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Controlled Amino Acid Therapy

 

What is CAAT?

CAAT is an amino acid– and carbohydrate-deprivation protocol using scientifically formulated amino acids. Research by Marco Rabinovitz, Ph.D., formerly of the National Cancer Institute, and Albert B. Lorincz, M.D., formerly of the University of Chicago, shows how beneficial amino acid deprivation therapy can be in treating cancer. 1

CAAT also includes a low-carbohydrate regimen that is personalized for each patient. Chi Van Dang, M.D., Ph.D., of the Johns Hopkins University School of Medicine, reported that cancer cells are such sugar junkies that glucose deprivation can contribute significantly to their demise. 2

CAAT has benefited patients across the United States, Canada, Europe, South America, and even in such faraway lands as New Zealand and India. Our hope is that CAAT can help you as well.

The following paragraphs will give you a more detailed explanation of CAAT. Please feel free to call us with any questions. We look forward to the opportunity to work with you. Click here to contact us.

The Science behind CAAT

The A.P. John Institute for Cancer Research was founded in 1978 by cancer scientist Angelo P. John, Sr., as a nonprofit organization. John, Sr., who specialized in molecular biology, invested more than 45 years in cancer research and studying its causation and treatment.

For more than two decades, the Institute has been focusing its investigative efforts on the role of amino acids in the cancer cell and how they differ from that role in normal cells. After the differences were identified, it was left to determine how amino acids in cancer cells could be altered or eliminated, causing their death. This research led to the development of Controlled Amino Acid Therapy (CAAT).

The objective of the CAAT protocol is to scientifically and strategically use the chemical reactions and interactions of amino acids, foods, and nutritional supplements to alter or impair the development of cancer cells by interfering with the five basic requirements of cell formation: structure, energy, blood vessels, growth hormones, and functions.

Because CAAT’s activity is so basic, it does not interfere with conventional therapies but rather complements and enhances their effectiveness. CAAT combined with chemotherapy or acting alone has stopped tumor growth, reduced tumor size, or eliminated tumors while improving one’s quality of life.

CAAT has benefited patients across the United States, Canada, Europe, South America, and even in such faraway lands as New Zealand and India. Our hope is that CAAT can help you as well.

The Scientifically Formulated Controlled Amino Acid Therapy

The immediate purpose of CAAT is to control a patient's amino acid intake. This is achieved by taking certain foods out of a person's daily food plan for a short time and by replacing them with a scientifically supported formula of amino acids. It is vital that the food plan that accompanies the amino acid formula be followed so not to offset any of the benefits created by depriving cancer cells of the nutrients they need to grow. Patients do not need to abandon their conventional cancer treatment, such as surgery, chemotherapy, radiation, and/or hormone treatments, nor is it recommended that they do so unless it has already failed them. CAAT works synergistically with chemotherapy and/or radiation to enhance their benefits, as demonstrated by Rabinovitz. His article on amino acid deprivation, such as used in CAAT, proves that it inhibits the working of phosphofructokinase and glycolysis, by which cancer cells create energy, simultaneously enhancing the benefits of chemotherapy while lessening its toxic side effects. CAAT has also proven to work successfully alone.

The CAAT Formulation

The most important component of CAAT is the scientifically formulated amino acid supplement, which consists of eight (seven essential) amino acids, citric acid, and small amounts of sodium benzoate. The CAAT supplement replaces most of the regular daily proteins found in meats, dairy, fish, beans (excluding green beans), and nuts, from which cancer cells can derive their energy. Taken two times a day, CAAT will nourish healthy cells while causing cancer cells to starve. Of course, all individuals have specific dietary needs, a fact that is taken into account and that will be explained by a specialist at the Institute when a patient begins CAAT.

Daily Food Intake

Disclaimer: The following food program is only a SAMPLE and should not be followed.

