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Old 29-04-2014, 09:33 AM   #301
jondoeuk
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Warburg Rules!
A Review of Thomas Seyfried’s Cancer As a Metabolic Disease

Once in a long while, a book comes along that revolutionizes our understanding of the cancer problem. Such a book is Cancer as a Metabolic Disease (Wiley 2012) by Thomas N. Seyfried, PhD. Formerly a cancer researcher at Yale University, Seyfried is a professor of biology at Boston College and the author of more than 150 PubMed- indexed scientific articles.

With its 400-plus pages, and over 1000 scientific references, Cancer as a Metabolic Disease covers very broad territory. It attempts to explain the essential nature of primary tumors and of metastases, at the same time providing practical advice on the management and prevention of cancer.

The book’s central message stands in stark contrast to the prevailing dogma in cancer research. But Seyfried’s approach is rational, methodical, and scientific. It is grounded in the fundamental biochemistry of cancer and is up to date. This book should be required reading for all scientifically literate people involved in the cancer problem. You need to buy, read, and assimilate this book in its entirety if you expect to thoroughly understand the debate over cancer.

As a result, we now have a thorough picture of how defects in metabolism drive the various changes seen in cancer, including its famous “genome instability.” It is an amazing intellectual achievement. Stephen Strum, MD, FACP, agrees. He has written as follows:
I am a board-certified medical oncologist with 30 years experience in caring for cancer patients and another 20 years of research in cancer medicine dating back to 1963. Seyfried’s Cancer as a Metabolic Disease is the most significant book I have read in my 50 years in this field. It should be required reading of all cancer specialists, physicians in general, scientific researchers in the field of cancer and for medical students. I cannot overstate what a valuable contribution Thomas Seyfried has made in writing this masterpiece.

I would prefer if every reader went out and bought a copy of this book immediately. (It is available on Amazon.) But Townsend Letter readers might appreciate a summary, so that they can at least become familiar with its major points.

The Somatic Mutation Theory
The conventional theory of cancer, subscribed to by the vast majority of scientists, is the somatic mutation theory (SMT; Fardon 1953; references below).

The basic premise of the SMT is that cancer is a genetic disease. While some forms of cancer are linked to inherited (or germ line) mutations, the primary thrust of the theory is that cancer typically originates in the course of a person’s lifetime as a result of a cascade of genetic injuries. These “somatic mutations” lead, step by step, from a quiescent normal cell to a lethally proliferating one.

Seyfried’s differences with the majority of his colleagues begin at this point, for he regards a normal cell as fundamentally proliferative, like primitive bacteria, and not naturally quiescent, as most biologists believe. Cancer, he says, involves a fundamental loss of control rather than the acquisition of numerous mutations that ultimately convey some hitherto-unsuspected ability to replicate wildly. There is not enough room in this article to explain his argument in detail, but I found it compelling.

“The SMT has not been rigorously tested, and several lines of evidence raise questions that are not addressed by this theory,” according to two professors at Tufts University School of Medicine, Boston (Soto 2011). Seyfried agrees. But the SMT has received a huge boost in the past 10 or so years due to scientists’ ability to sequence a cell’s genome (i.e., its complete collection of genes) and to do that economically. To sequence the first human genome cost around $3 billion. But news stories in 2012 announced that a person’s genome could now be sequenced in one day for a mere $1000 (Hayden 2012).

This increasingly easy access to a complete genomic analysis of both normal and malignant cells has led to the discovery of an incredible genetic diversity within cancer cells. Consider for instance this paragraph from Science magazine’s review of cancer research for the 40th anniversary of the War on Cancer:

We now know that there are usually between 1,000 and 10,000 somatic substitutions in the genomes of most adult cancers, including breast, ovary, colorectal, pancreas, and glioma….There are cancer types that generally carry relatively few mutations – for example, medulloblastomas, testicular germ cell tumors, acute leukemias, and carcinoids, whereas others, such as lung cancers and melanomas, have many more mutations (occasionally more than 100,000) Even within a particular cancer type, individual tumors often display wide variation in the prevalence of base substitutions” (Stratton 2011).

Imagine, then, trying to devise a treatment regimen that must target 1000, 10,000, or even 100,000 separate mutations! With new analyses of various cancer genomes emerging almost weekly, the variations among tumor cells have grown to gargantuan proportions.

Deciphering the human genome was a dazzling technical accomplishment. But it is not necessarily relevant to solving the cancer problem. Any theory of cancer as a single disease with many manifestations is now firmly rejected in favor of cancer as a “disease complex,” not just of 100-plus anatomically defined tumor types, but with 1000, 10,000, or 100,000 individual peculiarities. These highly individualized presentations of cancer supposedly require a correspondingly complex set of treatments in order to fully “personalize” drug therapy.

Theory of Metastases
Seyfried also proposes an uncommon theory of metastasis, in which wandering cells do not just break away from the primary tumor but are themselves either transformed macrophages or at least fusion cells made up of cancer cells and macrophages. I was surprised to learn that Prof. Otto Aichel of Germany proposed this theory in 1911. John Pawelek, PhD, of the Yale School of Medicine and the author of nearly 200 peer-reviewed papers, has revived this theory in our era (Lazova 2011).

In their famous “Hallmarks of Cancer” articles (2000 and 2011), Weinberg and Hanahan claim that genome instability is the essential “enabling characteristic” of all cancers, including metastases. But Seyfried proposes an alternative view; that is, that the key lethal flaw in cancer does not originate in the nucleus at all but in the mitochondria. Mitochondria are the power plants of the cell, where a person’s energy is created.

Through the tricarboxylic acid (TCA) cycle, mitochondria can turn one glucose molecule into ~30 packets of energy (i.e., adenosine triphosphate, or ATP. The theoretical yield in a normal cell is 38 ATP molecules from each oxidized glucose molecule. In practice the yield is usually between 29 and 30.) This process is called oxidative phosphorylation – or OxPhos, for short (Rich 2003).

Seyfried affirms the commonly held view that cancer originates in the impact of carcinogens (radiation, tobacco smoke, asbestos, etc.) but that this damage crucially affects the mitochondria, not only the nucleus. This damage causes chronic inflammation and respiratory insufficiency. Some cells, deprived of sufficient oxygen to function, simply die. But others, in order to survive, find a way to generate energy without the use of OxPhos. Like yeast growing in beer or bread, they inefficiently transform glucose into a very limited amount of energy, and produce as waste products carbon dioxide and lactic acid. This is fermentation among mammalian cells, and cells adopt it as a way of compensating for the breakdown of the TCA cycle. That is why it is called compensatory fermentation. This provides energy for a cancer cell’s survival and replication, provided that the patient in question provides an abundant supply of glucose or its carbohydrate precursors. That is why cancer is an avid “sugar junkie” and why FDG-PET scans (which detect a radioactive form of glucose) are now used all over the world to detect cancer.

Enter Otto Warburg
In its basic outlines, this theory of cancer is hardly new. In fact, it was propounded by Otto H. Warburg, MD, PhD, from 1923 until his death in 1970. Warburg won the Nobel Prize for this work in 1931. Warburg was indisputably one of the greatest scientists of biochemistry’s golden age. Then came World War II, with all its tragic consequences. After the war, Warburg’s claims that cancer ferments instead of engaging in healthy OxPhos came under withering attack from critics, primarily Prof. Sidney Weinhouse of Philadelphia (1909–2001), editor of Advances in Cancer Research.

Warburg’s point of view, says Seyfried, was fundamentally right. But, with the perspective of time, his theory had some weaknesses as well. For instance, it did not account for: (1) the role of tumor-associated mutations, which were increasingly coming to the fore in cancer research; (2) the entire phenomenon of metastasis; and (3) the molecular mechanisms of uncontrolled cell growth and how they related to impaired respiration. Even his student, the Nobel laureate Hans Krebs, finally agreed that the fermentation of glucose in the presence of oxygen (aerobic glycolysis) was merely a symptom of cancer, not (as Warburg maintained until his death) the cause. In the US, his chief American disciple, Dean Burk, PhD, cofounder of the National Cancer Institute (NCI), remained true to his fundamental vision.

The strongest evidence against Warburg was Weinhouse’s demonstration that many tumors continued to utilize oxygen while also engaging in fermentation. This seemed to show that OxPhos continued, while the cancer cell fermented as a side activity. If this were truly the case, then Warburg’s theory was fundamentally contradicted. Burk and a few others tried to salvage Warburg’s theory, but the data went against them. In fact, it was only fairly recently that Seyfried and others showed that this utilization of oxygen by tumors is without any energy-generating capacity. It is oxidation “uncoupled” from any normal or productive usage.

Due to the work of Prof. Peter Pedersen of Johns Hopkins University, Seyfried, and others, Warburg’s theory is now experiencing an unexpected revival. In 2011, Weinberg and Hanahan revised their 2000 Cell paper, to include “reprogramming of energy metabolism” as another (seemingly forgotten) hallmark of cancer (Pedersen 2007; Hanahan 2011).

The Nobel laureate Thomas D. Watson, PhD, codiscoverer of DNA’s molecular structure, has called into question the search for treatments based on genetic abnormalities and has urged his fellow scientists to turn toward a study of metabolism. In December 2010, Science magazine published a review of metabolic energetics in cancer. In it, Prof. Arnold J. Levine (codiscoverer of the p53 tumor suppressor protein) of the Institute for Advanced Study, Princeton, and a colleague restated the classic Warburg hypothesis. Studying altered metabolic pathways, they said, “could lead to a new approach in cancer treatments.”

