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  • Controlled Amino Acid Therapy (CAAT) have shown to drastically inhibit the growth of cancer cells 0 comments
    Apr 30, 2009 11:36 PM
    For those who are seeking a non-conventional treatment modality that aids in the fight against cancer, I invite you to inspect the rational and clinical evidence behind CAAT (Controlled Amino Acid Therapy). 
    Basically, CAAT is an amino acid and carbohydrate deprivation protocol using scientifically formulated amino acids. Research by Dr.Marco Rabinowitz of the National Cancer Institute and Dr. Albert B. Lorincz of the University of Chicago shows how beneficial amino acid deprivation therapy can be in treating cancer.  The objective of the CAAT protocol is to strategically use the chemical reactions and interactions of amino acids to alter or impair the development of cancer cells by interfering with their biochemical factory: DNA synthesis.
    The CAAT replaces most regular protein foods. It creates a deficiency in the amino-acid precursor pool in the patient’s body. The diet, also low in carbohydrates and certain other nutrients, is adequate in calories to sustain desirable body weight. The amino-acid formula contains an additive, sodium benzoate, that further deprives cancer cells of glycine. The liver uses glycine to detoxify and eliminate sodium benzoate from the body. (1) Therefore, when added to the CAAT amino-acid formula in non-toxic but physiological quantities, sodium benzoate helps deplete glycine in the body.
    This promising biological approach, which involves phytochemicals and herbs and deprivation of carbohydrates and certain amino acids, resembles chemotherapy because it inhibits DNA and protein synthesis, angiogenesis and also curtails mitotic signal transduction receptors on cellular membranes of cancer cells. This latter process affects receptor regions common to numerous tumor growth factors. Thus this new modality not only can enhance conventional medicine, it also allows oncologists the option to treat cancer patients with less toxic therapies.  Furthermore, this model reduces certain nutrients in the daily diet of cancer patients (such as specific amino acids, carbohydrates, vitamins B-6 and folic acid, and the mineral phosphorus). The reasons that the prevailing science upholds the concept of a biological-deprivation diet to benefit cancer patients are elaborated below:

    A.  Amino-acid deprivation diet as first phase of the CAAT model:

    Amino acids are the building blocks of all proteins. Some 20 amino acids are essential to life. Twelve of these can be synthesized within the body and are classified as non-essential, whereas the remaining eight, classified as essential, must be provided by the daily diet.

    Genes and chromosomes dictate the kind of proteins each cell will manufacture, using different combinations of amino acids. Some proteins, such as glutathione, contain only three amino acids--glycine, glutamic acid, and cysteine. Other proteins may contain as many as a hundred or more amino acids in their molecules. These proteins not only form the major components of the human cell structure but in the form of enzymes and hormones, control literally every chemical or metabolic reaction that occurs in cells during daily life.

    We know before one cancer cell can grow and divide, it must first synthesize and double its DNA contents. In any textbook on biology or biochemistry one learns that there are four amino acids essential to synthesis of DNA. These include glycine, glutamic acid, aspartic acid and serine. (1) Many of the most effective chemotherapeutic drugs, like 5-fluourouracil, work by preventing cancer cells from synthesizing normal DNA. An amino-acid deprivation diet, by decreasing the precursor pool of any of these four non-essential amino acids, can therefore work alone or synergistically with numerous chemotherapeutic drugs to inhibit DNA synthesis in cancer cells.

    However, since each of the four amino acids mentioned above can be synthesized within the body it would be very difficult to reduce the precursor pool of all four at the same time simply by reducing their amounts in the daily diet. The CAAT model therefore concentrates on the depletion in the body of only one of the four amino acids, the one called glycine. A glycine deficiency alone can inhibit DNA synthesis.

    An amino-acid deprivation diet can stop the growth of cancer cells because proteins are the major structural components of almost all cells, including cancer cells. Before a cancer cell can divide, it must double both its DNA and its entire protein content. Here again, reducing the precursor pool of certain amino acids–especially any of the essential amino acids--can impede the cancer cell’s ability to produce sufficient proteins to self-replicate.  An amino-acid deprivation diet also inhibits tumor growth by a process called angiogenesis. Depriving cancer cells of glycine impacts the building of new blood vessels, since blood vessels are composed primarily of proteins. One protein absolutely essential to the manufacture of new blood vessels is elastin. (3)

    Elastin contains some five amino acids--glycine, proline, leucine, isoleucine, and valine.(4) Twenty-five percent of the elastin molecule consists of glycine. It is interesting that cancer cells have an extra requirement for these five amino acids, compared with normal cells,(5)indicating that cancer cells depend much more upon angiogenesis for their growth and reproduction than are normal cells. This is understandable, since normal cells have a built-in system of blood vessels and do not need to build as many new ones as cancer cells.