— Breakfast

  • One-half grapefruit* or 1 orange or 6 ounces (177 milliliters) of fresh squeezed orange juice.
  • Approximately 0.35 to 0.42 ounces (10 to 12 grams) of Whey Enhanced Protein based on a person 150 pounds (63 kilograms) in weight. Read the label carefully if your weight varies from this.
  • A serving (as defined on the product packaging) of grits or plain polenta. Adding a small pat of butter and/or some cinnamon or other spices is fine.
  • One cup (237 ml) of green or black tea (sweetened with fructose as desired).

*Do not have one-half grapefruit if you are taking chemotherapy or radiation because the side effects of these treatments could be intensified.

Explanation: One-half grapefruit or 1 orange or 6 ounces (177 ml) of fresh orange juice is rich in the natural nutrients limonene and citric acid. Limonene helps shut down the Ras cancer gene,3 which is overactive in 90 percent of all cancers. Citric acid helps shut down glycolosis, which in turn helps starve cancer cells.4

Phosphorus is a nutrient that cancer cells must utilize in order to grow and reproduce.5 The Whey Protein product we suggest contains no phosphorous and contains no additional vitamins, so when used according to directions, it helps protect normal cells, maintain a normal appetite, and fight edema, swelling of the legs or other body parts as a result of fluid retention.

Whey protein is included in the daily menu of all advanced or metastatic cancer patients. When undergoing treatment for cancers that are stable or have regressed in size, patients have the option of including other proteins at breakfast such as cottage cheese, yogurt, or soy products. Eggs are allowed in the diets of patients with lymphoma and brain cancers.

Grits or cream of rice is the standard breakfast staple. Having one slice of white toast, half a plain bagel, or half an English muffin with a small pat of butter is okay up to several times a week, but not every day. Grits or white rice is the preferred carbohydrate at each meal. The other choices are options once the cancer is stable or reduced in size. Unrefined carbohydrates are included in the CAAT menu instead of whole grains to deprive cancer cells of vitamin B6, also known as pyridoxine, which they require to manufacture certain amino acids that CAAT aims to reduce. Grits is the preferred carbohydrate at all meals instead of rice or pasta because it helps deplete the amino acid, tryptophan, which is essential for the growth and spreading of cancer cells.6

Green or black teas, using fructose as the sweetener of choice (if using any at all), are rich sources of several compounds that help shut down glycolosis and cut off the energy supply to cancer cells. Also, green or black tea helps prevent certain hormones and tumor growth factors from stimulating cancer cells to grow and metastasize.7 Brassica teas can also be taken because they contain sulphoraphane, a nutrient that inhibits cancer growth, and also shuts down cancer genes.8

— Lunch

  • The controlled amino acid formula as directed
  • Generous amounts of one cooked vegetable or a combination of the following: asparagus, broccoli, cabbage, brussells sprouts, spinach, squash, and/or string beans
  • One serving (½ cup or 113 grams) of one of the following fresh fruits: pear, orange, blueberries, raspberries, or strawberries
  • One moderate serving of grits, corn, rice, or pasta with tomato sauce or butter added
  • One tablespoon (15 ml) of coconut oil
  • Eight to ten black or green olives
  • Two tablespoons (30 ml) of vinegar (with a minimum acidity of 5 percent) added to vegetables or food
  • One cup (237 ml) of green or black tea (sweetened with fructose as desired)

Explanation: Taking the controlled amino acid formula as instructed combined with the special food plan, reduces certain amino acids daily and is designed to replace most of the normal animal protein one would consume in a day. Cancer cells require the amino acids glycine, glutamic acid, aspartic acid, and serine to synthesize DNA, build new blood vessels, and duplicate their entire protein contents.9 They also require these and certain other amino acids to synthesize other proteins that act as growth-promoting hormones or tumor growth factors.10 CAAT impairs the synthesis of a protein called elastin, which is absolutely essential to the manufacture of new blood vessels.11 The controlled amino acid formula, food plan, and selected phytochemicals and herbs work efficaciously to attack cancer cells on all biological fronts.