So, the situation today is that almost nobody doubts that cancer cells exhibit both genetic and metabolic abnormalities. The conundrum is which abnormality is cause and which is effect. Even among those who stress the importance of metabolic targets, there is a belief that genes must be driving abnormal metabolism and not the other way around. Molecular biology is locked in a kind of genetic determinism.

Only Seyfried, Pedersen, and a few others have taken a truly Warburgian approach, unequivocally stating that cancer is a disease of injured mitochondria and its resulting compensatory fermentation and that this causes the genome to degrade in unpredictable ways.

In this comprehensive book, Seyfried shows that oxidative insufficiency and its resulting compensatory fermentation cause genome instability. “All hallmarks of cancer including the Warburg effect can be linked to impaired respiration and energy metabolism,” he writes (p. 26). These are “downstream effects of damaged mitochondrial function.”

He cites research showing that if you transplant a nucleus containing mutations from a cancer cell into a normal cell (from which the nucleus has been removed), this does not produce cancer cells (McKinnell 1969; Mintz 1975; Howell 1978; Harris 1988; Shay 1988; Li 2003; Hochedlinger 2004). But if you transplant a normal nucleus into a cancerous cell, the cell can now form tumors – again, presuming that the original nuclear material has been removed (Israel 1987; Israel 1988). These results show that nuclear gene mutations alone cannot produce tumors and that normal mitochondria can suppress tumor formation.

Seyfried also has a great deal to say about how this new-old conceptual view of cancer affects the proper idea of cancer, particularly a novel dietary treatment.

Seyfried’s book opens the door to a discussion of cancer as a metabolic disease. We now need a wide-ranging discussion of the fundamental nature of cancer. Is it genetically driven, as most believe, or in fact does mitochondrial insufficiency, followed by compensatory fermentation, drive genome instability? Seyfried makes a powerful case that, in effect, “Warburg rules,” and that control of cancer will come about by controlling fermentation.

In the tradition of Otto Warburg, Dean Burk, and Peter Pedersen, Thomas Seyfried has attempted to inform the world about the nature of cancer and of more effective ways that this scourge can be brought under control. I highly recommend Cancer as a Metabolic Disease to all readers who want the clearest statement yet of the metabolic cause and control of cancer. I look forward to a debate over its arguments, for this will almost certainly revolutionize the entire war on cancer.

References
Fardon JC. A reconsideration of the somatic mutation theory of cancer in the light of some recent developments. Science. 1953;117(3043):441–445.

Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000 Jan 7; 100(1):57–70.

———. Hallmarks of cancer: the next generation. Cell. 2011 Mar 4;144(5):646–674.

Harris H. The analysis of malignancy by cell fusion: the position in 1988. Cancer Res. 1988;48:3302–3306.

Hayden EC, Nature News Blog. The $1,000 human genome: are we there yet? [blog post]. Scientificamerican.com. Jan. 10, 2012.

Hochedlinger K, Blelloch R, Brennan C, et al. Reprogramming of a melanoma genome by nuclear transplantation. Genes Dev. 2004;18:1875–1885.

Howell AN, Sager R. Tumorigenicity and its suppression in cybrids of mouse and Chinese hamster cell lines. Proc Nat Acad Sci U S A. 1978;75:2358–2362.

Israel BA, Schaeffer WI. Cytoplasmic suppression of malignancy. In Vitro Cell Dev Biol. 1987;23:627–632.

———. Cytoplasmic mediation of malignancy. In Vitro Cell Dev Biol. 1988;24:487–490.

Lazova R, Chakraborty A, Pawelek JM. Leukocyte-cancer cell fusion: initiator of the warburg effect in malignancy? Adv Exp Med Biol. 2011;714:151–172.

Levine AJ, Puzio-Kuter AM. The control of the metabolic switch in cancers by oncogenes and tumor suppressor genes. Science. 2010;330(6009):1340–1344.

Li L, Connelly MC, Wetmore C, Curran T, Morgan JI. Mouse embryos cloned from brain tumors. Cancer Res. 2003;63:2733–2736.

McKinnell RG, Deggins BA, Labat DD. Transplantation of pluripotential nuclei from triploid frog tumors. Science. 1969;165:394–396.

Mintz B, Illmensee K. Normal genetically mosaic mice produced from malignant teratocarcinoma cells. Proc Nat Acad Sci U S A. 1975;72:3585–3589.

Nebeling LC, Miraldi F, Shurin SB, Lerner E. Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports. J Am Coll Nutr. 1995;14(2):202–208.

Pedersen PL. Warburg, me and Hexokinase 2: Multiple discoveries of key molecular events underlying one of cancers’ most common phenotypes, the “Warburg Effect”, i.e., elevated glycolysis in the presence of oxygen. J Bioenerg Biomembr. 2007;39(3):211–222.

Rich PR. The molecular machinery of Keilin’s respiratory chain. Biochem Soc Trans. 2003;31(Pt 6):1095–1105.

Shay JW, Werbin H. Cytoplasmic suppression of tumorigenicity in reconstructed mouse cells. Cancer Res. 1988;48:830–833.

Soto AM, Sonnenschein C. The tissue organization field theory of cancer: a testable replacement for the somatic mutation theory. Bioessays. 2011;33(5):332–340.

Stratton MR. Exploring the genomes of cancer cells: progress and promise. Science. 2011;331(6024): 1553–1558.

Watson JD. To fight cancer, know the enemy. New York Times. August 6, 2009

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Old 30-04-2014, 12:43 PM   #303
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According to Boston College professor and cancer research scientist Thomas Seyfried, the very origin of cancer is in dispute. His recently published book Cancer as a Metabolic Disease is having a dramatic impact on the field of integrative oncology.
   
To quote Ralph Moss, "Once in a long while, a book comes along that revolutionizes our understanding of the cancer problem. ... You need to buy, read, and assimilate this book in its entirety if you expect to thoroughly understand the debate over cancer."
   
The war on cancer has not been won. In his book, Seyfried meticulously explains why it is not a genetic disease and says that we will not likely make any substantial progress until we recognize and direct our therapies toward the true cause of cancer.
   
Seyfried will be a keynote speaker at the Oncology Association of Naturopathic Physicians (OncANP) 3rd annual conference this coming February 14, 2014 in Scottsdale, Arizona (www.oncanp.org).
   
As I am a member of the conference speaker committee, the Townsend Letter very graciously gave me the opportunity to interview Seyfried to highlight his work and appearance at our conference.

Michael Uzick: How did you become involved in researching the effects of ketogenic diets in cancer?

Thomas Seyfried: We had been doing research on the biochemistry of tumors for decades, particularly lipid metabolism. We knew there were certain kinds of lipids expressed in tumor cells and we were mainly interested in figuring out what kind of function the lipids might have. At the same time, we had a parallel study on the genetics of epilepsy and one of my students talked to me about the ketogenic diet as a therapy for epilepsy. We took the natural models that we had developed and evaluated ketogenic diets for epilepsy and we became very involved in the mechanisms by which ketogenic diets affect epileptic seizures. We found that the majority of the therapeutic benefit of the ketogenic diet came from calorie restriction. One of my other colleagues knew that calorie restriction could be effective against tumors, so we tried this and we saw how powerful it was in blocking tumors. This has been known for a hundred years. Then we just put them together and found out that if you restrict calories on the ketogenic diet you can actually get better therapeutic benefit than either alone. So, it was a fortuitous combination of research activities that were taking place in the lab at the same time.

MU: Your book, Cancer as a Metabolic Disease, challenges the current scientific paradigm on the origin of cancer. Can you describe the current paradigm and how you came to question it?

TS: The current view now, without any question, is that cancer is a genetic disease. If you go on the National Cancer Institute website or you read any of the major articles published in Nature and Science, often the articles will start with, "Cancer is a genetic disease." I think that this has become dogma. It became clear to us as we did our research that the therapeutic benefits we were seeing from calorie restriction had their origin with Otto Warburg. But if he was correct, why are we talking about genes? The gene theory became predominant following Watson and Crick's evidence that DNA is the genetic material and finding all the mutations in cancer cells. One thing led to another and, among the powers that be, the gene theory won out. The gene theory seemed to be more consistent, and there were mutations that seemed to be either provoking the growth of the tumor or failing to suppress the tumor. The entire field was built on this foundation, that genes are regulating this entire process. But if one goes back in the literature, one can see clear disconnects in the linkage between nuclear genetic problems and the origin of the disease. For example, Darlington had clearly shown that there were carcinogens that did not damage the nuclear DNA, but did cause cancer. He concluded that cancer could not be a nuclear genetic disease. It had to be something in the cytoplasm and he alluded to factors that were related to the mitochondria. That's exactly what Warburg had said, but Warburg's theory had been discredited because it was observed that you could see normal respiration in cancer cells. Of course the genetic argument is that the metabolic issues are due to oncogenes and that's where the big controversy is and I looked at that very carefully and was able to parse it out. It turns out that the oncogenes are responding to the abnormal metabolism of the cell and we were able to show this. It is actually the abnormal metabolism of the cell that's dictating the genetic mutations. This is where my book challenges the field. It provides credible scientific evidence that seriously questions the notion that cancer is a genetic disease. And I think you are not going to make major advances in the field of cancer until this becomes more widely recognized.

MU: You mentioned that Warburg was discredited because some cancer cells were found to have normal respiration. Can you explain how this is possible?

