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Each year we gain more and more knowledge about the prevention, causation, and treatment of cancer.

This contemporary knowledge provides us with a better understanding of the role that diet and nutrition can play in the treatment of this widespread and challenging set of diseases.

Cancer cells require the same amino acids, carbohydrates, fats, vitamins, and minerals for their growth and reproduction as do normal cells—but in different quantities. This fact alone raises the question about whether or not a nutritious diet can actually help fight cancer. Or does an otherwise nutritious diet help fuel the growth of cancer?

The prevailing concept behind providing cancer patients a wholesome diet is the belief that this builds up the immune system to fight cancer better. Scientific evidence shows that the immune system not only does not attack cancers that develop within the body of their host but that the immune system can actually increase the risk of developing cancer, especially cancer of the breast1,2. Some evidence shows that one type of macrophage that composes part of the immune system secretes toxic disease-causing chemicals in creating an inflammatory response.3

The immune system can protect the body against pathogens—viruses, bacteria, fungi, molds, and the like, but it is the Detoxification System that protects body cells against toxic cancer-causing chemicals and from the development of cancer. Teams of scientists at the world’s leading cancer research centers, including a team at the Johns Hopkins University School of Medicine, headed by Paul Talalay, M.D., have all published studies and confirmed that each of the trillions of cells that compose the human body contains a cancer detoxification system.4 This system is composed of numerous enzymes, such as superoxide dismutase, catalase, glutathione, and epoxide hydrolase, to name just a few. These enzymes are supported in their work of detoxifying cancer-causing chemicals by nutrients called anti-oxidants and phytochemicals. These nutrients are contained in foods and beverages consumed daily.5

Numerous studies published over the past several years support the concept that typical modern nutrition or what is often considered good nutrition can fuel cancer growth.6 Emerging evidence shows that diets deprived of certain amino acids can enhance the benefits of chemotherapy or radiation therapy and that diets lacking glucose can kill cancer cells. For example, Marco Rabinowitz, Ph.D., reported in the Journal of the National Cancer Institute that a drug that prevents cancer cells from utilizing either of the amino acids histidine or tryptophan can disable their energy supply. Without sufficient energy, cancer cells cannot expel toxic chemotherapeutic drugs as they normally do and are therefore more susceptible to killing by these drugs.7

Craig Albright, Ph.D., formerly of the University of North Carolina, removed the antioxidants C and E from the diets of animals bred to develop breast cancer. He reports that when compared to control animals on a regular diet, the animals on the deprivation diet developed fewer cancers and the least number of metastases. He concluded that excess apoptosis (cell death) contributed to fewer tumors in the antioxidant-deprived animals.8

Chi Van Dang, M.D., Ph.D., of Johns Hopkins University School of Medicine, found that most cancer cells, when deprived of glucose, will self-destruct.9

In addition, Yong J. Lee, Ph.D.,10,11 currently of the University of Pittsburgh School of Medicine, and Douglas Spitz, Ph.D.,12 of the University of Iowa have published studies showing that carbohydrate deprivation kills cancer cells, both in vitro and in vivo, Furthermore, such carbohydrate deprivation has no adverse effects on normal cells.

David Kritchevsky, Ph.D., published in Journal of the National Cancer Institute that when he reduced carbohydrates only 10 percent in the diets of laboratory animals, he could reduce tumor size. When he fed cancerous animals a diet in which carbohydrates were reduced by 40 percent, their tumors disappeared completely.13

Albert B. Lorincz, Ph.D., formerly of the University of Chicago, conducted a small trial with several advanced cancer patients. He reduced tumor size in most patients who ate a diet restricted in the amino acids tyrosine and phenylalanine. He provided these patients a liquid formula, developed by Mead Johnson, deficient in both these amino acids.14 This diet resembles the diet given to children with phenylketonurea (PKU).

Catherine A. Elstad, Ph.D., of Washington State University, and others have increased the survival rates in animals with melanomas by reducing their daily intake of the same amino acids, tyrosine and phenylalanine.15

Cancer scientist Angelo P. John, Sr., published some results in the October 2001 issue of Medical Hypotheses (57:4, 429–31).16 Here he explains the biochemical reasons that most cancer cells must rely almost exclusively upon the glucose derived from carbohydrate foods as their major supply of nutrients. John’s discovery that cancer cells have defective mitochondria and must therefore depend largely upon glycolysis and glucose for nutrition can have a major impact on the treatment of cancer if its implications are acted upon.

Certain supplements, including phytochemicals, also help stop the growth of cancers. Use of these supplements is supported by the latest science, which demonstrates their physiological action in the body. One example is d-Limonene, which has an antiproliferative effect on lymphoma and other cancers.17 Another is calcium D-glucarate, which can help reduce estrogen levels in the body and help in preventing breast cancer.18 Yet another is Vitamin D, which seems to have a protective effect against colon cancer.19

As mentioned above, numerous studies have been published showing that amino acid and carbohydrate-deprivation diets, plus certain supplementation, can cause cancerous tumors to regress and often disappear from the bodies of their hosts.

Based on these facts, John, Sr., a cancer scientist who specialized in molecular biology, designed a protocol called Controlled Amino Acid Therapy (CAAT). CAAT’s selective amino acid and carbohydrate-deprivation formula was designed to work synergistically with chemotherapy and radiation therapy to kill cancer cells.

CAAT attacks cancer in many of the same ways as drugs do. Before a cancer cell can divide in two, it must duplicate its DNA and other cell contents. Because cells are composed primarily of protein, which needs amino acids to regenerate itself, reduction of the precursor pool of amino acids through CAAT can prevent cancer cells from reproducing. Cancer cells also depend upon amino acids to synthesize their DNA and their numerous tumor growth factors.