The generous amounts of one cooked vegetable or a combination of vegetables helps keep normal cells healthy. They are low in carbohydrates and proteins and high in phytochemicals that help fight cancer. Patients can eat these vegetables and salads whenever they wish.

The eight to ten olives are rich in squalene and oleic acid, nutrients that have been reported to inhibit certain cancer growth factors.12 The calories in olives help control body weight and the consumption of olives and olive oil is ketogenic, that is, it increases ketones in the blood because the liver produces ketones when it metabolizes fat. Ketones help fight cancer by impairing glycolysis,13 a process cancer cells depend almost exclusively on for their daily energy supply. Vinegar and fructose increase the body's production of both acetic and citric acids, which help fight cancer by shutting down glycolysis.14 Normal cells derive most of their daily energy supply from the Krebs or citric acid cycle, whereas cancer cells derive most of their daily energy from glycolosis.

— Dinner

  • The controlled amino acid formula as directed
  • Generous amounts of one cooked vegetable or a combination of the following: asparagus, broccoli, cabbage, brussells sprouts, spinach, squash, and/or string beans
  • One serving (½ cup or 113 grams) of stewed plums with fresh cream and fructose or 4 ounces (118 ml) of orange juice if plums are not in season
  • Avocado salad with lettuce, tomatoes, celery, and onions, with a dressing of lemon juice and coconut or olive oil
  • Two tablespoons (30 ml) of vinegar (with a minimum acidity of 5 percent) added to vegetables or other food
  • One serving of grits, corn, pasta, or rice with garlic and butter or tomato sauce added
  • One cup (237 ml) of green or black tea (sweetened with fructose as desired)

Mid-Evening Snack

  • A ketogenic cocktail made of 2 ounces (30 ml) fresh cream, ½ ounce (7.5 ml) each of coconut and olive oils, and 1 tablespoon (15 ml) fructose
  • A serving of a homemade gelatin dessert made with fructose and with whipped cream added either on top or stirred into the mixture before it sets (vegans can use a gelatin substitute such as KoJel® or Natural Desserts Unflavored, both by VIP Foods, and add fruits and fruit juice), 1 plum, or 4 ounces (118 ml) of orange juice
Explanation: A gelatin or gelatin-substitute dessert helps satisfy the appetite. Plums contain quinic acid, which is converted into benzoic acid in the body, which in turn helps to deplete the availability of the amino acid, glycine, essential to the synthesis of DNA by cancer cells, and the proteins that cancer cells require to build new blood vessels and their tumor growth factors. Prunes are also a good source of quinic acid as are whole coffeeberries and Cape Jasmine fruit (gardeniae fructus) should you be able to obtain this fruit easily in your geographic area.15If you are underweight, take 2 ounces (59 ml) of light cream and 1 ounce (30 ml) of olive or coconut oil as needed to maintain your weight.

— Optional Meal

Three to 4 ounces (85 to 113 grams) of veal, fish of choice, beef, chicken breast, and one slice of white bread. Consume this meal a minimum of 3 hours before or after taking the amino acid formula.

Explanation: The optional meal is taken only by patients who are 10 or more pounds (4.5 kg) underweight or who have albumin levels below normal. CAAT provides sufficient protein to maintain the health of normal cells and adequate amounts of calories to maintain desired body weight. Any proteins taken in excess of amounts recommended in the diet will counteract its benefits.

Special Diets

A special diet will be created for any cancer patients whose ability to consume food and liquids has placed them in a critical situation. For patients using a feeding apparatus or who have become too weak or lethargic to eat and drink the daily minimum amount for survival, we will break up the total breakfast, lunch, and dinner into portions to be consumed every 2 waking hours until they are capable of returning to a daily diet as outlined above.