TS: Most of the work that challenged Warburg's theory was done in culture. When you grow mammalian cells in culture, they take on characteristics that they don't generally have when growing in vivo. For example, if you take normal cells and grow them in culture, invariably they produce lactic acid. This doesn't happen in vivo. Muscle will produce lactic acid when it's under incredible physiologic stress, until there's enough oxygen returning to the system to suppress the formation of lactic acid. So there are a number of artifacts of the in vitro system that compromised the view of cancer as a disease of respiration. Now, when you look in vivo at cancer cells, invariably most cancers will have structural aberrations in their mitochondria. In breast cancer the majority of aggressive breast tumors have no mitochondria. So there's no way that these cells could have normal oxidative phosphorylation. So none of this is discussed in the literature. They just ignore it. I went back and looked at it and I said, "You can't say respiration in cancer cells is normal when there's so much evidence to say it isn't."

MU: Let's assume that everyone agrees all cancer cells have damaged respiration. But then the question becomes, which came first – damage to the genes or the abnormal respiration?

TS: If you go into the literature, the studies reveal the answer. If oncogenes are the drivers of this disease, why is it that when you take the nucleus from a tumor cell and put it into a normal cytoplasm, the nucleus is no longer capable of producing the disease? And now within the last year people have been able to transplant mitochondria. So if you transplant normal mitochondria into a tumor cell's cytoplasm, you suppress the tumorgenic phenotype. And if you transplant abnormal mitochondria into a normal cytoplasm, you can produce developmental abnormal cells or dead cells. You can actually stimulate oncogene upregulation. So it tells me that the mitochondria are calling the shots.

MU: Your research has shown that a CRKD [calorie-restricted ketogenic diet] significantly inhibits brain cancers and in your book you have suggested that this dietary intervention should be effective in every kind of cancer. Can you explain how a CRKD impacts cancer?

TS: So why are tumor cells producing lactate if they have normal respiration? We have blood cancers that have plenty of oxygen in the environment, yet they still produce lactic acid. Cancer cells are producing lactic acid because they can't get sufficient energy through normal respiration, and must therefore use fermentation instead. Fermentation usually occurs in the absence of oxygen, not in the presence of oxygen. So what’s going on here? The simplest explanation and the one supported by a variety of different studies, is that their respiration is damaged or insufficient in some way. Now ketones are an alternative fuel, which evolved to substitute for glucose when our food intake was suspended. Our bodies will transition to stored fat for energy, which is broken down to ketone bodies which can then be burned by all of the tissues, especially the brain. But you need good mitochondria to metabolize ketones. These have been shown to be abnormal in many different kinds of cancers. So the tumor cells can't transition to the alternative fuel that normal cells evolved to use. This seems like a very simple way to put pressure on cancer cells without toxicity.

MU: I understand how ketones are involved. But where does the caloric restriction come in? Why does that become important?

TS: We gave animals unrestricted ketogenic diets and the tumor cells grew just as fast, or even faster sometimes, than a standard high-carbohydrate diet. So we said, what's going on here? There's a diet with zero carbohydrate and the animals are eating as much as they want and when we looked at their blood, their blood sugars were very high. So it turns out if you eat large amounts of fat in a ketogenic diet you get insulin insensitivity, which then increases the level of sugar, and the cancer cells are fat and happy using this. So you have to restrict the diet. Because the glucose is now low and the ketones must be retained to be used for energy.

MU: So if caloric restriction is required, how can one maintain this approach in order to target cancer?

TS: You know the issue is, how long should you do this? I have to admit in some of my earlier publications, we were pretty hyped on the calorie restriction aspect of it. We were probably going a little overboard on how many calories you need to restrict. Only after we saw rather substantial regression of tumors or stabilization in people who cut down to maybe 1500 calories a day, which is not anywhere near a heavily restricted diet, did we begin to see that each individual is a unique metabolic entity. Some people require minimal restriction and other people require more restriction. If you look in the literature, a lot of people are using ketogenic diets to remain in a healthy state at low weight. And people can maintain this for years and they seem to be very healthy. Now I'm not saying all cancer patients need to maintain for the rest of their lives a state of low glucose and elevated ketones. I suggest they do it until there is clear evidence that the disease has been arrested or stabilized. And then there's a likelihood one could transition off of this, as they would for any kind of therapy.

MU: Valter Longo, PhD, will also be speaking at the OncANP conference about his research looking at the benefit caloric restriction during the administration of chemotherapy. Do you have any thoughts on Longo's research and any parallels between your own?

TS: You know I agree, I think what he's seeing is real and I think it's important. I have heard of and spoken to people, physicians who have done therapeutic fasting on some of their patients for as much as 30 days and have seen cancer regression in some patients. Water only, you know without any chemo. So if you fast with only water like the Longo group does, the body goes into defense mode. And what I think is happening is a lot of these tumor cells become very compromised under these stressed conditions. Here's where the mutations play an important role in allowing these therapies to work. Many of these cancer cells are loaded with all kind of mutations. And what those mutations do is prevent those cells from making the correct adaptations to the new stressful environment, so they now become in a much more compromised state. So if you give chemo under this therapeutic fasting condition, those cells are going to be less able to deal with the chemo and die faster than the normal cells, which are able to make these adjustments to this new metabolic state. I think it's another view of the same kind of approach. There are metabolic approaches to managing cancer that people need to recognize.

MU: Your book opened my mind to the idea of ketones as anticancer agents. I specialize in enhancing the effectiveness of conventional therapies while reducing their toxicity. I was surprised by the number of studies showing that ketones, at least in vitro, enhance the effectiveness of several chemotherapeutic agents.

TS: The question is, are they toxic in vivo? We have a paper that's under review now with my colleague Dominic D'Agostino and his graduate student Angela Poff at the University of South Florida. He has evidence that elevated ketones can in fact be toxic to the tumor cells. In my earlier writings, we were considering the ketones to be largely protective of normal cells and basically tumor cells just can't use them. But now we have evidence that they may in fact be toxic to the tumor cells. So it's a one-two hammering of the tumor cells. You're pulling away their glucose, forcing an alternative fuel they can't use, and potentially an alternative fuel that will actually kill them.

MU: I see a general fear among cancer patients about losing weight. Medical oncologists for the most part recommend that patients eat ice cream and high carbohydrate foods so as to not lose weight. When you have a patient who is already starting off thin, is there reason to be concerned?

TS: For those patients, we know that the ketogenic diet will cause some initial weight loss, but it also maintains muscle mass. Tisdale showed this years ago in England. So, there's a certain way to do this and the patient's weight can be stabilized. Cachexia is a very dangerous situation but you can institute a ketogenic diet, and yes, initially there will be some weight loss, but the weight will stabilize.

MU: Currently the NIH (National Institutes of Health) lists eight clinical trials under way or completed examining the effects of ketogenic diets in patients with cancers. Have you been involved with any of studies and do you think your research has played a role in the interest in this topic?

TS: Our studies were motivated by Linda Nebeling's 1995 case report on the therapeutic efficacy of the KD in two children with malignant brain cancer. Our research has certainly established the evidence for the current interest and I am excited that some members of the medical community find our approach to cancer management interesting and worthy of patient application. I have helped with protocols for some studies, but not for others. I am not presently participating in any of the studies. I can only hope that the PIs of these studies know what to do, and how to collect and interpret the data.
   
These studies are all in combination with either radiation or chemotherapy. My preference is to start metabolic therapy with GBM (glioblastoma multiforme). This is a devastating type of brain cancer. Metabolic therapy with a restricted KD could be done with a few tumors where you know the conventional standard of care doesn't work at all. You would choose those kinds of patients and do a clinical trial based on historical controls and see what the outcome would be and see if you could get some level of survival that would match or be better than the conventional standard of care.

MU: Since the publication of your book, have you become aware of more successful cancer cases using your approach?

TS: We are hearing about more cases for sure. I know only of a few, that I've participated in directly, where people are really collecting the key biomarkers to establish the therapeutic efficacy. So the people whom I do know that are responding fairly well are showing me very careful and comprehensive daily blood glucose and ketone values. We have documented blood work from some individuals that go over years. I think up to about 2 years for the most part and sometimes longer.
   
I have data on a dog, if you can believe; you know dogs respond really well to this therapy, I never saw such responses in some. We have a good case-controlled report we are working on now out of Greece where the person had non-small cell lung cancer metastasized to the brain. He's been on the metabolic therapy now for 4 years and he seems to be doing well. But these are all anecdotal reports. Nevertheless, if you do the case studies correctly, like we did for the Italian woman, that we published in Nutrition & Metabolism, there's a very comprehensive case report that served as a basis for others.
   
There are some people out there, like any media thing, they'll say, "Oh, the ketogenic diet cures cancer." We know there's no evidence for that. We haven't used it long enough to know if anybody is going to be cured from cancer using a ketogenic diet. All we can say is that the ketogenic diet has the potential to arrest the growth of the tumor. Now whether it's cured in the long run, who knows? It's going to take a long time to figure out whether these people are cured or not.

MU: In your book you mention 2-deoxyglucose as an adjunctive treatment to the CRKD. Many integrative oncology specialists are using DCA (dichloroacetate) in a similar way. Are there any new or exciting metabolic therapies to go along with a CRKD?

TS: Well, I think this is going to be the future. I mean the ketogenic diet by itself is just like step number one. As I said, you bring the patient into a new metabolic homeostasis where ketones become the predominant metabolic fuel and glucose is reduced. At that point now your tumor cells are under metabolic stress to a much greater extent than the normal cells. Now you can have add-ons, you have DCA, you can have 3-bromopyruvate, phenylbutyrate, there are approaches that are attempting to control the glutamine issue with respect to cancer. I think hyperbaric oxygen from the work I've seen with Dominic D'Agostino has tremendous potential, and the mechanism of action become clear once you recognize that cancer is a metabolic disease. The important thing is that in most cases the patient does not need to be harmed by these approaches. So many patients are harmed today from the current standard of care. Some drugs have very little effect when used alone, can have tremendous affect when matched together with CRKD. So there's a lot to be hopeful about I think in the future.

