteristics of the cancerous activity also happen to be normal immune system functions.

The immune system is complex and much remains unknown about it. The immune system is actually three distinct systems with three distinct functions. Within our immune system there exists a complex system with the responsibility of identifying foreign antigens that are deemed to be enemies of the body. In addition to identifying these enemies, the immune system also has a complex system which is responsible to destroy any and all identified threats. The immune system has control of an arsenal of specialized cells for the purpose of carrying out this mission, and a complete lymphatic system to deliver these specialized cells to the targeted areas. And on top of all that, and of principal interest to this alternate approach to cancer, the immune system is also responsible for the repair of any damage that may have occurred during this onslaught. This rival theory for explaining the root cause of cancer will be specifically concerned with this third branch of the immune system, namely the repair function.

 The mechanism that starts the repair process is triggered when the body experiences some form of trauma. Clearly once this process has been set in motion, there needs to be a corresponding mechanism in place to inform the body of when the healing process has been completed. That is to say, the body must be made to know when to start, and when to stop the rapid formation of scar tissue, so that the immune system may end this elevated activity, and restore itself to the level of activity that existed prior to the trauma. It doesn't require too much imagination to realize that the inability to shut off this ‘repair process’ would result in a situation indistinguishable from what we presently call ‘cancer’. So 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 not receiving a signal as to when to stop. There must be a stop code. The absence of a stop code would result in the relentless formation of scar tissue, which is  synonymous with cancer.

 

Cancer becomes much less mysterious if we simply 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 new growth, by way of inflammation (again because it is its job to do so).

 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 leaves the cancer alone would become easily explained if the cancer were a function of a defective 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. This explanation would justify the association between cancer and the lymphatic system. It can also be explained why cancer is a modern disease and has been referred to as a ‘western disease’ if we take into consideration how western societies have treated their immune systems in the last half century.

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 A close examination of tumor tissues reveals that there are similarities between the formation of scar tissue (with its accompanying inflammation) 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), 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.”
 Notice that the tissues manufactured from this scar tissue method are given the attribute of being “functionally and cosmetically inferior” to normal tissue replacement. There would be no reason to expect that a fault in the p53 gene that allowed the cell to go on to reproduce itself over and over, would have this attribute of being functionally and cosmetically inferior. But ‘functionally and cosmetically inferior are attributes given to both cells manufactured by the immune system, and cell thought to be manufactured by cancer.

 

If cancer was a disease of the cell losing the ability to replicate itself in a controlled manor, then we would expect to see uniformity between the cancer tumor and the parent cell that had lost this ability to replicate itself in a controlled manner. We should not expect to see uniformity between cancers themselves (if this uniformity did not first exist between the parenting cells). But 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.

"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

"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

"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

"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 that comes to mind is, ‘If a fault in the DNA is causing this tissue growth, why is the daughter cell even distinguishable from the normal cell?’

All of this uniformity seems to imply that there is a common theme in all cancers, which in turn supports the proposition that there could be a single source of manufacture. It is impossible for the DNA model to account for this anomaly of uniformity. Yet it is an obvious deduction if the cancers were being manufactured by our immune system. A pattern of uniformity would be necessary if the immune system were held to be responsible for the generation of all these tissues. The cancer cell is distinguishable from the normal cell because it was manufactured by a different process then normal cell replacement. Since there are only two ways in which a cell can be manufactured, and only one of the two methods can account for the uniformity issue, and the fact that the new cell is even distinguishable from the parent cell, then it follows that the ‘repair’ aspect of our immune system is responsible for this non requested cell growth we call cancer.

 The belief that cancer cells can somehow become unrecognized by the immune system is a necessary stratagem of the present DNA theory. Yet the only occurrence in nature in which our immune system tolerates the existence of foreign cells to live in its domain is when the cells are from an identical twin. To give credence to the concept that some cells are unrecognizable to the immune system, we could phrase this phenomena to read ’ cells from an identical twin are unrecognizable to the immune system ’. We would then have one occurrence of this ‘unrecognizable’ phenomenon. But this begs the question, why? The answer I believe is intuitive. These cells go unrecognized because they have the same characteristics as the body’s own cells, and therefore the immune system does not recognize these cells as being any different. From this it can be concluded that since cancer cells are also treated in a similar manner to cells that are not recognized as being different, then they too are deemed to be not foreign. To say that they are not foreign is equivalent to saying that they are domestic, or rather, a legitimate part of the body. If there were any other occurrences in which living cells were granted the same privileges as the cancer cells, then this conclusion would not have any merited. Since there are no other occurrences (other than an identical twins) in which this phenomenon can be observed to occur, I feel that this conclusion is warranted, namely that cancer cells are a legitimate product of the body, and their function asserts that they are a part of our immune system.