Weight Gain and Loss

The CAAT food plan provides approximately 20 percent of its calories in the form of carbohydrates. Calories need not be a focal point or counted daily. It is recommended that all patients combat their cancers by keeping their body weight at normal or slightly below normal levels based on their particular frame size. Patients' desired body weights are regulated by their metabolic rates, which in turn are regulated by their blood levels of thyroxine, cortisone, insulin, and the amounts of fats and oils in their diets. Several studies have reported the therapeutic action of caloric reduction on malignant tumors in animals. Klurfeld and Kritchevsky, for example, report that in laboratory animals, cancerous tumors regress when their caloric intake is reduced by 10 percent—and are even eliminated from the body when the carbohydrates are reduced by 40 percent.16 Obese patients will find that following the CAAT diet will help them gradually and systematically lose their excess weight, which in turn will help increase the efficiency of the CAAT protocol because weight loss increases the amount of ketones in the bloodstream, which in turn has an anticarcinogenic effect. Underweight patients should not gain weight unless they are more than 10 pounds (4.5 kg) below normal levels. If a patient is underweight as a result of anorexia nervosa17 or cachexia,18 such illnesses must be addressed before CAAT can begin.

Reasons for Using Fructose and Vinegar to Treat Cancer

Nobel Prize winner Otto Warburg, M.D., Ph.D., discovered more than 50 years ago that all cancer cells produce inordinate amounts of lactic acid because they do not receive sufficient amounts of oxygen.19

In 2001, A.P. John, Sr., published the first study to show that cancer cells produce excess amounts of lactic acid because they have defective mitochondria. This causes cancer cells to break down glucose into lactic acid and then glycogen instead of carbon dioxide and water. This outcome forces cancer cells to depend almost exclusively on glycolysis as their major source of energy.20

Douglas Spitz, Ph.D., currently Director of the Free Radical Radiation Biology Program at the University of Iowa, and Yong J. Lee, Ph.D., currently Professor of Surgery in the Department of Pharmacology and Chemical Biology at the University of Pittsburgh, with other cancer researchers published studies showing that when cancer cells are deprived of glucose, their energy supply is cut off, causing them to die.21 Therefore, shutting down glycolysis would be one means of destroying cancer cells.

The A.P. John Institute for Cancer Research discovered that both acetic and citric acids could inhibit the activity of a key enzyme in glycolosis called phosphofructokinase, thereby shutting down the process of glycolosis. We were the first to introduce both the ingestion of vinegar and fructose as treatments for cancer because they either contain acetic acid or cause the body to produce it.

Keep in mind, CAAT is much more than just a "diet;" it is an amino acid–, carbohydrate-, and glucose-reduction protocol that scientifically and strategically uses the chemical reactions of amino acids, foods, and nutritional supplements to impair the development of cancer cells, thus starving them to death. Clinical trials have already been done with humans using amino acid–deprivation formulas with much success.22

 