MU: You have written about glutamine being a specific fuel for cancer cells. Several clinical trials have shown that high doses of glutamine significantly reduce chemo- and radiation-related side effects, without interference in outcomes. This has become a controversial issue among naturopathic oncologists. Can you address this concern about glutamine?

TS: The glutamine issue is a really important one. If you go into the basic scientific literature, you see numerous papers in top scientific journals. It's pretty well recognized among the individuals who do basic research that glutamine together with glucose act as a powerful synergistic metabolic stimulus to tumor cells.
   
So let's talk a little about glutamine. OK, well first of all we know that glutamine is the most abundant amino acid in the body. And it's used extensively by cells of the immune system, like macrophages and lymphocytes, as a prime fuel. In burn patients they give glutamine infusions. You have to jack up the immune system to fight the bacteria. Certainly glutamine is going to be a good metabolite to restore some level of immune function.
   
On the other hand we have to recognize that many of the metastatic cancer cells are part of the immune system. There's a number of articles from John Pollack at Yale, Melisa Wong at Oregon, and a number of others showing that the cancer metastatic cell is a fusion hybrid between an immune cell like a macrophage and some cancer stem cell. So you have this hybrid cell that has the characteristics of both a stem cell and an immune cell. So what's going to happen to that cell when it gets the glutamine? Of course the cell is going to be rescued. So you're enhancing one aspect of the immune system. Well, on the other hand you could potentially be rescuing cells for eventual reoccurrence sometime down the road. So again you have to make your treatments in line with what we understand about the metabolism of the tumor cell. And the evidence in the literature is huge that glutamine for many different cancers is a primary fuel that is used by tumor cells, especially those tumor cells that have some level of mitochondrial function.
   
We have a model of metastatic cancer we developed here at Boston College. It's one of the best models for systemic metastasis; it's brutal. It just rips through the mouse's body from the tip of his nose to the tip of his tail. This tumor doesn't respond to anything. We gave them DON (6-diazo-5-oxo-L-norleucine), which is a toxic drug, it's a glutamine analog (cannot be metabolized). We were able to really knock out metastatic cancer throughout the body of the mouse, except the spleen. It turns out the spleen is kind of like a sanctuary for cells like macrophages and these kinds of cells.
   
We just wanted to use it to get some concept of the role of glutamine. Because we couldn't stop this tumor using calorie restriction alone. The glutamine issue has to be carefully dealt with, I think. We recommended phenylbutyrate (Buphenyl) that's metabolized to phenyl acetate, which binds to glutamine and you excrete it. This will lower some levels of glutamine. And there has to be more cross-talk between the basic scientists and the clinicians about this glutamine issue.

MU: I'm not aware of any treatment which cancer cells cannot ultimately resist. Why can't cancer cells develop the ability to use ketones as a fuel source?

TS: You know, burning ketones requires normal mitochondria. Ketones are even more efficient than fatty acids, which uncouple, and they are more efficient than pyruvate. So ketones are a wonderful, highly sophisticated fuel that reduces oxygen free radicals, but in order to do that your mitochondria must be in good shape. And as I've mentioned and I've shown over and over again, the mitochondria of tumor cells are compromised in one way or another, making them less able to use ketone bodies for energy. That's the reason they ferment. They are fermenting because their mitochondria are insufficient. So, how are they going to adapt, unless they grow new mitochondria? And if they generate new mitochondria, they will be able to burn ketones, but they will no longer be cancer cells. So it's very hard to get around this.
   
If cancer is viewed as a metabolic disease, then these kinds of ideas and these kinds of understandings become more apparent. Why are all these other cancer cells adapting to the drugs and other therapies? Because you're not targeting their metabolic fuels. If you target their metabolic fuels that they absolutely require, they are not going to do very well. If you're not targeting their glucose or glutamine issues, they look like they're adapting. You're just making them more likely to ferment than respire. Then you get cancer cells that have no mitochondria. All right, well, those cells should be remarkably sensitive to the CRKD. So it's going to take time for this to sink into the minds of people that work in this area.
   
We have so many ways to manipulate this metabolic therapy. Not only with the diet as the main platform, but then the add-on drugs and hyperbaric oxygen. And I am hopeful we will be able to come up with an approach that is effective for the management of cancer without toxicity for the majority of people who suffer with this disease. It's just a matter of time. I think this is what's going to happen, but how long that time will be I don't know; I'm hopeful that it won't take too long.



Thomas N. Seyfried, PhD, has taught and conducted research in the fields of neurogenetics, neurochemistry, and cancer for more than 25 years at Yale University and Boston College. He has published more than 150 scientific articles and book chapters and is on the editorial boards of Nutrition & Metabolism, Journal of Lipid Research, Neurochemical Research, and ASN Neuro.
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Old 01-05-2014, 05:34 AM   #304
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Old 03-05-2014, 02:26 AM   #305
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Given the extent of published research pieces finding a positive relationship between glyphosate (the active ingredient in Monsanto’s best-selling herbicide RoundUp) and cancer, it isn’t very jaw-dropping anymore to hear of a new study coming to similar conclusions. Indeed, one new review and a series of meta-analyses of 30 years-worth of research has found that Monsanto’s RoundUp could be causing blood cancers in the lymph glands, specifically non-Hodgkin lymphoma (NHL).

The review focused on 30 years-worth of epidemiologic research on the connection between NHL and exposure to ingredients used in agricultural pesticides. The researchers examined the results from 44 papers, which found an association between NHL and 21 pesticide chemical groups and 80 active ingredients. The meta-analyses showed that phenoxy herbicides, carbamate insecticides, organophosphorus insecticides and the active ingredient lindane, an organochlorine insecticide, were positively associated with NHL.

In a handful of papers, associations between pesticides and NHL subtypes were reported; B cell lymphoma was positively associated with phenoxy herbicides and the organophosphorus herbicide glyphosate.

Diffuse large B-cell lymphoma was positively associated with phenoxy herbicide exposure. Despite compelling evidence that NHL is associated with certain chemicals, this review indicates the need for investigations of a larger variety of pesticides in more geographic areas, especially in low- and middle-income countries, which, despite producing a large portion of the world’s agriculture, were missing in the literature that were reviewed.”


But of course this isn’t the only study to find a connection between pesticides, glyphosate, and cancer. One groundbreaking study has found that glyphosate is responsible for fueling breast cancer by increasing the number of breast cancer cells through cell growth and cell division. The effects are so potent, in fact, that the cancer cell proliferation is driven even when we’re talking about RoundUp in the parts-per-trillion (PPT) range.

These are just a few of the countless studies revealing the many dangers of RoundUp, pesticides, and glyphosate. It is these findings that are causing nations around the world to limit pesticide use, or ban the ingredients altogether. Sri Lanka became the first country to ban Monsanto’s toxic RoundUp Ready chemical, glyphosate, in light of recent studies linking it to chronic kidney failure, while a full suspension of glyphosate is being demanded by the Brazilian Federal Public Prosecutor in the Federal District. What’s more, the Netherlands have passed a similar ban to Russia, Tasmania, and Mexico, disallowing the used of glyphosate-laced herbicides by the general public.

It is time the United States makes a move of it’s own. Just how many studies need to reveal glyphosate’s dangers before we ignite a ban of our own?

http://naturalsociety.com/meta-analy...-lymph-tissue/

http://www.ncbi.nlm.nih.gov/pubmed/23756170

http://www.ncbi.nlm.nih.gov/pubmed/24762670
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Old 04-05-2014, 04:52 AM   #306
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Right now, the government is deciding whether to pass a new law, the Medical Innovation Bill, that will help doctors to find new treatments safely and responsibly for cancer and other diseases.

For Alex Smith's son Harrison, 8, who has Duchenne – a 100% fatal condition – and those with cancer and other diseases it is a matter of life and death.

Standard treatments for rare cancers and other less common diseases often don’t work. And in many cases they haven’t changed or been improved for years.

This leaves the patient with a terminal illness no hope, no choice and no chance.

The law makes it hard for doctors to try new treatments – even when they know that standard procedures are not going to cure the patient.

Offering only the standard procedure guarantees the doctor will not be sued.

Safely trying something new leaves the doctor open to litigation and the loss of his or her job.

This is why current law is a barrier to innovation – it creates a culture of defensive medicine in the NHS.

The Medical Innovation Bill will remove this barrier and help doctors innovate safely on behalf of their patients.

Jeremy Hunt, Health Secretary, said: “The government should do whatever is needed to remove barriers that prevent innovation which can save and improve lives. The Medical Innovation Bill…correctly identifies the threat of litigation as one such barrier."

Help us ensure the Government keep their promise.

"The Bill seeks to support doctors who endeavour to act in the best interest of their patients without the fear from litigation.

"It deters from irresponsible experimentation but encourages a much needed attitude change of innovation in the provision of care to patients."

Professor Ahmed Ashour Ahmed, Professor of Gynaecological Oncology, Consultant Gynaecological Oncology Surgeon and Scientist, University of Oxford

http://www.change.org/en-GB/petition...nnovation-bill
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Old 05-05-2014, 12:58 PM   #307
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The latest push by the NCI is called the Cancer Genome Atlas Project. Its stated mission: “To systematically explore the entire spectrum of genomic changes involved in more than 20 types of human cancer.” The goal of this ambitious project is to once and for all, find and sequence all of the genetic mutations responsible for cancer. But so far the search for causative mutations has remained elusive – in fact, to date, the data suggests that mutations are not involved in ways previously assumed. The genetic mutational profile of any given cancer type looks different form person to person, rendering it impossible to claim mutations are definitely responsible for the origin of the disease. To be sure, some genes are mutated more frequently than others, but it appears that no single gene, or even any combination of genes, is absolutely necessary for the development of a tumor within a person. And to make things even more confusing, the mutational profile is different from cell to cell within the same tumor, rendering development of drugs that target mutations next to impossible. The drug targets not only change from person to person, but even within the tumor of a single individual.