 

The theory of natural selection relies heavily on a fundamental maxim called the ‘Borel-Cantelli lemma’ which is a theorem about sequences of events. The theorem is perhaps best exemplified with the cliché that if an infinite number of monkeys sat at an infinite number of typewriters and randomly press keys, they would eventually produce the complete works of Shakespeare. If we grant that this would eventually happen, then the same logic used to conclude this, would compel us to admit that there would, in the process be generated an unfathomable volume of typewritten gibberish. So where then is the gibberish in the field of cancer? If a single case of cancer is the culmination of a series of events, then it would be expected that there should exist a multitude of occurrences in which the entire chain of events did not occur. To address this anomaly, the scientific community has placed the entire blame on our p53 chromosome. If the orderly reproduction of our DNA is the responsibility of our p53 gene, then a defect in this one gene could be the ‘common denominator’ and then be used to account for all cases of mutated cell growth. That is to say; if the one gene responsible to oversee the orderly division of cells is itself defective, then the un-orderly division of cells could occur. This then becomes the ‘root cause’ of cancer from the perspective of the DNA model of cancer. It is mathematically comprehendible how the DNA of an individual cell might go astray, and starts to reproduce itself repeatedly as outlined in our present cancer theory, but this event would be limited to grow only to the size that could be supported by the existing blood supply. It would yield at best, a 'pea' sized growth. If the defect that we call ‘cancer’ were in fact shown to be the p53 gene reproducing the cell in an uncontrolled manor, there should be occurrences in which the cell did reproduce itself, but the accompanying blood supply did not happen. The scientific community acknowledges the need to address the blood supply issue, and with great difficulty, have postulated a complex chain of events that is both mathematically and logically absurd. This ‘root cause’ of cancer must therefore also have the attributed powers of being able to induce pathological angiogenesis which is the abnormal rapid proliferation of blood vessels. These cancer cells, we are told, release molecules that attract our endothelial cells, which then set out to successfully build a blood vessel system to get the much needed nutrients to the site. This amazing task is performed by a cell that is already deemed to be defective and in a nutrient and oxygen starved environment. All this must be identified as needed, set in motion, and successfully accomplished, all before the cell succumbs to its seemingly perilous situation. But the Borel-Cantelli lemma principal holds that if enough cells experience this, some are bound to go on and achieve the observed outcome. But how many mutated cells do not achieve the angiogenesis stage? And what becomes of them? Are they successfully dealt with by our immune system and disposed of? There would be evidence of this, and the observable evidence from the present dogmatic confines is that the immune system is doing nothing with cancer. It is interesting to note here that the principal method of combating cancer is chemotherapy. This cancer fighting protocol is described as a process of poisoning the entire body with the hope that the weak cancer cells will be the first ones to die. And chemotherapy is the most effective protocol at our disposal. We are further told that these cancer cells take on an immortal status, and acquire the ability to disguise themselves, and recruit allies in their defense, and a multitude of other special powers that are attributed only to cancer cells. When we examine this supernatural chain of events, and the obstacles that the cancer must overcome, and the safeguards that are in place to prevent these occurrences from happening the way they are described, one must ponder the likelihood of this occurring even once in a species with just over six billion members. The mathematical likelihood of acquiring cancer in your lifetime is approaching one in every two persons if you are male, and one in three if you are female.

 

One could point out that cancer activity can be clinically observed. If it were in fact, a normal body function, then why does it shows up on tests designed to indicate cancerous activity? The tests show heat being generated. The by-product of this unauthorized work being performed by this arm of the immune system; namely the cancer cells stimulating the rapid cell division and inflaming the area with increased blood flow, etc… is heat. This “heat” being generated is then interpreted as the immune system battling with the foreign antigen that is causing the cancer. But the irony in all this is that no foreign antigen can be found or observed at the cancer site, and the immune system has already been dismissed from the scenario, and labelled as not recognising and not objecting to the presence of the cancer. Every cell that can be observed in the cancerous area is legitimate. It would be prudent to ask the question ‘why would the immune system wait until this proposed antigen took up residency in the cell’s DNA before it amassed any objection to this antigen’s presence?’ If there were no activity, the area would operate at body temperature, and register as cold (not register). This is why cancer cannot be observed as it flows through the body. It can only be observed when it takes up residency and starts to inflame and stimulate the cell division in a new area. If, on the other hand, cancer were caused from some antigen inducing the DNA of a tissue to malfunction, and this antigen encountered an immune response, then we should be able to observe this cancerous activity as it moved to a new location. The fact that cancer cannot be observed as it moves throughout the body gives support to the premise that cancer is a legitimate part of the immune system.