    The amino-acid deprivation diet also thwarts the growth of cancer cells by inhibiting their production of various tumor growth factors. Almost every cancerous tumor requires these tumor factors for growth and metastasis; normal cells do not have the same necessity. With the exception of steroid hormones, almost all tumor growth factors, such as epithelial growth factor, hepatocellular growth factor, insulin-like growth factor, vascular endothelial growth factor, and the Ras gene protein growth factor, are proteins, composed of amino acids. Again, reducing any essential amino acid in the daily diet can affect protein synthesis and therefore the production of tumor growth factors in the body as well. (6,7)

    Earliest studies with amino-acid deprivation diets occurred in the early forties. In 1944, Kocher (8)reported in Cancer Research that a lysine deprivation diet failed to stop the growth of cancers in laboratory animals. White, (9) working with cysteine, also reported no benefits in treating cancer in laboratory animals with the amino-acid deprivation diet. In those days all of the amino acids had not been isolated in pure form, and the scientists could study only the ones available at the time.

    However, in 1965, Lorincz reported in the Nebraska Journal of Medicine (10) a reduced tumor size in cancerous animals treated with a phenylalanine-deprivation diet. In 1966, he reported similar findings in Fed. Proc.(11) In 1967 in the Journal of the American Medical Association,(12) Lorincz published a further study showing the benefits to cancer patients taking a diet low in phenylalanine. In 1969, he reported the benefits of treating advanced cancer patients with a diet restricted in the amino acids phenylalanine and tyrosine (Journal of the American Dietetic Association) (13).

    B.  Carbohydrate-deprivation diet

    The second phase of the CAAT model includes a carbohydrate-deprivation diet. Lee (14) and Spitz (14)and their teams list more than twenty studies supporting their discovery that a glucose-deprivation diet causes apoptosis in cancer cells. Consider also that use of the PET scan to detect or monitor cancer is based upon the fact that cancer cells feed almost exclusively upon glucose for their major source of energy.

    The benefits that can be derived by reducing the amount of carbohydrates in the diets of cancer patients are now compelling because most cancers depend largely upon carbohydrates or glucose as their major fuel source. (15) A recent paper in Medical Hypotheses (16) details why cancer cells cannot burn carbohydrates or fats in their mitochondria, as do normal cells, but must rely almost exclusively upon glycolysis and the metabolism of glucose for their daily energy. Most energy for normal cells comes from the burning of fats, carbohydrates, and amino acids in the Krebs cycle. Cancer cells, however, must extract almost all their energy from glycolysis, a process that utilizes only glucose. Lee and others have shown that cancer cells enter apoptosis when deprived of glucose.

    Several other studies have reported the therapeutic benefits of carbohydrate- or glucose-deprivation diets. Kritchevsky, for example, reports that in laboratory animals cancerous tumors regress when their dietary carbohydrates are reduced by 10 percent—and are even eliminated from the body when the carbs are reduced by 40 percent. (17)

    Another means to impair metabolism of cancer cells and deprive them of energy is to inhibit phosphofructokinase, an enzyme that plays a key role in glycolysis. (18,19) Citric acid and ketones have been reported in textbooks to inhibit the activity of this enzyme. The addition of citric acid in nontoxic but physiological amounts to the CAAT amino-acid formula can help impair glycolysis and increase the benefits of the CAAT protocol. A diet low in carbohydrates can increase the amount of ketones in the blood and thus helps inhibit phosphofructokinase and glycolysis, robbing the cancer cell of its energy needs. (20)

    Prevailing science now shows numerous phytochemicals and herbs that can also serve as biological weapons to combat cancer. These are included in the CAAT model. Such biological weapons include tocotrienols, limonene, curcumin, and green tea.