Of the 700 targeted drugs developed to date, only one, Gleevec, has made a difference. Even Gleevec, with all its success, is not a cure but is a lifetime therapy, not eliminating the disease, but managing it. These new “targeted” drugs can cost up to $100,000 per treatment, and offer no increase in survival time – the relationship between price and value is completely broken when it comes to oncology treatment. Call this what it is, it is taking advantage of people when they are at their most vulnerable.

One sentence that is worth repeating can sum up the sequencing data from the Cancer Genome Atlas Project – No mutation has yet to be identified that is reliably diagnostic of any type of cancer.

http://www.singlecausesinglecure.org...ory-of-cancer/

(Good luck http://www.cancerresearchuk.org/supp...lised-medicine )


Review of ‘The Truth in Small Doses: Why We’re Losing the War on Cancer-and How to Win It’

Once again Clifton Leaf has generated a rich, circumspect, and sobering narrative on the war against cancer. Leaf takes readers on an expansive journey — one minute your sitting with him in a cancer ward, sharing a profoundly human, and personal moment between him and his father – the next your traveling through sub-Saharan Africa with a one-eyed surgeon in an old station-wagon, piecing together epidemiological clues, detailing the mechanics of an unknown cancer. All together, Leaf’s book explores every subtle nuance – around hidden corners — under every stone; he looks everywhere in search of one question: “how did we get here?” (‘here’ being the position we are in today — no closer to cures as when Nixon originally declared the war on cancer)

In the email correspondence I’ve personally had with Clifton I can tell you this — he is one of the smartest, most genuine, generous, and hard-working individuals I’ve ever encountered. He is a National treasure. So what I’m about to write has nothing to do with Clifton personally — it is just that we have arrived at different conclusions to the same question: “how did we get here?”

I picture Clifton’s book as a skyscraper — the building itself represents our countries losing effort in the war against cancer. The top-floor has a broken window — that is our governments collective denial concerning the ‘real’ cancer burden. The 8th floor has broken pipes — they represent our broken ‘cancer culture,’ a system that constricts bold science, encourages caution, and bogs-down creativity with bureaucracy. And the first floor is terrible-management of the war itself — a system that forces researchers to spend 50% of their time applying for grants. Inefficient and redundant layers of decision makers. A glaring lack of a common language and standards within the science itself – adding to inefficiency and confusion. Clifton explores every floor on his hands and knees, with a flash-light in one hand, and a magnifying glass in the other — cataloging every cracked tile, leaky air vent, and dripping faucet. It is just that there is one place Clifton forgets to look — and paradoxically — it is the place he urges us to go throughout the book: the foundation.

The foundation of the war against cancer has glaring, exposed, and obvious cracks — but only a handful of creative, intrepid, and bold-scientists are urging us to look where nobody else is looking. Clifton celebrates the creativity and boldness of a handful of scientists throughout his book, who were able to break with convention, and identify the hidden-details of cancer, resulting in great-leaps forward. In the first chapter Clifton tells the wonderful story of a Dutch-educated, Chinese Indonesian, working in a lab in Sweden, who did something extraordinary — he counted.

It was established dogma — written in every textbook, preached by the institutional leaders — that the human cell contained 24 chromosomes. Nobody questioned it. That is until Joe Hin Tjio, who didn’t know any better than to not question firmly establish theology written in script — Tjio didn’t know he wasn’t supposed to believe his own eyes. Tjio counted 23.

Sure enough the textbooks has to be rewritten – the serious scholars had to clear their throats, shuffle their feet, and admit they were wrong. All because one man, working alone at 2 in the morning, had the courage of conviction to trust his own eyes and shrug off the shackles of convention and groupthink. In fact, others, many others, had also counted 23, but thought they had counted wrong — that is the power and inertia of entrenched dogma.

Clifton celebrates examples like Tjio throughout his book — the men and women who think outside the box — he says over and over again these are the people we need to nurture – and we should dictate the conditions necessary for them to thrive.

Back to the skyscraper. The cracks in the foundations are covered by the most firmly established tenant in cancer biology — that mutations to DNA cause cancer. Under this unquestionable premise, the first chapter in every biology textbook, are festering cracks that explain so much — yet so few notice them. The cracks are the metabolic theory of cancer — that states it is dysfunction of metabolism that causes cancer, and that mutations to DNA are just a side-effect. The cracks explain why Gleevec alone is the only success story in the era of ‘targeted therapies.’ They explain why the data from the Cancer Genome Atlas Project is virtually incomprehensible. They explain why the therapies that target metabolism have exhibited remarkable results.

The entire cancer complex — the doctors, the pharmaceutical companies, the academic researchers, the huge charitable foundations, all in all, a multibillion dollar massive institution — are all banging around inside this huge, dilapidated, and crumbling skyscraper trying to figure out how to fix it – when all it needs is a new foundation, and yet nobody is looking there.

While Clifton urges America to change the conditions in order to nurture the next-generation of Tjio’s — I think they are here right now, it’s just that they can’t get anyone to listen. They are Thomas Seyfried of Boston College, Peter Petersen of John Hopkins, and Dominic D’Agostino of the University of South Florida. They are swimming against a current with biblical inertia.

But the beautiful thing about science is that it exists in the realm of physical law — the truth always revels itself in time. And it will again. I love how Clifton compares the war against cancer to going to the moon — because the real category of both endeavor is engineering. As dauntingly complex as cancer seems — the metabolic theory simplifies it. Cancer researches will tell you, the seemingly infinite heterogeneity of mutations, not only from individual to individual, but within individual tumors, renders cancer incurable. A check-mate.

Clifton tells the tale of the fabled Matterhorn. When it was thought the Matterhorn could not be summited, after countless failed attempts — a single man looked at it differently. Edward Whymper, a wood engraver, and artist from London, who had never before scaled a mountain, decided to try a route nobody else had tried. He decided to try the Northeast side. It was here that Whymper found something inconceivable to the entire climbing community — a nature-made, hidden staircase leading to the top.

Maybe, just maybe, the metabolic theory is this hidden staircase.

http://www.amazon.com/The-Truth-Smal.../dp/1476739986
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Old 06-05-2014, 03:31 PM   #308
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http://www.youtube.com/watch?v=5LDc5TxOcvA

http://www.youtube.com/watch?v=sBjnWfT8HbQ

http://www.youtube.com/watch?v=A-_UY-WnH1k
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Old 12-05-2014, 08:24 AM   #309
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Interleukin 21 may boost Herceptin http://www.upi.com/Health_News/2006/...0961152902592/
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Old 15-05-2014, 10:07 PM   #310
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Virotherapy, or the use of oncolytic viruses (OVs) to kill cancer cells,

by Chris Woollams

This article is about another ´Alternative´ Cancer Treatment. Namely, that of using common viruses to kill cancer cells whilst leaving healthy cells unharmed. Oncolytic viruses are live viruses that replicate selectively and, ideally, enthusiastically in tumour cells, but not in healthy cells. There are a number of strategies in, what is now called, virotherapeutics. Technical advances are increasing tumour specificity and replication rates and great advances have been made in the last decade. However, some viruses that replicate well in laboratory tests are much slower in real life situations where cancer tumours erect more barriers.

Virotherapy has been around for 15 years or more - indeed we even have an article on the successes of their ´Virotherapy´ programme from the MD Anderson Cancer Center in Texas covering a couple of patients with lung cancer, who lived more than 10 years after treatment.

Early clinical trials have shown great potential, and some viruses are currently in late stage clinical trials.

Furthermore common viruses may be genetically modified to enhance their attack on cancer cells, and/or to prevent harm to healthy cells and/or to overcome cancer tumour barriers. Although they are most usually referred to as oncolytic viruses (OVs), they are sometimes erroneously called cancer vaccines. Genetic engineering has led to some of these viruses becoming a novel form of gene therapy. Some are modified to become genetic ´carriers´ to disrupt some particular genetic feature of the cancer.

Rarer cancers, and mainstream cancers

About 9 years ago CANCERactive ran a story about researchers lead by Professor Moira Brown in Scotland using the Herpes virus in an attempt to kill brain cancer cells (see Example 9). Her work has progressed and patients have seen extended survival times. Her team believes that the herpes virus could be used to treat many different types of cancer.

In Cancer Watch, our cancer research centre, we have brought you many more studies. Put ´viruses used to kill cancer cells´ into your Internet search engine and you will see that this is a huge and developing area of Alternative Cancer Treatment, especially in America where people with rarer cancers (for which orthodox medicine often offers little) are brought into a trial on many new ´alternative´ treatments with potential - like virotherapy, dendritic cell therapy and others. Some 20 viruses are in early stage trials. Nine viruses are in Phase I and phase II trials with ovarian cancer, for example.

In 2013 Cancer Watch covered research on prostate cancer where a genetic modification involves a protein which is cleaved by Prostate Specific Antigen (PSA) making the virus extremely aggressive to the cancer.

Moira Brown´s research team see no reason why their herpes virus should work with all manner of cancer tumours.

But matters are a little slower in Europe - In 2009 Ark Therapeutics issued results of a Phase III Clinical Trial on an adenoviral vector dubbed TK, but the marketing application has been rejected by the European Medicines agency for being underpowered and failing to show sufficient efficacy. They are making an appeal.

Key Issues?

