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From the Townsend Letter
November 2015

Refocusing Our Efforts Against Cancer
review by Ira L. Goodman, MD, FACS, ABIHM, FAARM
iraleegoodman@gmail.com
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Tripping over the Truth:
The Return of the Metabolic Theory of Cancer Illuminates
a New and Hopeful Path to a Cure

by Travis Christofferson
CreateSpace Independent Publishing Platform 
© 2014; paperback; 296 pp.

This is a very important book that could reframe the War on Cancer and establish a new paradigm. Mr. Christofferson is not an MD, but it would be a mistake to ignore this book based on that. There have been several other non-MD authors who have contributed much in the scientific literature, including Ralph Moss on cancer, Robert Whitaker and Kirsch on psychotropic drugs, and Norman Cousins. The book was well written and at times read like a detective novel; I could not put it down. It will be difficult to do it justice in this short summary.
   
The book's fundamental message is that cancer is not primarily caused by somatic mutations in the nuclear DNA as the current research and theories propose. The DNA damage noticed in many cancers (although not all) is the result, rather than the cause, of the disease, which, according to the author, is primarily from damage to the cells' respiration apparatus. Cancer cells use fermentation instead of the normal oxidative phosphorylation. In other words, the mitochondria and cytoplasmic environment are the common ground where all cancers start and where we should focus.
   
As Warburg said decades ago, the primary cause of cancer is the cells' replacement of normal respiration (oxidative phosphorylation) with fermentation and cancer cells' voracious appetite for only glucose as opposed to normal cells' ability to utilize ketones as well as glucose. There are many secondary causes of cancer (pollutants, X-rays, etc.) but they all result in the primary defect just mentioned. The author carefully takes you through the research of Otto Warburg starting in the 1920s and progresses through the discoveries of Pedersen, Ko, D'Agostino, and Seyfried at Boston University. Detailed bios of these giants, as well as the evolution of their thinking, add to the logic and intrigue of their work.
   
The fact that the death rates from cancer are about the same now as they were in the 1950s and that chemotherapy directed against targeted mutations has been an abysmal failure in terms of survival benefit (only Gleevec out of the 700-plus targeted drugs has shown real clinical and durable efficacy). Even Herceptin only works in a minority of select cases with modest results in terms of survival. A nice summary of the history of the evolution of chemo is present in the book.
   
Yes, we are getting better at poisoning , burning, and cutting, but only minimally and not enough to affect overall survival statistics significantly. That is because, according to the author, with the exception of the above-mentioned scientists, we are on a multibillion-dollar wild goose chase after the wrong target (nuclear DNA). The fact that the intratumoral DNA mutations vary considerably (DNA analysis of the same tumor from different locations within the primary tumor) and intertumoral DNA analysis (DNA samples of the same type of tumor from different patients) also varies significantly should make it clear to the most casual observer that we are barking up the wrong tree. This is also proven by the high degree of intrametastatic DNA variability (DNA differences between metastases and the primary tumor in the same patient). In other words, if you take two biopsy samples from the same tumor, the DNA mutations will not usually be the same! The same is true if you take biopsies from different patients' primary tumors even if they are the same kind of cancer, or if you take biopsies of individual metastases and compared them to the primary tumor. The mutations are all over the board, which proves in my mind that these mutations are secondary to the primary cause and it is foolish to try and go after this moving target.  
   
Does the pharmaceutical industry think that we should design multiple targeted drugs for each person's individual cancer when it is well known that the mutations change over time in the same cancer? DNA mutations are clearly a moving target. 
   
What is driving these mutations is the mitochondrial health in the cytoplasm. Seyfried proves this with his elegant nuclear transfer studies that he outlines in his 2012 book Cancer As a Metabolic Disease.  His experiments have been duplicated. He replaces the nucleus of a normal cell with that of a cancer cell and transplants that clone into a mouse. If the DNA mutation theories were correct, this new cell should become malignant, but it does not! He then replaces the nucleus of a cancer cell with a normal nucleus, and what happens? Cancer grows anyway, since the mitochondria and cytoplasm are still defective in the resulting clone.  The nucleus appears to be irrelevant, and only the damaged cytoplasm rules. There is much more detail about these experiments in the book.
   
The development of drugs such as 3BP (3-bromopyruvate), which inhibits hexokinase 2 and corrects the abnormal functioning of the mitochondria, show great promise; but the funds are not there for phase III trials. There are other drugs being looked at as well. Mention is also made of the ketogenic diet as a method of starving cancer cells, which cannot metabolize ketones as can normal cells. This has been used with great success in some forms of cancer. It makes you wonder if the cachexia seen in advanced cancer is the body's final attempt to induce ketosis as a defense against the tumors.
   
This book clearly has too much detail to properly describe here, but I think that this author has hit the nail on the head in regard to refocusing our efforts against the disease that is killing more people than ever in spite of the billions dollars spent on the War On Cancer. I am sure that Pharma would be happy to continue to develop more downstream targeted treatments with their big price tag whether it be immunotherapy or mutation intervention. The cancer surgeons would be happy to continue as before, and the entire cancer industry needs to be fed. The name of the game is clearly prevention and treatment against cancer's common-denominator defect: that of the mitochondria and cytoplasm. As Louis Pasteur said on his deathbed: "The microbe is nothing; it's the soil."  In the case of cancer, I believe that the cells' mitochondrial and cytoplasmic health are the primary common-denominator defect which leads to downstream DNA mutations at times. Remember, there are times when no mutations can be found in the nuclear DNA in spite of cancer's being present. The cells' "soil" is the cytoplasm, and once that is damaged, the mitochondria send signals to the nucleus which result in nuclear mutations. It is well known that the more aggressive cancers have the most disrupted mitochondrial appearances and function. Directing pharmaceutical treatments against the nucleus in one way or another is missing the point. It may work and has worked transiently, but the overall result has been bad. Treatments against cancer should bolster all your cells and make you feel better, not worse. Hyperbaric oxygen, adequate cellular nutrition, perhaps exposure to ketones, drugs that target the aberrant respiration of cancer cells, and certain electrical treatments that can increase cellular voltage (Ondamed, Tennant, etc.) should be used primarily in an effort to address the root cause before the big guns of chemo, radiation, and surgery are unleashed. Sometimes a bird's-eye view of this disease helps more than continued efforts down the same reductionist tracks.

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