 

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). The fundamental difference between a benign tumor and a cancerous tumor therefore becomes a product of the timing of when it is discovered. If we were to discover a tumor ‘after the fact‘, the body has stopped, and there is a mass of scar tissue that is currently not undergoing any development. If however, we were to stumble upon this exact 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 warranted, but then it received the ‘stop code’, and the immune system ceased this elevated activity. In a cancerous tumor, either the cells do not receive the ‘stop code’, or we 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 lets leave it alone, 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 point of time in the past. The benign scar tissue has already been manufactured by the immune system, and is now dormant. Everyone freely accepts that the inactive scar tissue was manufactured by 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 the immune system, though be it a defective one.

The immune system accepts this benign tumour as part of the ‘self’, for the same reason that it accepts the cancer; because it possesses all the characteristics of the legitimate body cells. The cancer cells that created the tumour, and then stopped, have either been reclaimed by the immune system, and may function normally in the future, or they may travel to another part of the body (through the lymphatic system) and start to stimulate cell division at a new location. These tumours that the cancer cells unnecessarily produce, are not marked for destruction because they posses all the characteristics of the body’s own cells. The immune system is designed to recognize the body’s own cells so as not to attack itself. These mutated cells will not be attacked by the immune system either, because they are legitimate body cells. This explanation would help us to understand why the body’s own immune system is useless against fighting cancer. This also makes sense of the fact that all attempts to employ the immune system into attacking the cancer cells have failed. And it also justifies why the three oncological approaches that have shown to be the most successful treatments for combating cancer are the only three procedures that make no attempt at employing the immune system in the first place.  These three most successful protocols for fighting cancer are chemotherapy, radiation, and surgery. All other scientific studies and protocols that presently offer treatment to cancer patients tend to focus on the immune system. These studies have two things in common:

1) they are unsuccessful at curing cancer, and

2) they all try to stimulate; enhance; activate; invigorate; boost; assist etc., the immune system.

There are only three cancer treatments that make no attempt at employing the immune system. Coincidentally, these three treatments have over the years, proven to be superior to the multitudes of cancer fighting regimes that try to employ our immune systems.  Note however that these three most successful protocols for fighting cancer, all inadvertently incorporate the immune system by placing a workload on it. In all of these cases, the immune system must come on the scene to repair the damage that has been inflicted onto the tissues of the various sites. Placing a workload on the immune system provides a workout, or exercise for it.  All the other protocols try to enhance, strengthen, and invigorate the immune system into a conflict with the cancer cells. This new framework for viewing cancer would help us to understand why these protocols fail to achieve their objective, and further help to account for why the protocols that do not involve the immune system are the most successful. From the vantage point of viewing cancer as a function of a defective immune system, we can understand why the most successful protocols continue to be the most successful. The DNA theory for explaining cancer offers no insight as to why some protocols are more, or less, effective than others. Why for instance would a patient who underwent surgery to remove a cancerous tumor, not go on to enjoy the same level of health as a patient who underwent a non cancerous surgery? When a medical professional discovers an active tumor being produced, he or she may opt to surgically remove the tumor and the offending cancer cells that made it (excisional 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 also contain the offensive cancer cells. They test the removed tissue and confirm that it was indeed cancerous. They then close up the wound and hope that they have managed to remove all of the cancerous tissue. They must now wait until the immune system has had time to heal up the surgical wound before testing the area, because the elevated activity and the inflammatory nature of the healing process will read as hot. So now we have the defective immune system, which might one day be shown 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, receives a signal that the healing is complete, 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 relentlessly. The poor surgeon is mystified that they could have missed some of the cancer cells. The 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, perhaps, is what causes it to flourish. Exposing the cancer to the light and air is a 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. Since the immune system may have already shown to be defective, it is conceivable to hold that sometimes it does turn out to inflict the area with a new cluster of cancerous activity, despite how diligent and careful the surgeon had performed. If faulty DNA were the cause of the cancerous activity, then mathematically, the individual who underwent the surgical removal of the offensive tissue should be granted the same bill of health and have the same survival statistics as anyone who had undergone a similarly invasive surgery. Unfortunately the statistics do not support this optimistic view. This patient might still possess a faulty immune system that is capable of generating these unwanted tissues.

