The following is a rebuttal to self proclaimed "medical writters" about Insulin Potentiation Therapy IPT or IPTLD.
I will start by sharing a comment made by R.W. Moss about chemotherapy (extract reproduced from a public source at http://www.whale.to/c/moss.html): “RM: Chemotherapy is machismo practiced to the N'th degree. It is a war in which you are the battleground, lucky you, I mean you have to treat your body better than that. The folks that bring you the toxic chemicals that cause the cancer are then kind enough to bring you toxic chemicals that allegedly…..”
Yes IPT/IPTLD works, it is a treatment alternative for lasting and successful outcomes. #InsulinPotentiationTherapy #IPT© or #IPTLD®, it is a metabolic supported chemotherapy. It involves fasting, insulin and chemotherapy. This is not a miracle product or the cure that is hidden from you. It is a safe treatment alternative. Not all patients will benefit. Consult your case: www.iptldmd.com .
I have undertaken to write this rebuttal because insulin potentiation therapy (IPT/ IPTLD) has helped multitudes of people with cancer who had already undergone the conventional route of surgery, chemotherapy and radiation and whose oncology team explained that there was “nothing else we can do.” I have personally had hundreds of these types of patients come to our center and, guess what? There was and is something that can be done to be restored to health.
It is clear that the self called "medical writers" and editors R.Baratz, RW Moss, J Jones, have not studied the protocols or the science behind insulin potentiation therapy (IPT/IPTLD). Their position regarding IPT/IPTLD as reflected in their writings posted on their Blogs has either evolved out of hearsay or their imagination, not honest research into the subject matter, which indicates that they are attempting to alter people’s opinion regarding this chemotherapy delivery system by ‘reference to “authority,” rather than by utilizing factual information in an effort to inform or educate. The following is a definition of this fallacious way of arguing utilized by Dr Baratz, MD, DDS, PhD:
“Argument from authority (also known as appeal to authority) is a fallacy of defective induction, where it is argued that a statement is correct because the statement is made by a person or source that is commonly regarded as authoritative. The most general structure of this argument is:
* Source A says that p is true.
* Source A is authoritative.
* Therefore, p is true.
This is a fallacy because the truth or falsity of a claim is not related to the authority of the claimant, and because the premises can be true, and the conclusion false (an authoritative claim can turn out to be false). It is also known as argumentum ad verecundiam (Latin: argument to respect),argumentum ad potentiam (Latin: argument to power), or ipse dixit (Latin: he himself said it).”
Even a cursory evaluation of the science underlying IPT/IPTLD reveals that all cancer cells studied have, not only many more insulin receptors on their surfaces, but that those receptors have up to a 60% greater affinity (stickiness) than usual insulin receptors on non-cancerous cells. Also, what becomes clear from an earnest evaluation of the research into this matter is that there is a 43% homology between insulin receptors and IGF-1 receptors. This aspect of receptor status regarding cancerous cells is an additionally, rather salient aspect of how it is that IPT/IPTLD works to target cancerous cells as well as increase the effectiveness of the chemotherapeutic agent(s) administered. Under these conditions, lower administered doses carry equal, if not more of a “punch.” IGF-1 receptors, once activated, initiates cells to begin dividing, which is a stage of the cell cycle wherein cells are more vulnerable, hence more easily and effectively eliminated. Although cancerous cells have an autocrine function (produce their own insulin and IGF=1), this is occurring at all times which stimulates and fuels their growth during all phases of the cell cycle. However, when this is purposely activated during treatment with a cytotoxic agent, there is greater destruction of the malignant cells being targeted.
Any physician who has worked in an emergency department knows that when a patient arrives in an unconscious condition, the standard protocol usually calls for a dose of naltrexone and a dose of glucose. The naltrexone to counteract opiate overdose and the glucose counteract insulin overdose. The protocol requires both of these agents since there is no information regarding how the person became unconscious. When glucose is administered intravenously (IV) to someone who is suffering from an insulin overdose, they quickly begin to regain consciousness and are often confused, wondering where they are and how they got there. In the vast majority of cases, the person who was “comatose” (unconscious) from insulin having produced a potentially lethal hypoglycemic state returns to normal with no long term, adverse effects. Although the duration that the person was “comatose” is never precisely known, clearly, it must have included, at least a few minutes prior to the ambulance’s arrival plus the duration of the ambulance ride to the ER.