References

  1. M. Rabinovitz, "Consequences of Amino Acid Deprivation in Combination with Chemotherapy," Journal of the National Cancer Institute 87 (1995): 142. A.B. Lorincz, "Tumor Response to Phenylalanine-Tyrosine-Linked Diets," Journal of the American Dietetic Association (Feb. 1968): 198–205; __________ and R.E. Kuttner, “Response of Malignancy to Phenylalanine Restriction,” Nebraska Medical Journal 50 (1965): 609. ___________________, “Suppression of Advanced Malignancy Disease by Restricting Phenylalanine Intake,” Federation. Proceedings 25 (1966): 360. ____________________, “Tumor Inhibition Limiting Amino Acid Diets,” (Abstr.) Journal of the American Medical Association 200 (1967): 211. ____________________, and M.B. Brandt, “Tumor Response to Phenylalanine-Tyrosine Limited Diets,” Journal of American Dietetic Association 54 (1968): 198–205.
  2. C.V. Dang, A.L. Simons, D.M. Matson, K. Dornfeld, and D.R. Spitz, "Glucose Deprivation–Induced Metabolic Oxidative Stress and Cancer Therapy," Journal of Cancer Research Therapy 5 (2009) Supplement 1: 52–56.
  3. M. Dollinger, E. Rosenbaum, and G. Gable. “Lung: Non-Small Cell Cancer,” in Everyone’s Guide to Cancer (Kansas City, KS: Andrews McMeel Publishing, 1997), 537 and E. Karp and S. Broder, “Oncology and Hematology,” Journal of the American Medical Association 271 (1994): 1693–95.
  4. H.A. Harper, V.W. Rodwell, and P.A. Mayes, “Metabolism of Carbohydrates and Lipid Metabolism,” in Review of Practical Physiological Chemistry (Los Altos, CA: Lange Medical Publications, 1979), 370 and M. Rabinovitz, “Consequences of Amino Acid Deprivation in Combination Chemotherapy,” Journal of the National Cancer Institute 87 (1995): 142.
  5. H. Harper, V. Rodwell, and P. Mayes. “Nucleotides,” in A Review of Physiological Chemistry (Los Altos, CA: Lange Medical Publication, 1979), 132.
  6. C.A. Opitz, U.M. Litzenburger, F. Sahm, M. Ott, I. Tritschler, S. Trump, T. Schumacher, L. Jestaedt, D. Schrenk, M. Weller, M. Jugold, G.J. Guillemin, C.L. Miller, C. Lutz, B. Radlwimmer, I. Lehmann, A. von Deimling, W. Wick, and M. Platten, "An Endogenous Tumour-Promoting Ligand of the Human Aryl Hydrocarbon Receptor," Nature 478 (2011): 197–203. George C. Prendergast's review of this article, "Why Tumours Eat Tryptophan," Nature 478 (2011): 192–94, presents a succinct summary of the preceding article, draws connections from it to past research, and spots the potential the discovery of Opitz et al. has for the future of cancer research.
  7. A. Khafif, S.P. Schantz, T.C. Chou, D. Edelstein, and P.G. Sacks, “Quantitation of Chemopreventive Synergism Between (-) Epigallocatechin-3-Gallate and Curcumin in Normal, Premalignant Human Oral Epithelial Cells,” Carcinogenesis 19 (1998): 419–24.
  8. J. Huang, C. Plass, and C. Gerheauser, "Cancer Prevention by Targeting the Epigenome," Current Drug Targets Dec. 15, 2010 (Epub ahead of print) http://www.ncbi.nlm.nih.gov/pubmed/21158707.
  9. H. Harper, V. Rodwell, and P. Mayes, “Metabolism of Purine and Pyrimidine Nucleotides,” in Review of Physiological Chemistry (Los Altos, CA: Lange Medical Publications 1979), 442. See also the Doctors/Oncologists page of this Web site for further information on this topic.
  10. N. Allen and T. Key, “Plasma Insulin-Like Growth Factor-1, Insulin-Like Growth Factor-Binding Proteins, and Prostate Cancer Risk: a Prospective Study,” Journal of the National Cancer Institute 93 (2001): 649 and K. Burroughs, S. Dunn, C. Barrett, and J. Taylor, “Insulin-Like Growth Factor-1: a Key Regulator of Human Cancer Risk,” Journal of the National Cancer Institute 91 (1999): 579.
  11. P.B. Hawk, B.L. Oser, and W.H. Summerson, “Proteins: Their Classification and Properties,” in Practical Physiological Chemistry (New York: McGraw-Hill Book Company, 1955), 183.