It is all very complex. One issue is to now start to pick some ´winners´ amongst the basic viruses, and some ´winners´ amongst the modified versions. In that way there can be more focus towards finding one really powerful treatment. Another issue is that off immunity: that of maximising the attack on cancer cells, but minimising any undesirable effects in the body.

This is not meant to be our usual type of article but more a briefing, providing some examples of work currently under development. What I observe is that virotherapy research is widespread and takes many different forms. Phase III Clinical Trials are in the offing, but the lack of them has not stopped some top cancer centres going ahead already and using the treatment on patients, especially with rarer cancers:


Example 1: In 2006 researchers at the Mayo Clinic were testing the use of the Measles virus. ´We are looking at better ways to treat some of the most lethal cancers´, said Dr. Eva Galanis, oncologist and lead researcher on the glioblastoma multiforme project in the measles virus investigation. ´We have shown in the laboratory and in several animal models that measles virus strains can significantly shrink glioma tumors and prolong animal survival´.

This Mayo Clinic work with strains of the measles virus was unique at the time. The called the viruses vaccines or oncolytic viruses. Early work looked at cancers including glioblastoma multiforme, recurrent ovarian cancer and multiple myeloma

Example 2: Dr. Kevin Harrington, working at The Royal Marsden Hospital, London for the Institute of Cancer Research, studied 17 patients found that use of the Herpes virus with chemotherapy and radiotherapy can help kill cancer cells in most patients. It does this in three ways: By direct attack on the cancer cells, multiplying inside them; the genetic modification is designed to produce a protein to activate the immune system; the virus itself causes a rapid increase in the immune system against it (and the cancer cells it is living in).

The treatment was most effective with early stage cancers - the study was with cancers of the head and neck area. 93% showed no recurrence of cancer after surgery and 82% of patients still did not show any recurrence of the disease more than two years later.

The herpes virus is genetically manipulated so that it attacks and thrives in cancer cells but cannot infect healthy cells.

The worry, of course, is that the genetically modified virus does cause health problems years later, maybe even to the population at large. (August 2010; Journal of Clinical Cancer Research).

Example 3: Researchers at Georgetown Lombardi Comprehensive Cancer Center, part of Georgetown University Medical Center, are conducting a clinical trial using the Reovirus. Normally, you have experienced this virus at least once by the age of 5, causing coughing and diarrhea, but sometimes no symptoms. Apparently, the researchers found that the virus grows like gangbusters inside cancer cells, because of a specific attribute of a cancer cell, namely that the Ras gene is dominant and making it divide paridly. In healthy cells the p53 gene suppresses the Ras gene. Researchers are currently conducting a Phase II Clinical Trial with small cell lung cancer patients. Again, the virus has been genetically modified to prevent harm to healthy cells.

Example 4: Drugs can be made from the virus: Researchers at Oncolytics Biotech Inc., of Calgary, Canada, have developed a therapeutic drug, REOLYSIN, from the same Reovirus and are conducting multicenter clinical trials for a variety of cancers. Renowned American Hospital Cedars-Sinai is one of those participating, and in this case is looking into recurrent gliomas, the most common and deadly brain cancer.

"Although not every glioma cell line has an activated Ras pathway, Ras activation is very common in these malignant brain cancers. In lab tests and animal studies, the reovirus appears to target Ras-activated tumor cells and leave normal cells alone," said a spokesperson from Cedars-Sinai.

Example 5: Dalhousie Medical School have proven that Reovirus can infect and kill breast cancer stem cells (September 2009). This breakthrough finding was published in Molecular Therapy, the journal of the American Society of Gene Therapy.

Dr Lee, head researcher said, It is only within the past few years that the scientific community has understood the full significance of cancer stem cells and the urgent need to find a means of eliminating them (Ed: Actually, UK embryologist John Beard in 1906 told the world but his work was ignored until picked up by William Kelley then Dr Gonzalez from the 1970s. Oh, but they really were Alternative Doctors!)

Cancer stem cells are essentially mother cells, explains Dr. Lee, Cameron Chair in Basic Cancer Research at Dalhousie Medical School. They continuously produce new cancer cells, aggressively forming tumours even when there are only a few of them.

Cancer stem cells are difficult to kill as they respond poorly to chemotherapy and radiation. As Dr. Lee notes, You can kill all the regular cancer cells in a tumour, but as long as there are cancer stem cells present, disease will recur. Dr. Lee is optimistic that his team has found the key to destroying cancer stem cells.

Example 6: Boston University School of Medicine (BUSM) presented their findings in the Journal of Virology on December 2010. They were using a virus, vesicular stomatitis virus (VSV), to kill cancer cells. VSV is supposedly not an important cause of ill health in humans.

In cancer cells a major signaling pathway, called the AKT signaling pathway, is frequently turned on and AKT signaling is a cell survival signal, helping to keep the cancer cells alive. VSV can switch off the AKT pathway and cause cancer cell death. VSV can also prompt the immune system to produce interferon which also targets the diseased cancer cell.

Example 7: Memorial Sloan Kettering Cancer Center in New York are now getting in on the act. As recently as May 2011, Joyce Wong M.D. published findings looking at oncolytic viruses to infect cancer cells, and especially stem cancer cells in pancreatic cancers The researchers have looked at a number of such common viruses, all modified to avoid harm to healthy cells.

Example 8: Viruses can also be genetically modified to be carriers. For example: In December 2009, (Molecular Therapy0 Ohio State University researchers looked at modifying viruses so that they carried a gene which made a protein that could block tumour blood cell formation.

Looking at brain tumours, research leader Balveen Kaur, associate professor of neurological surgery said, "This is the first study to report the effects of vasculostatin delivery into established tumors, and it supports further development of this novel virus as a possible cancer treatment," "This study shows the potential of combining an oncolytic virus with a natural blood-vessel growth inhibitor such as vasculostatin. Future studies will reveal the potential for safety and efficacy when used in combination with chemotherapy and radiation therapy," she says.

The work still needs to be trialled with humans. In this study researchers injected the cancer-killing virus, called RAMBO (for Rapid Antiangiogenesis Mediated By Oncolytic virus), directly into human glioblastoma tumors growing either under the skin or in the brains of mice.

Example 9: Professor Norman Nevin, chair of the UK gene therapy committee believes the UK is at the forefront of oncolytic virus work. For example, his committee gave the go-ahead several years ago for a team at Glasgow University (Southern General Hospital), lead by Professor Moira Brown, to treat 100 patients with gliomas using a genetically modified form of the herpes virus. Here initial findings and the development work has been covered in Cancer Watch in October 2013 (see HERE).

In conclusion

Hopefully this briefing, on a subject that has grown rapidly in the last few years, will help you to make more informed choices on your options for cancer treatment over the coming years.

http://www.canceractive.com/cancer-a...0kill%20cancer


Could measles cure cancer? Experimental virus treatment leaves 49 year old woman in complete remission
Two patients underwent the treatment, which researchers stress was at the earliest stage of human trials
Were injected with high dose of an engineered version of the measles virus
49-year-old woman now in complete remission

Researchers have revealed a proof of principle clinical trial that used a high dose 'blast' of a specially engineered version of the measles virus to cure cancer.

Two patients underwent the treatment, which researchers stress was at the earliest stage of human trials.

Both patients responded, showing reduction of both bone marrow cancer and myeloma protein, with one, a 49-year-old woman, experiencing complete remission of myeloma - and has been clear of the disease for over six months.

Mayo Clinic researchers say the result demonstrated that virotherapy, destroying cancer with a virus that infects and kills cancer cells but spares normal tissues, can be effective against the deadly cancer multiple myeloma.

'it’s a very simple concept,' said Stephen Russel of Mayo Clinic Molecular Medicine, who led the study.

'Viruses naturally come into the body and they destroy tissue.'

He hopes the idea could eventually lead to a new treatment, and the team are also testing the measles virus’s effectiveness at fighting ovarian, brain, head and neck cancers and
mesothelioma.

'We recently have begun to think about the idea of a single shot cure for cancer and that’s our goal with this therapy.

'These patients were not responsive to other therapies and had experienced several recurrences of their disease.'

The findings appear in the journal Mayo Clinic Proceedings.

Two patients in the study received a single intravenous dose of an engineered measles virus (MV-NIS) that is selectively toxic to myeloma plasma cells.

Both patients responded, showing reduction of both bone marrow cancer and myeloma protein.

One patient, 49-year-old Stacy Erholtz, experienced complete remission of myeloma and has been clear of the disease for over six months.

Multiple myeloma is a cancer of plasma cells in the bone marrow, which also causes skeletal or soft tissue tumors.

This cancer usually responds to immune system-stimulating drugs, but eventually overcomes them and is rarely cured.

'I received enough apparently to vaccinate a hundred million people, which was alarming and I was happy to hear that after the fact,' she said.

'I think it’s just remarkable. I -- who would have thought?'

In their article, the researchers explain they were reporting on these two patients because they were the first two studied at the highest possible dose, had limited previous exposure to measles, and therefore fewer antibodies to the virus, and essentially had no remaining treatment options.

Angela Dispenzieri, a Multiple Myeloma Expert who worked on the project, said 'There’s some suggestion that it may be stimulating the patient’s immune system to further recognize the cancer cells or the myeloma cells and help mop that up more effectively than otherwise.'


Oncolytic virotherapy – using re-engineered viruses to fight cancer – has a history dating back to the 1950s.

Thousands of cancer patients have been treated with oncolytic viruses from many different virus families (herpesviruses, poxviruses, common cold viruses, etc.).

However, this study provides the first well-documented case of a patient with disseminated cancer having a complete remission at all disease sites after virus administration.