  1. K. Jagdeep, "Effect of Dietary Vitamin E on Spontaneous or Nitric Oxide Donor-Induced Mutations in a Mouse Tumor." Journal of the National Cancer Institute 2000; 92: 1429–32.
  2. T. Stewart, "Incidence of De-Novo Breast Cancer in Women Chronically Immuno- Suppressed after Organ Transplantation." The Lancet 1995; 346: 796–802.
  3. D.L. Laskin," Macrophages and Inflammatory Mediators in Chemical Toxicity: A Battle of Forces." Chemical Research in Toxicology 2009; 22 (8): 1376–85.
  4. P. Talalay, "Sensitivity to Carcinogenesis Is Increased, and Chemoprotective Efficacy of Enzyme Inducers is Lost in nrf2 Transcription Factor-Deficient Mice." Proceedings of the National Academy of Sciences 2001; 99: 1207–12.
  5. S.D. Hursting, "Mechanism-Based Cancer Prevention Approaches: Targets, Examples, and the Use of Transgenic Mice." Journal of the National Cancer Institute. 1999; 91: 215–25
  6. For example, S.C. Larsson, L. Bergkvist, and A. Wolk, "Milk and Lactose Intakes and Ovarian Cancer Risk in the Swedish Mammography Cohort." American Journal of Clinical Nutrition 2004 80 (5): 1353—57 and H. Liu, D. Huang, L.G. Boras, N. Nissen, and A.P. Heaney, "Fructose Induces Transketolase Flux to Promote Pancreatic Cancer Growth." Cancer Research 2010 70 (15): 6368—76.
  7. M. Rabinowitz, "Consequences of Amino Acid Deprivation in Combination Chemotherapy." Journal of the National Cancer Institute 1995; 87: 142.
  8. C. Albright, Science News 2000; 159: 248.
  9. C.V. Dang, "Unique Glucose Dependent Apoptotic Pathway Induced by CMYC." Proceedings of the National Academy of Sciences 1998; 95: 1511–16.
  10. Y.J. Lee, S.S. Galolforo, C.M. Berns, J.C. Chen, B.H. Davis, J.E. Sim, P.M. Corry, and D.R. Spitz, "Glucose Deprivation-induced Cytotoxicity and Alterations in Mitogen-Activated Protein Kinase Activation Are Mediated by Oxidative Stress in Multidrug-Resistant Human Breast Carcinoma Cells." Journal of Biological Chemistry 1998; 273: 5294–99.
  11. Y.J. Lee, S.S. Galolforo, J.E. Sim, L.A. Ridnour, J. Choi, H.J. Forman, P.M. Corry, and D.R. Spitz, "Dominant-Negative Jun N-Terminal Protein Kinase (JNK-1) Inhibits Metabolic Oxidative Stress during Glucose Deprivation in a Human Breast Carcinoma Cell Line." Free Radical Biology 2000; 28: 575–84.
  12. D.R. Spitz, J.E. Sim, L.A. Ridnour, S.S. Galoforo, and Y.J. Lee, "Glucose Deprivation-Induced Oxidative Stress in Human Tumor Cells." Annals of the New York Academy of Sciences 2000; 899: 349–62.
  13. D. Kritchevsky, "Can Reducing Caloric Intake Also Help Reduce Cancer?" Journal of the National Cancer Institute 90: 1766–68.
  14. A.B. Lorincz, R.E. Kuttner, and M.B. Brandt, "Tumor Response to Phenylalanine-Tyrosine-Limited Diets." Journal of the American Dietetic Association Mar 1969; 54(3): 198–205.
  15. C.A. Elstad, G.G. Meadows, C.J. Aslakson, and J.R. Starkey, "Evidence for Nutrient Modulation of Tumor Phenotype: Impact of Tyrosine and Phenylalanine Restriction," in Diet and Cancer: Markers, Prevention, and Treatment, ed. M.M. Jacobs, 171–83 (New York, NY: Plenum Press, 1994).This article also appeared in the journal Advances in Experimental Medicine and Biology 1994; 354: 171–84.
  16. A. John, "Dysfunctional Mitochondria and not Oxygen Insufficiency Cause Cancer Cells to Produce Inordinate Amounts of Lactic Acid: Its Impact in the Treatment of Cancer." Medical Hypotheses 2001; 57: 429–31.
  17. M.G. Manuele, M.L. Barreiro Arcos, R. Davicino, G. Ferraro, G. Cremaschi, and C. Anesini. "Limonene Exerts Antiproliferative Effects and Increases Nitric Oxide Levels on a Lymphoma Cell Line by Dual Mechanism of the ERK Pathway: Relationship with Oxidative Stress." Cancer Investigation 2010; 28 (2):135–45 and P.M. Vigushin, G.K. Poon, A. Boddy, J. English, G.W. Halbert, C. Pagonis, M. Jarman, and R.C. Coombes, "Phase I and Pharmokinetic Study of D-Limonene in Patients with Advanced Cancer." Cancer Chemotherapy and Pharmacology 1998; 42 (2): 111–17.
  18. A.S. Heerdt, C.W. Young, and P.I. Borgen, "Calcium Glucarate as a Chemopreventive Agent in Breast Cancer." Israel Journal of Medical Science 1995; 31 (2&3): 101–05.
  19. V. Tangpricha, J.N. Flanagan, L.W. Whitelatch, C.C. Tseng, T.C. Chen, P.R. Holt, M.S. Lipkin, and M.F. Holick, 25-hydroxyvitamin D-1alpha-hydroxylase in Normal and Malignant Colon Tissue. Lancet 2001; 357 (9269): 1673–74.
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- Debbie - Cervical Cancer

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