With insulin potentiation therapy (IPT/IPTLD), no one is ever allowed to become, even slightly neurologically impaired and, of course never allowed to lose consciousness. IV glucose is administered immediately if even the slightest neurological impairment becomes evident, e.g., slurred speech and glucagon is available to be used if the glucose does not immediately reverse the condition. Although glucagon is always available, it has never been necessary to use it. Glucagon is a hormone like insulin, produced in the pancreas by the Islets of Langerhans cells. Insulin is produced by the beta cells while glucagon is produced by the alpha cells. They are the ‘yin and yang’ of blood glucose homeostasis. Glucagon has the opposite effect of insulin and therefore, is its natural ‘antidote.’ NO ONE HAS EVER DIED FROM INSULIN POTENTIATION THERAPY. The same cannot be said of conventionally delivered, high dose chemotherapy. As indicated previously, even a cursory evaluation of the protocols used in IPT/IPTLD make it clear that this concern discussed in Blogs like Quack Watch, Moss Reports regarding the potential neurological impairment resulting from acute hypoglycemia brought about by insulin from this therapeutic modality could never occur if one follows the established protocols.
Why have there been no clinical trials using insulin potentiation therapy? As is commonly known, most clinical trials are expensive and funded by pharmaceutical companies attempting to receive FDA approval for use of a drug or device. No pharmaceutical company has to date accepted the offer to fund a clinical trial utilizing IPT/IPTLD nor even attempted to develop a clinical trail in order to prove that one can use 90% less of a chemotherapeutic drug that has already received FDA approval for its use. The stockholders simply would not allow this. It would not be considered a fiscally sound use of corporate money. The only human trail was performed in Uruguay and funded by the government (reference included). The lead investigator, Dr Lasalvia, is a well respected member of the American Society of Clinical Oncology and the results of his small trail clearly demonstrated that insulin plus a lower dose of a chemotherapeutic agent was more effective than either the drug alone or insulin alone. Although there are similar trials being performed in other countries where funding can be obtained from sources other than pharmaceutical companies, none of the studies have been concluded at this time.
In conclusion, IPT/IPTLD has been used successfully since 1930. Since 1997 it was introduced to many countries for neurological infectious, other infectious diseases, i.e., Lymes, and cancer of almost every type, and all stages (I – IV). With this long history of successful use of a modality to deliver drugs in a targeted fashion, minimal side effects (toxicities) and with no deaths, it is truly a human tragedy that this modality has not been evaluated here in the United States beginning with animal models and progressing to humans, as do all of the drugs that receive FDA approval. To merely criticize and attempt to dissuade further evaluation of something with such great potential benefit to humans is not only a tragedy but should be an embarrassment to the scientific community at large.
How very easy it is to proclaim your self a “medical writer or critic” and think you can rule a lifetime legacy as “quackery”. These ignorant “critics” do a couple of Google searches, a few hour research on an 8-decade tradition and actually believe they are experts in the theme. What a truly pathetic existence they must have. The good name of my grandfather and my father have been under attack for decades now, attack on my protocol “Insulin Potentiation Therapy” and this will be tolerated no more. Self proclaimed medical writers that abuse of their (?) prestige, like Robert Baratz, Jonathan Jones and Ralph W Moss, come out! They have been attacking my lifetime work and placing doubt over the effectiveness of IPT©- IPTLD® with no solid foundation, except non-medical opinions. But these are the “low blows” of a coward, who attacks behind comfortable desks and think they can undo a lifetime achievement from a laptop and steal a life saving treatment to cancer patients. The testimony of IPT©- IPTLD® s effectiveness is living and breathing in every cancer patient that lives today in remission, beating in every healthy patient worldwide who overcame cancer when no other doctor gave them hope. IPT©- IPTLD® is hope and mere verbal attacks from you ignorant selfish people, who have no courage to tell it to my face, can undo. My office is open for discussion with you “Quackery Cowards” and dare to say these things to my face. I am not hiding like you are. Unlike you people, I do have moral standards and courage to fight my opponents out in the open. I do not hide behind comfortable desks, I don’t offend or attack other professional’s based on Google searches and post whatever comes to mind. You are dealing with human lives, and they have the right to know TRUTH, and the TRUTH is that IPT©- IPTLD® is a successful alternative cancer treatment, proven for decades to save patients lives. The theoretical proof is here in my office, if you want it, come and get it! Stop tainting my family’s good name and stop poisoning peoples mind with LIES, take a stand and come out you Cowards! You’ve done enough damage. Think you know more about IPT? PROVE IT!