  12. For example, H.L. Newmark, "Squalene, Olive Oil, and Cancer Risk: A Review and Hypothesis," Cancer Epidemiology, Biomarkers & Prevention 6 (1997): 1101 and J.A. Menendez, S. Ropero, R. Lupu, and R. Colomer, "Dietary Fatty Acids Regulate the Activation Status of Her-2/neu (c-erB-2) Oncogene in Breast Cancer Cells," Annals of Oncology 15 (2004) 1719–21.
  13. G. Yellen, "Ketone Bodies, Glycolysis, and KATP Channels in the Mechanism of the Ketogenic Diet," Epilepsia 49 (Supplement 8) (2008): 80–82. This article explains that a ketogenic diet has shown remarkable efficacy in the treatment of drug-resistant epilepsy.
  14. J.W. Anderson and S.R. Bridges, "Short-Chain Fatty Acid Fermentation Products of Plant Fiber Affect Glucose Metabolism of Isolated Rat Hepatocytes," Proceedings of the Society for Experimental Biology and Medicine 177 (1984): 372–76. Acetic acid is one of the short-chain fatty acids.
  15. S. Kayano, H. Kikuzaki, N.F. Yamada, A. Aoki, K. Kasamatsu, Y. Yamasaki, T. Ikami, T. Suzuki, T. Mitani, and N. Nakatani, "Antioxidant Properties of Prunes (prunus domestica L.) and their Constituents," Biofactors 21 (2004): 1–4; coffeeberry (accessed on November 20, 2011); and H.J. Kim, E.J. Kim, S.H. Seo, C.G. Shin, C. Jin, and Y.S. Lee, "Vanillic Acid Glycoside and Quinic Acid Derivatives from Gardeniae Fructus," Journal of Natural Products 69 (2006): 600–03. Prunes have also beens shown to counter osteoporosis: S. Hooshmand, S.C. Chai, R.L. Saadat, M.E. Payton, K. Brummel-Smith, and B.H. Arjmandi, "Comparative Effects of Dried Plum and Dried Apple on Bone in Postmenopausal Women," British Journal of Nutrition 106 (2011): 923–30.
  16. D.M. Klurfeld, C.B. Welch, M.J. Davis, and D. Kritchevsky, "Determination of Degree of Energy Restriction Necessary to Reduce DMBA-Induced Mammary Tumorigenesis in Rats during the Promotion Phase," Journal of Nutrition 119(2) (Feb. 1989): 286–91 and D. Kritchevsky, M.M. Weber, and D.M. Klurfeld, "Dietary Fat versus Caloric Content in Initiation and Promotion of 7,12-Dimethylbenz(a)Anthracene-Induced Mammary Tumorigenesis in Rats," Cancer Research 44(8) (Aug. 1984): 3174–77.
  17. Anorexia nervosa is an eating disorder that makes people lose more weight than is considered healthy for their age and height. Persons with this disorder may have an intense fear of weight gain, even when they are underweight. They may diet or exercise too much, or use other methods to lose weight. Source: MedlinePlus
  18. Cachexia is the loss of body weight and muscle mass, and weakness that may occur in patients with cancer, AIDS, or other chronic diseases. Source: NIH Genetics Home Reference.
  19. O. Warburg, "On the Origin of Cancer Cells," Science 123 (1956): 309–14.
  20. A.P. John, Sr., "Dysfunctional Mitochondria, not Oxygen Insufficiency, Cause Cancer Cells To Produce Inordinate Amounts of Lactic Acid: the Impact of this on the Treatment of Cancer," Medical Hypotheses 57 (2001): 429–31.
  21. D.R. Spitz, "Glucose Deprivation-Induced Oxidative Stress in Human Tumor Cells," Annals of the New York Academy of Sciences 899 (2000): 349–62 and Y. Lee, "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 and Medicine 28 (2000): 575–84.
  22. A.B. Lorincz and R.E. Kuttner, "Tumor Inhibition Limiting Amino Acid Diets," (Abstr.) Journal of the American Medical Association 200 (1967): 211 and Medical News, "Amino Acid Restriction for Cancer," Journal of the American Medical Association 200 (1967): 31–46.
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I am diagnosed with Stage 4 breast cancer and start CAAT and femara 2 months ago. My CA 27-29 dropped 57 points. I look forward to my clear diagnosis....

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