 

 When the immune system is healthy and functioning properly, these cancer cells are kept at bay and in harmonious balance with the rest of the system (identify and destroy), so most people live out their lives oblivious to this second method of cell generation. It is only when something goes astray that we come to know of their presence. Thus, cancer cells are only thought of as being bad.

 

 This ‘scar tissue’ model does not yet attempt to account for the various forms of cancer that a defective immune system may choose to take. Why does the defective immune system start to randomly multiply the tissues of the breast in some individuals, and the lung tissue in others? The statistical evidence tends to support that there is a hierarchy amongst tissue types. There are different types of tissues in the body, and the observable data supports that some of these tissue types are simply easier then others for a defective immune system to stimulate into unnecessarily forming scar tissue. Cancer appears to be an ‘opportunistic disease’. That is to say, the immune system will ‘pick-on’ or stimulate the tissue that it finds to be the easiest tissue to do so with within a given individual. We can look at the various links (environmental links; lifestyle links; heredity links; etc.) as antigens that either promotes a tissue type towards being the easiest tissue, or the link may demote a certain tissue away from being the likely candidate from which the defective immune system can operate. Tobacco smoke or asbestos dust has been linked to cancer of the mouth, oesophagus and lung. Using this new model we can view these tissues as having been weakened by these antigens and now represent the easiest forms of tissue that this individual is in possession of. If this individual also possesses the requisite faulty immune system, then this person will get cancer, and it will be a cancer of one or more of these weakened tissues.

Conversely, a high fibre diet has been linked to a decrease in the number of colon, anal and intestinal cancer patients. Using this new model we can view the high fibre diet as having strengthened the tissues in this region away from being the easiest tissue from which the defective immune system can operate. If colon cancer can be averted by implementing a high fibre diet, then it may turn out to merely be a pyrrhic victory. The patient who avoids colon cancer by eating a high fibre diet, will ultimately succumb to some other type of cancer if they already posses the requisite weakened immune system, and do nothing to change this. Again, the evidence tends to support this belief, which has led to the dilemma whereby doctors manage to overcome one type of cancer, only to have the patient succumb to another type. The supporters of the DNA model dismiss this dilemma by saying that the patient was merely allowed to live longer and thus was permitted the time necessary to acquire some other type of cancer.(*1) But the real problem is that the doctors and scientists are devoting their efforts in treating the attacked tissues, while ignoring what is attacking them, namely the immune system itself.

This hierarchy of tissue types tends to show that our melanin cells appear to be one of the easiest cells from which a defective immune system can wreck havoc. One of the best ways to demonstrate this principle is to look closely at malignant melanoma. One of the most bizarre anomalies in the field of cancer research is in regards to melanoma. Melanoma has been linked to sun damage, yet it is 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 because of the location, could not be attributed to sun damage. The 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 adapted 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 would view these melanin cells as no longer be 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 an opportunistic faulty immune system will discover to be easier to stimulate into this unwanted tissue. This same trend can also be observed by studying the cancers of Northern Europe and comparing these to countries closer to the equator in Southern Europe. The statistics support that countries nearer to the equator, have lower incidence of melanoma but 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 principle can be applied across the board in explaining why some types of cancer are more uncommon then others. The rarer forms of cancer have a cell structure that is more difficult for the defective immune system to stimulate into scar tissue. This new vantage point is the only viable means with which to address the anomaly as to why African Americans (and Hispanic Americans) suffer disproportionately with a number of cancers and heart disease.

 

 We have always been aware that people who share the same culture, same lifestyle, same access to health services and facilities, 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 from one form of cancer, then by using this new model we would expect that the numbers would have to be compensated for in other forms of cancer. We see a prime example of this prediction by examining cancer in African Americans. They share the same culture as the North American Caucasians, and yet they could be considered to be genetically immune from acquiring skin cancer due to their darker pigmentation. Thus we see African Americans with alarmingly higher rates of lung cancer, for instance. Studies were conducted to see if they perhaps smoked more to account for this discrepancy. However, it was determined that they actually smoke less. It was then postulated that although they smoke less, perhaps they inhale deeper. It is absurd to generalize that an entire group of people who are known to smoke less then Caucasians, are inhaling deeper, merely to attempt to give credence to this observation and prevent it from becoming yet one more anomaly surrounding this disease. 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. 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 cause of cancer (skin), then they therefore must fall into one of the other categories of cancer, in this case, the number two (lung) cause of cancer. 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 phenomena can only b