    Specific areas targeted with such weapons include receptor regions common to numerous tumor growth factors. Cancer cells use these receptor regions to transmit mitogenic signals into their nuclei. Some tumor growth factors are Tyrosine Kinase (NYSE:TK), Ras Protein (NASDAQ:RP), Epithelial Growth Factor (NYSE:EGF), and Insulin-like Growth Factor -1 (IGF-1). (21)

    The tocotrienols, found in vegetable oils, belong to the vitamin E family. In cancer cells, they exert their anti-mitogenic effects by impairing a process called isoprenylation, (22) which is essential to activate the receptor regions of EGF, TK, and Ras protein. D-limonene, (23)contained in citrus fruits, can also curtail the activity of these three mitogens. It works downstream from the tocotrienols. Curcumin, major ingredient of the popular herb turmeric, is reported to have a powerful inhibitory effect on the activity of TK and Protein Kinase C. (24) Green tea contains a compound called epigallocatechin 3-gallate (EGCG). This substance shuts down the maleate-aspartic acid shuttle, a major function involved in conversion of glucose into energy during glycolysis. (25)

    Dietary deprivation or restriction of the vitamins folic acid and pyridoxine (vitamin B-6) and the mineral phosphorus are further valuable components of the proposed CAAT model. Since folic acid is essential to DNA synthesis, its deprivation in the diet can help inhibit DNA synthesis in cancer cells. The important chemotherapeutic drug methotrexate works similarly, by preventing cancer cells from utilizing folic acid, thereby inhibiting DNA synthesis.

    The body utilizes pyridoxine to synthesize the non-essential amino acids, including glycine. Its restriction in the diet can also help impair the synthesis of DNA and the amino acids necessary for cancer cells’ growth and reproduction. Phosphorus is an essential constituent of ATP, GTP, UTP and CTP all of which together control (26) the function of every metabolic reaction that occurs in every cell of the human body. A low phosphorus diet, which results when animal proteins are reduced in the diet (animal protein foods are among the richest sources of phosphorus), helps create a deficiency of ATP. Consequently, glycolysis is impaired, and cancer cells find it difficult to grow, reproduce, or even to sustain life.

    A discussion of the possible role that antioxidants play in cancer treatment may be deferred because results of studies reported to date are contradictory. However, evolving evidence suggests that the benefits, or lack of benefits, of antioxidant supplementation depend upon the oxidative stages the cancer cells are in. If they are in a state of high oxidative stress, then antioxidants may protect them against apoptosis. (27) The fact that many drugs, including adriamycin and mitomycin C , as well as radiation therapy, cause apoptosis by increasing production of pro-oxidants suggests that antioxidants should be withheld until the oxidative status of cancerous tumors is ascertained.

    Additionally, the effects of biological targeted therapies like CAAT which interfere with specific functions in cancer cells, causing them to die, has also been reported in The New England Journal of Medicine, The Journal of the National Cancer Institute, Clinical Cancer Research and The Journal Of Cellular Biochemistry. It is now evident that not only drugs, but specific biological compounds, such as those employed by CAAT, can attack such sites on cancer cells.

    • Dr Albert B. Lorincz of the University of Chicago conducted several trials with cancer patients, reducing tumor size in most of them who were fed a formula reduced in certain amino acids, the treatment employed by CAAT.
    • Dr. Chi Van Dang, of the Johns Hopkins School of Medicine, and Dr. Douglas Spitz of the University of Iowa report how carbohydrate deprivation, a part of the CAAT protocol, kills cancer cells while having no effect on normal cells.
    • Dr. Pascal J. Goldschmidt of the Johns Hopkins Medical School reports that scientifically supported dietary supplements, such as those included in CAAT, may be helpful in treating certain cancers.
    • Dr. Marco Rabinowitz of the National Cancer Institute reports that amino acid deprivation, such as Controlled Amino Acid Therapy (CAAT), inhibits phosphofructokinase, shuts down energy supply to cancer cells and thereby enhances the benefits of chemotherapy.
    • Dr. Joel Evans, Honorary Co-Chairman of the Physicians Advisory Board to the U.S. Congress, lectured at Yale’s Cancer Center on cancer and nutrition, discussing Controlled Amino Acid Therapy and citing the notable recovery his patient experienced since using CAAT.

    1. Hawk PB, Oser BL, Summerson WH. Urine physiological constituents. In: Practical Physiological Chemistry. New York, McGraw Hill Book Company, Inc. 1944:804.
    2. Harper Harold, Rodwell Victor, Mayes Peter. Metabolism of Purine & Pyrimidine Nucleotides. In: Review of Physiological Chemistry. Los Altos, CA: Lange Medical Publications 1979;442.
    3. Niederhumber J, Brenan MF, Menck H. The National Cancer Data Base Report on Pancreatic Cancer. Cancer 1995;76:1671-7.
    4. Harper Harold, Rodwell Victor, Mayes Peter. Epithelial, Connective and Nerve Tissues. Review of Physiological Chemistry, Los Altos, CA: Lange Medical Publications 1979;660.