The second patient in the paper, whose cancer did not respond as well to the virus treatment, was equally remarkable because her imaging studies provided a clear proof that the intravenously administered virus specifically targeted the sites of tumor growth.

This was done using high-tech imaging studies, which were possible only because the virus had been engineered with a 'snitch gene' - an easily identifiable marker - so researchers could accurately determine its location in the body.

More of the MV-NIS therapy is being manufactured for a larger, phase 2 clinical trial.

The researchers also want to test the effectiveness of the virotherapy in combination with radioactive therapy (iodine-131) in a future study.

http://www.dailymail.co.uk/sciencete...remission.html
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Old 19-05-2014, 03:04 PM   #311
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Angelina Jolie’s Mastectomy: How Genes Relate to the Metabolic Origin of Cancer
Posted on May 17, 2013 by Travis Christofferson in Featured with 1 Comment

Angelina Jolie’s May 14th op-ed in the New York times about her recent preventative double mastectomy was touching, courageous, and informative. Most remain unaware of genetic predispositions to cancer including the BRAC1 gene. The fact is, inherited mutations that result in an increased predisposition to acquire cancer are rare. Only 5 to 7 percent of all cancers can be attributed to inheriting faulty genes. The vast majority of cancers arise spontaneously – being attributed to environmental insults like carcinogens, radiation, and viruses.

Women in general have a 12% lifetime risk of getting breast cancer. Women with a defective BRAC1 gene have approximately five times that risk – or on average, a 60% chance of getting breast cancer in their lifetimes.

A genetic test using a blood test can usually detect genes like BRAC1. There are no guidelines for recommending the test, and the test can cost several thousand dollars but may often be covered by insurance companies if women have risk factors that justify it. Women may be at higher risk for having the BRAC1 mutation if they have close family members diagnosed with breast or ovarian cancer at an early age, as in the case of Angelina Jolie

In Angelina Jolie’s case, a preventative double mastectomy reduces her risk of breast cancer from 87% to less than 5%.

You are probable wondering; If inheriting defective genes like BRAC1 increases your chances of acquiring cancer – isn’t that evidence that cancer is a genetic disease and not a metabolic disease?

While it is certainly true that inherited mutations in genes can predispose an individual to a greater cancer risk – it is also true that in almost all cases of inherited cancer risk, the defective genes manifest in damage to the mitochondria – the metabolic origin of the disease.The image to the left is of labeled BRAC1 protein, clearly showing it located within the mitochondria. Experimental evidence also implicates BRAC1 as being integral in the biogenesis of mitochondria and therefore oxidative energy creation. So one can easily conclude that a defective BRAC1 does not cause cancer by itself – but rather predisposes one for cancer because it inhibits the function of the mitochondria, and therefore the ability to generate energy through oxidative pathways.

In the vast majority of cancers – the cases that arise spontaneously – there is no initial genetic defect that precipitates the transformation of a normal cell into a cancerous cell. Rather, spontaneous cancer originates from mitochondrial damage followed by the genomic instability that leads to genetic mutations – mutations that have nothing to do with the origin of the disease.



BRAC1 located in the mitochondria

http://www.singlecausesinglecure.org...gin-of-cancer/
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Old 19-05-2014, 04:03 PM   #312
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Rapid Response of Glioblastoma Multiforme with the Ketogenic Diet: A Case Report
Posted on April 25, 2013 by ocadmin in Featured with 0 Comments

Glioblastoma Multiforme (GBM) is the most aggressive form of brain cancer. Median time of survival is about 15 months from diagnosis. Standard therapy for GBM includes surgical resection followed by concomitant radiation and chemotherapy and is able to extend GBM patients’ lives by approximately 1 year.

Like all cancers GBM is highly dependent on glucose for survival and is unable to transition to ketone body metabolism for energy due to damaged mitochondria. The metabolic intransigence http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2949862/ of tumor cells provides a clear route for therapeutic exploitation. Normal brain cells are able to obtain all the necessary energy requirements from ketone bodies where cancer cells cannot http://www.ncbi.nlm.nih.gov/pubmed/19159745. The restricted ketogenic diet (R-KD) is a simple, non-toxic therapy that reduces circulating blood glucose levels while raising ketone bodies in the blood stream. Substantial experimental evidence demonstrates the efficacy of the R-KD in reducing tumor growth rates by exploiting the impaired ability of the cancer cell to A 65 year old woman was admitted to Arcispedale Santa Maria Nuova, Reggio, Italy on December 5th, 2008. She presented with numerous neurological symptoms and was subsequently diagnosed with Glioblasoma Multiforme. After an incomplete surgical resection the patient began a restricted ketogenic diet the next day. Three weeks later she began the standard treatment protocol of chemotherapy and radiation.

MRI and PET scans preformed 2.5 months from the time of diagnosis found no evidence of any tumor tissue. The patient’s response to this therapeutic approach, complete regression within 2.5 months, is unusual. In fact, no prior reports are documented, describing complete regression within this time frame, to the author’s knowledge. This case study demonstrated that the R-KD was well tolerated. It also suggests the legitimacy of targeting defective tumor metabolism therapeutically, as the observed response from the patient would be unlikely from standard treatment alone.utilized oxidative energy production.

Even though the results of this single case report http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874558/ are stunning, drawing conclusions is speculative due to the sample size. However, the compelling results of metabolic therapies have been substantiated repeatedly in mice – one mouse study even demonstrating a complete cure http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341352/ of invasive brain cancer when combing the R-KD with radiation. Sadly, this is where these studies have been left – probably because a simple diet, and the molecules that target metabolism and exhibit efficacy, so far cannot be patented and charged for. These studies demonstrate an established mechanism of action based on defective tumor cell metabolism and open up tremendous therapeutic possibilities – especially as an adjunctive therapy. The R-KD differentiates the physiology of the cancer cell and the normal cell, greatly enhancing the efficacy of other therapies while attenuating the delirious effects to normal cells. We don’t want these promising avenues to be closed. That is our mission.



MRI scan reviling multiple large multi-centric mass involving the right hemisphere pole.



No clear evidence of tumor tissue or associated edema was seen 2.5 months after diagnosis

http://www.singlecausesinglecure.org...ma-multiforme/
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Old 20-05-2014, 09:08 PM   #313
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Free video Cancer as a Metabolic Disease: Impaired Mitochondrial Function and Tumorigenesis
By Thomas Seyfried , PhD http://digivisionmedia.com/lectures/...-seyfried-phd/
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Old 21-05-2014, 11:06 PM   #314
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A groundbreaking 14 year study was published in the Journal of Clinical Oncology in December 2004 called “The Contribution of Cytotoxic Chemotherapy to 5-year Survival in Adult Malignancies”. Researchers at the Department of Radiation Oncology at the Northern Sydney Cancer Center studied the 5-year survival rates of chemotherapy on 22 types of cancers in the US and Australia. They studied 154,971 Americans and Australians with cancer, age 20 and older, that were treated with conventional treatments, including chemotherapy. Only 3,306 had survival that could be credited to chemotherapy. Study Results: “The overall contribution of curative and adjuvant cytotoxic chemotherapy to 5-year survival in adults was estimated to be 2.3% in Australia and 2.1 % in The USA” Study Conclusion: “As the 5-year survival rate in Australia is now over 60%, it is clear that cytotoxic chemotherapy only makes a minor contribution to cancer survival. To justify the continued funding and availability of drugs used in cytotoxic chemotherapy, a rigorous evaluation of the cost-effectiveness and impact on quality of life is urgently required.” The fact that chemo only contributes on average about 2% to the overall survival rate is very alarming, and probably something your doctors didn't tell you. It is important to remember that the “2.1% average” can be deceptive. Some cancers do respond better to chemo than others. According to this research, the best results from chemotherapy are treating Testicular Cancer where it is 41.8% effective, and Hodgkins Disease where it is 35.8% effective, still not great. You can read and download the entire study HERE http://chrisbeatcancer.com/wp-conten...r-survival.pdf . Make sure you look at the tables on page 3 and 4 which show the survival rate for each type of cancer in the US and Australia. You will notice that the survival rate for some cancers after chemo treatment has a dash (-). That means ZERO effectiveness of chemotherapy toward 5 year survival. Yet it is still prescribed as a treatment for these cancers today, many years after this study was published. Although not mentioned in their research, chemo does have a better success rate on leukemia and some childhood cancers. Nowhere in the study does it say that the 3,306 patients (2.1%) that made it to the five year mark were actually cancer free. The only thing we know is that they were “still alive” at the five year mark. You could assume that some of them still had cancer, their cancer came back (did it really go away, were/are the tests that good at picking up small traces of the cancerous cells??) and/or died of cancer later. I would really like to see a follow up on how many of the 5-year survivors actually lived to the 10 year mark. I imagine the results wouldn't be great. However as far as I know that study hasn't happened.

The “2% chemo efficacy” comes from an Australian study into the contribution of chemotherapy to 5-year cancer survival, and the researchers claimed to have found that the average benefit of chemotherapy was about 2%. So: the study is about the contribution of chemotherapy to survival and not about survival of patients having chemotherapy. So they wanted to know what the contribution was of chemotherapy to 5-year survival. The therapies to treat cancer are: surgery, radiotherapy, hormonal therapy and/or chemotherapy. The researchers wanted to know to what extent chemotherapy contributed to five-year-survival of cancer patients. Of all 154,971 patients whose files were examined, in 3306 of these, 5-year survival could be attributed solely to chemotherapy. In 98% of the patients, 5-year survival was due to a combination of factors, of which chemotherapy sometimes also was a factor and sometimes was not. They did not differentiate between cancers for which chemotherapy is the primary treatment and cancers for which chemotherapy is only given as an adjuvant. This is the case in most solid cancers, for which surgery is the primary – and by far the most effective – treatment. They did not differentiate between early stage cancers (tumour <1cm, no mets in lymph nodes), for which chemotherapy often is not even indicated, and late stage, incurable cancers which had already metastasized at the time of diagnosis, some even quite extensively. There may be more 'flaws' in the study. Also i would like to see a new 10 year study that follows children up to the age of 18 and adults over this age up to 70 or even older. It would need to look at all stages, primary and adjuvant treatments. Also different types of personal treatment; just surgery, chemo and/or radio, two of them together and all three, also hormonal therapies would need to be taken into account also.

