institute for cancer research

Each year we gain more and more knowledge concerning the prevention, causation, and treatment of cancer. This newer knowledge provides us with a better understanding of the role that diet and nutrition can play in the treatment of this dreaded disease.

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 feeding cancer patients a wholesome diet is the belief that this builds up the immune system to fight cancer better. The scientific evidence shows that the immune system not only doesn’t 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 breast^1,2. Some evidence shows that macrophages and other white blood cells that comprise the immune system secrete toxic cancer-causing chemicals in order to kill the infectious organisms that infiltrate the cells of the body. Unfortunately, these toxic weapons of the immune system enter normal cells and thereby increase their risk of cancer.

The immune system can protect the body against pathogens--viruses, bacteria, fungi, molds, etc.--but it is the Detox 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 Johns Hopkins University School of Medicine, headed by Dr. Paul Talalay, have all published studies and confirmed that each of the trillions of cells that comprise the human body contains a Cancer Detox System³. This Detox System is composed of numerous enzymes, such as superoxide dismutase, catalaze, 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 the foods and beverages of the diet⁴.

Numerous studies published over the past several years, including this year, support the concept that good nutrition can fuel growth in most cancers. Also emerging evidence shows that diets deprived of certain amino acids can enhance the benefits of chemotherapy or radiation therapy and that diets deprived of glucose can kill cancer cells.

For example, Dr. Rabinowitz⁵ 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 the drugs.

Dr. Albright⁶ of the University of North Carolina has taken the anti-oxidants 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 anti-oxidant-deprived animals.

Dr. Chi Van Dang,⁷ of Johns Hopkins University School of Medicine, also found that most cancer cells, when deprived of glucose, will self-destruct.

In addition, five teams of scientists, including Drs. Yong and Hunt of George Washington University, Dr. Spitz of the University of Iowa, Dr. Lee of the University of Southern California, and Dr. Blackburn of William Beaumont Hospital,^8,9,10 have all 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.

Dr. Kritchevsky¹¹ published in Journal of National Cancer Institute that when he reduced the carbohydrates only 10 percent in the diets of laboratory animals, he could reduce tumor size. When he fed cancerous animals a diet with a 40-percent reduction in carbohydrates, their tumors disappeared completely.

Dr. Lorincz¹² 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 fed these patients a liquid formula developed by Mead Johnson and deficient in both of these amino acids. This diet resembles the diet given to children with PKU.

Dr. Meadows¹³ of the University of Washington has increased the survival rates in animals with melanomas by reducing their daily intake of the same amino acids, tyrosine and phenylalanine.

Cancer scientist Angelo P. John published some results in the October 2001 issue of Medical Hypotheses (57:4, 429-431).¹⁴ 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 will dramatically impact the future treatment of cancer.

There are also certain supplements, including phytochemicals, that help stop the growth of cancers. Use of these supplements is supported by the latest science that demonstrates their physiological action in the body. One example is d-Limonene, which can stop the action of the Ras oncogene and which is over-active in 90 percent of all cancers. Another is calcium D-glucarate, which can help reduce estrogen levels in the body and help in treating breast cancer.

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.

With this information Angelo P. John, Sr., a cancer scientist who specializes in molecular biology, designed a protocol called Controlled Amino Acid Therapy (CAAT). CAAT’s 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. Before a cancer cell can divide in two, it must duplicate its DNA and other cell contents. Since cells are composed primarily of protein, by reducing the precursor pool of amino acids, CAAT can prevent cancer cells from reproducing. Cancer cells also depend upon amino acids to synthesize their DNA and their numerous tumor growth factors.

Here is an actual case history from our work:

A 38-year-old woman enrolled in CAAT during April 2001. She had recurrent breast cancer that had metastasized to the bone at the time of enrollment. Her 25-37 tumor marker was elevated to 132. She had taken tamoxifen but, despite the fact she was estrogen positive, her tumors continued to progress.

Her CAAT diet contained approximately 15 to 20 percent carbohydrates and included our special amino acid formula. Taken twice daily, it substitutes for most of the animal protein in her diet.

To help inhibit production of estrogen in her body we supplemented her diet with d-limonene, squalene, and the tocotrienols. These are natural phytochemicals that can reduce the production of cholesterol. Cholesterol, of course, is a precursor of estrogen synthesis in the body. All these nutrients decrease epithelial growth factor (EGF), which is also a potent mitogen for breast cancer cells. She also took calcium d-glucarate to enhance elimination of estrogen from her body.