    5. Holm H, Staedt E, Schlickeiser G., Gunther H.J., Leweling H. Substrate balances across colonic carcinomas in humans. Cancer Res 1995;55:1373-1378

    6. Allen Naomi, Key Timothy. Plasma Insulin-Like Growth Factor-1, Insulin-Like Growth Factor-Binding Proteins, and Prostate Cancer Risk: a Prospective Study. J Natl Cancer Inst 2001;93:649.

    7. Burroughs Kevin, Dunn Sandra, Barrett Carl, Taylor Jack. Insulin-Like Growth Factor-1: a Key Regulator of Human Cancer Risk. J Natl Cancer Inst 1999;91:579.

    8. Kocher, R.A., Effects of a low lysine diet on the growth of spontaneous mammary tumors in mice and on nitrogen balance in man Cancer Res. 1944;4:251.

    9. White, J., Andervont, H.B., Effect of a diet relatively low in cystine on the production of spontaneous mammary gland tumors in strain C3H female mice. J. Nat. Cancer Inst. 1943;3:449.

    10. Lorincz, A.B., Kuttner, R.E., Response of malignancy to phenylalanine restriction. Nebraska Medical Journal 1965;50;609.

    11. Lorincz, A.B., Kuttner, R.E., Suppression of advanced malignancy disease by restricting phenylalanine intake. Fed. Proc. 1966;25:360.

    12. Lorincz, A.B. Kuttner, R.E., Tumor inhibition limiting amino acid diets. (Abstr.) Journal American Medical Association. 1967;200:211.

    13. Lorincz, A.B., Kuttner E., Brandt M.B., Tumor Response to Phenylalanine-Tyrosine Limited Diets. Journal of American Dietetic Society. 1968;54:198-205.

    14. Lee Yong. 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 & Medicine 2000;28:575-584.

    15. Spitz, D.R. Glucose Deprivation-Induced Oxidative Stress In Human Tumor Cells Annals of he New York Academy of Sciences. 2000;899:349-362.

    16. Quillin Patrick, Cancer’s sweet tooth, Nutrition Science News 2000;4:1-8.

    17. John A.P. Dysfunctional mitochondria, not oxygen insufficiency, cause cancer cells to produce inordinate amounts of lactic acid: the impact of this on the treatment of cancer. Med Hypotheses 2001;57:429-431.

    18. Kritchevsky D. Journal of the National Cancer Institute 1998;90:1766.

    19. Harper HA, Rodwell VW, Mayes PA. Metabolism of carbohydrates and lipid metabolism. In: Review of Practical Physiological Chemistry. Los Altos, California: Lange Medical Publications, 1979:370.

    20. Rabinowitz M. Consequences of amino acid deprivation in combination chemotherapy. Journal of the National Cancer Institute 1995;87:l42.

    21. Ibid., Regulation of carbohydrate and lipid metabolism, 371.

    22. Adjei Alex A. Blocking Oncogenic Ras Signaling for Cancer Therapy. J Natl Cancer Inst 2001;93:1062-1072.

    23. Dollinger M, Rosenbaum E, Gable G. Lung: non-small cell cancer. In: Everyone’s Guide to Cancer Kansas City: Andrews McMeel Publishing 1997:537.

    24. Karp Ejudith, Broder Samuel. Oncology and Hematology. JAMA 1994;271:1693-1695.

    25. Ruey Long Hong, William Spohn, and Mien-Chie Hung. Curcumin Inhibits Tyrosine Kinase Acivity of p185neu and Also Depletes p185neu1. Clinical Cancer Research 1999;5:1884-1891.

    26. Khafif A, Schantz SP,. Quantitation of chemopreventive synergism between (-) epigallocatechin-3-gal... and curcumin normal, premalignant human oral epithelial cells. Carcinogenesis 1998;19:419-424.

    27. Harper Harold, Rodwell Victor, Mayes Peter. Nucleotides.In: A Review of Physiological Chemistry, Los Altos, CA: Lange Medical Publication, 1979;132.

    28. Spitz, D.R. Glucose Deprivation-Induced Oxidative Stress In Human Tumor Cells. Annals of the New York Academy of Sciences: 2000;899:349-362.


    Disclosure:  Author does not own any securities realted to the above mentioned product.

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