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Old 22-05-2014, 03:38 AM   #315
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Maitake MD-fraction Mushroom Extract http://www.saisei-mirai.or.jp/gan/ma...ction_eng.html http://www.mskcc.org/cancer-care/herb/maitake http://www.cancer.org/treatment/trea...take-mushrooms
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Old 22-05-2014, 03:41 AM   #316
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GcMAF experiences http://www.gcmaf.eu/gcmaf-products/p...s-experiences/
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Old 22-05-2014, 10:22 PM   #319
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Deuterium-depleted water http://www.ncbi.nlm.nih.gov/pubmed/23076183 http://en.wikipedia.org/wiki/Deuterium-depleted_water http://www.deuteriumdepletion.co.uk/index.php
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Old 24-05-2014, 04:18 AM   #320
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Orthomolecular Medicine News Service, January 24, 2013
Antioxidants Prevent Cancer and Some May Even Cure It

Commentary by Steve Hickey, PhD

(OMNS Jan 24, 2013) It is widely accepted that antioxidants in the diet and supplements are one of the most effective ways of preventing cancer. Nevertheless, Dr. James Watson has recently suggested that antioxidants cause cancer and interfere with its treatment. James Watson is among the most renowned of living scientists. His work, together with that of others (Rosalind Franklin, Raymond Gosling, Francis Crick, and Maurice Wilkins) led to the discovery of the DNA double helix in 1953. Although his recent statement on antioxidants is misleading, the mainstream media has picked it up, which may cause some confusion.
Antioxidants: What's Going On

Dr. Watson claims to have discovered that antioxidants promote the growth of late stage metastatic cancers. He says that this is "among my most important work since the double helix." [1] We agree that the finding is fundamentally important, although it was not uniquely Watson's discovery. Rather, it is standard orthomolecular medicine and has been known for years. [2,3] Within the body, antioxidant levels act as a signal, controlling cell division. In healthy cells and benign tumors, oxidants tend to increase cell proliferation, whereas antioxidants inhibit it. By contrast, the malignant tumor environment can be so strongly oxidizing that it is damaging and triggers cell death by apoptosis. In this case, antioxidants may help tumor cells proliferate and survive, by protecting the cells against oxidation and stimulating the malignancy to grow. For this reason, antioxidants may sometimes be contraindicated for use with malignant tumors, although there are particular exceptions to this.
And Oxidants?

The balance between oxidants and antioxidants is a key issue in the development of cancer, as has been known for decades. Watson appears to be behind the times in his appreciation of nutritional medicine and, surprisingly, to have misunderstood the processes of oxidation and reduction as applied to cancer. He correctly asserts that reactive oxygen species are a positive force for life; this is basic biology. They are also involved in aging, chronic illness, and cancer. Oxidants also cause free radical damage, thus the body generates large amounts of antioxidants to prevent harm and maintain health.

Back in the 1950s Dr. Reginald Holman treated the implanted tumors of experimental rats, by adding a dilute solution of hydrogen peroxide to their drinking water. [4] Hydrogen peroxide, an oxidant, delivers a primary redox (reduction/oxidation) signal in the body. The treatment cured more than half the rats (50-60%) within a period of two weeks to two months, with complete disappearance of the tumors. Holman also reported four human case studies, concerning people with advanced inoperable cancer. Two patients showed marked clinical improvement and tumor shrinkage. (Please note: we are not suggesting that people should consume hydrogen peroxide.) He published his findings in Nature, one of the most prestigious scientific periodicals of the day and, of course, the same journal that had presented Crick and Watson's double helix papers, just four year earlier.

Orthomolecular medicine has advanced since those days; we now have safer and more effective techniques with which to attack cancer. Intravenous vitamin C is a good example. [5] Nevertheless, both modern orthomolecular and conventional treatments often rely indirectly on increasing hydrogen peroxide levels, and thus deliberately causing free radical damage within the tumor. Watson correctly identifies oxidation and free radical damage as primary mechanisms through which radiation and chemotherapeutic drugs slow cancer growth. He also states that cancer cell adaptation to oxidation is the method by which it becomes resistant to such treatment, although once again, this has been standard in cancer biology for decades. We agree with some of Watson's assertions: that cancer research is overregulated; that a primary aim should be to cure late stage cancers; and that a cure for cancer could be achievable, given 5-10 years of properly targeted research. [6] However, we think he should become more familiar with progress in orthomolecular medicine, which is currently leading the way.
How Does Cancer Grow?

Cancer develops when cells multiply in the presence of oxidation and other damage. According to micro-evolutionary models, cells become damaged and change their behavior, growing uncontrollably, and act like the single-celled organisms from which they originally evolved. The cancer cells' individualism overwhelms the cooperative control processes that are essential to a complex multicellular organism. Importantly, antioxidants limit oxidative damage and thus inhibit early benign cancer growth, preventing cancer from developing.

As cancers become malignant, they exhibit incredible genetic diversity. Whereas a benign tumor is like a colony of similar abnormal cells, a malignant tumor is a whole ecosystem. At this late stage, some (but not all) antioxidants can indeed promote cancer cell growth. Thousands of different cell types coexist: cooperating, competing, and struggling to survive. A consequence of the anaerobic conditions that prevail during the early development of a malignancy is that cancer cells differ from healthy cells, in that they have been selected for the way they generate energy (i.e. anaerobically, using glucose). This is the well-known Warburg effect [7], another finding from the 1950s. [8]
How Does Cancer Stop?

Certain "antioxidant" substances, such as vitamin C, are able to exploit the differences between cancer and healthy cells; they kill cancer cells while helping healthy cells. [9] Such substances have the ability to act either as antioxidants or as pro-oxidants, depending on their environment. In tumors, they act as pro-oxidants, producing hydrogen peroxide that attacks the cancer; whereas, in healthy cells they act as protective anti-oxidants.

The dual nature of these substances is crucial, because standard chemotherapy or radiation harms healthy cells almost as much as it does cancer cells. The idea of a drug with a limited selective activity against cancer cells has apparently impressed Watson, who suggests that "highly focused new drug development should be initiated towards finding compounds beyond metformin that selectively kill [cancer] stem cells." [10] Metformin is an antidiabetic drug that acts against cancer by lowering blood glucose levels. Interestingly enough, carbohydrate reduction and other methods of "starving the cancer" are standard methods in orthomolecular cancer therapy. [2]

Selective anticancer agents of the kind Dr. Watson advocates are already known to exist: they include vitamin C, vitamin D, vitamin K, alpha-lipoic acid, selenium, and others. A research agenda to investigate the synergistic operation of such substances in cancer treatment is required urgently. It is time for conventional medicine to come to terms with their failure in cancer research and embrace selective orthomolecular methods. The public should stick with nutritional therapies while we wait, perhaps for some time, for medicine to focus on patients rather than profits. Don't be warned off the very substances that can most help you.

References:

1. Watson J. (2013) Nobel laureate James Watson claims antioxidants in late-stage cancers can promote cancer progression, The Royal Society, latest news, 09 January, http://royalsociety.org/news/2013/wa...xidants-cancer.

2. Hickey S. Roberts H. (2005) Cancer: Nutrition and Survival, Lulu Press.

3. Hickey S. Roberts H.J. (2007) Selfish cells: cancer as microevolution, 137-146.

4. Holman R.A. (1957) A method of destroying a malignant rat tumour in vivo, Nature, 4568, 1033.

5. http://www.doctoryourself.com/RiordanIVC.pdf, http://www.riordanclinic.org/researc...minc/protocol/ and http://www.doctoryourself.com/Radiation_VitC.pptx.pdf

6. Lettice E. (2010) James Watson: 'cancer research is over regulated' The Guardian, Friday 10 September, http://www.guardian.co.uk/science/20...ancer-research.

7. Gonzalez M.J. Miranda Massari J.R. Duconge J. Riordan N.H. Ichim T. Quintero-Del-Rio A.I. Ortiz N. (2012) The bio-energetic theory of carcinogenesis, Med Hypotheses, 79(4), 433-439.

8. Warburg O. (1956) On the origin of cancer cells, Science, 123(3191), 309-314.

9. Casciari J.J. Riordan N.H. Schmidt T.L. Meng X.L. Jackson J.A. Riordan H.D. (2001) Cytotoxicity of ascorbate, lipoic acid, and other antioxidants in hollow fibre in vitro tumours, Br J Cancer, 84(11), 1544-1550. http://www.nature.com/bjc/journal/v8.../6691814a.html

N.H. Riordan, H.D. Riordana, X. Menga, Y. Lia, J.A. Jackson. (1995) Intravenous ascorbate as a tumor cytotoxic chemotherapeutic agent, Med Hypotheses, 44(3), 207-213, http://www.sciencedirect.com/science...0698779590137X

10. Watson J. (2013) Oxidants, antioxidants and the current incurability of metastatic cancers, Open Biology, January 8, doi: 10.1098/rsob.120144.

http://orthomolecular.org/resources/omns/v09n02.shtml
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