To reduce production of the mitogenic prostaglandin hormones, we suggested to her oncologist a Cox -II inhibitor called Celebrex (a prescription drug). She also took over-the- counter nutrients, such as EPA, curcumin, silymarin, and resveratrol. Curcumin inhibits EGF growth factor activity in cancer cells. The patient also took olive leaf extract, to help induce apoptosis, plus vitamin D to activate phosphatases. These de-activate mitogenic enzymes called kinases¹⁵.

Anti-oxidants should not be taken when cancer cells are growing rapidly because they can protect cancer cells from apoptosis. Nor should anti-oxidants be taken in combination with drugs like adriamycin and mytomycin C, which also increase oxidation of cancer cells. Furthermore, anti-oxidants should never be taken when patients are receiving radiation therapy, for the same reasons mentioned above.

This breast cancer patient has completed her seventh month of CAAT treatment. Her 25-37 tumor marker has dropped each month to its present normal level of 17, and her latest CAT scan shows no evidence of her metastatic bone cancer. Most patients stay on CAAT 6 to 9 months and then return to an otherwise wholesome diet along with proper supplements, including anti-oxidants.

Calories need not be a focal point or counted daily. Patients’ desired body weight is regulated by their rate of metabolism, which in turn is regulated by their blood levels of thyroxine, cortisone, and insulin. plus the amount of oils and fats in the diet.

Patients are allowed to eat vegetables and salads ad libitum (depending on the type of cancer, medical information, and their blood work). Vegetables are generally low in carbohydrates, proteins, and especially in certain amino acids that are already reduced in the daily diet. CAAT’s amino acid formula (depending on the type of cancer) is designed to replace most animal protein in the diet.This research with scientifically designed diets and proper supplementation is a powerful weapon that supports and complements conventional therapies. Bio-nutritional protocols such as CAAT can mean the difference between survival and death for these individuals.

REFERENCES

1. Jagdeep, K. 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: l429-1432.
    
2. Stewart, Thomas. Incidence of de-novo breast cancer in women chronically immuno- suppressed after organ transplantation. The Lancet l995; 346: 796-802.
    
3. Talalay,Paul. Sensitivity to carcinogenesis is increased, and chemoprotective efficacy of enzyme inducers is lost in nrf2 transcription factor-deficient mice. Procedings of the National Academy of Sciences 200l; 99: l207-l2l2.
    
4. Stephen D. Hursting. Mechanism-Based Cancer Prevention Approaches: Targets, Examples, and the Use of Transgenic Mice. Journal of the National Cancer Institute. l999; 9l: 2l5-2l0.
    
5. Rabinowitz, M., "Consequences of Amino Acid Deprivation in Combination Chemotherapy." Journal of the National Cancer Institute l995; 87: l42.
    
6. Albright, Craig. Science News 2000; l59: 248.
    
7. Dang, C.-V. Unique glucose dependent apoptotic pathway induced by CMYC. Proceedings of the National Academy of Sciences l998; 95: l511-l5l6.
    
8. Yong, J. 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 l998;273: 5294-5299.
    
9. Spitz,Douglas. Dominant-Negative Jun N-Terminal Protein Kinase (JNK-1) Inhibits Metabolic Oxidative Stress during Glucose Deprivation in a Human Breast Carcinoma Cell Line 2000; 28: 575-584.
    
10. Spitz, Douglas. Glucose Deprivation-Induced Oxidative Stress in Human Tumor Cells. Reactive Oxygen Species 2000; 899-902.
     
11. Kritchevsky, David. Can Reducing Caloric Intake Also Help Reduce Cancer? Journal of the National Cancer Institute 90: l766-l768.
     
12. Lorincz, Albert. Tumor Response to Phenylalanine-Tyrosine-Limited Diets. Journal of the American Dietetic Association Feb. l968; l98-205.
     
13. Meadows,J. Survival of mice fed the low Tyrosine/Phenylalanine diet. Aadv. Exp. Med. Biol. 1994; l71-l84.
     
14. John, Angelo. 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 200l; 57: 429-43l.
     
15. Tangricha, Vin. 25-hydroxyvitamin D-1&-hydroxylase in normal and malignant colon tissue. Lancet 200l; 357: l673.