Publications and Essays on IPT, also Supportive Studies – Published clinical and in-vitro studies that support the use of insulin as a biologic response modifier.
1)Poster Presentation at the Third Annual Comprehensive Cancer Management Conference, Washington, DC June 2000
Primary Breast Conserving Treatment for Breast Cancer Using Biologic Response Modification with Insulin in Combination with Non-Toxic Low-Dose Chemotherapy. Steven G. Ayre, M.D.
2)Insulin Shows Promise
Oncology News, 1991, 17(4):1,7
3) Ayre SG, Perez Garcia y Bellon D, Perez Garcia Jr D. Neoadjuvant low-dose chemotherapy with insulin in breast carcinomas. Eur J Cancer. 26:1261-2, 1990
4) Ayre SG, Perez Garcia Y Bellon D, Perez Garcia Jr D. Insulin potentiation therapy: a new concept in the management of chronic degenerative disease. Medical Hypotheses 20:199-210, 1986
5) Lippman ME, Dickson RB, Kasid A, et al. Autocrine and paracrine growth regulation of human breast cancer. J Steroid Biochem 24:147-154, 1986
4) Hilf R. The actions of insulin as a hormonal factor in breast cancer. In: Pike MC, Siiteri PK, Welsch CW, eds. Hormones and Breast Cancer, Cold Spring Harbor Laboratory, 1981, 317-337.
6) Cullen JK, Yee D, Sly WS, et al. Insulin-like growth factor receptor expression and function in human breast cancer. Cancer Res 50:48-53, 1990
6) Holdaway IM, Freisen HG. Hormone binding by human mammary carcinoma. Cancer Res 37:1946-1952, 1977
7) Papa V, Pezzino V, Constantino A, et al. Elevated insulin receptor content in human breast cancer. J Clin Invest 86:1503-1510, 1990
8) Sporn MB, Todaro GJ. Autocrine secretion and malignant transformation of cells. N Engl J Med 308:487-490, 1980
9) Jaques G, Rotsch M, Wegmann C, et al. Production of immunoreactive insulin-like growth factor 1 and response to exogenous IGF-1 in small cell lung cancer cell lines. Exp Cell Res 176:336-343, 1988
10) Nakanishi Y, Mulshine JL, Kasprzyk PG, et al. Insulin-like growth factor-1 can mediate autocrine proliferation of human small cell lung cancer cell lines in vitro. J Clin Invest 82:354-359, 1988
11) Lee PDK, Rosenfeld RG, Hintz RL, Smith SD. Characterization of insulin, insulin-like growth factors I and II, and growth hormone receptors on human leukemic lymphoblasts. J Clin Endocr Metab 62:28-35, 1986
12) Colman PG, Harrison LC. Structure of insulin/insulin-like growth factor-1 receptors on the insulinoma cell, RIN-m5F. Biochem Biophys Res Commun 124:657-662, 1984
13) Zapf J, Froesch ER. Insulin-like growth factors/somatomedins: structure, secretion, biological actions and physiological role. Hormone Res 24:121-130, 1986
14) Papa V, Constance CR, Brunetti A, et al. Progestins increase insulin receptor content and insulin stimulation of growth in human breast carcinomas. Cancer Res 50:7857-7862, 1990
15) Stewart AJ, Johnson MD, May REB, Westley RB. Role of insulin-like growth factors and the type I insulin-like growth factor receptor in the estrogen-stimulated proliferation of human breast cancer cells. J Biol Chem 265:21172-21178, 1990
16) Eppenberger U. New aspects in the molecular growth regulation of mammary tumors. In: Eppenberger U, Goldhirsch A, eds. Recent Results in Cancer Research, Vol. 113: Endocrine Therapy and Growth Regulation of Breast Cancer. Berlin-Heidelberg, 1989, 1-3
17) DeLeon DD, Bakker B, WIlson RL, et al. Demonstration of insulin-like growth factor (IGF-I and IGF-II) receptors and binding protein in human breast cancer cell lines. Biochem Biophys Res Commun 152:398-405, 1988
18) Karey KP, Sirbasku DA. Differential responsiveness of human breast cancer cell lines MCF-7 and T47D to growth factors and 17B-estradiol. Cancer Res 48:4083-4092, 1988
19) King GL, Kahn CR, Rechler MM, Nissley SP. Direct demonstration for separate receptors for growth and metabolic activities of insulin and multiplication-stimulating activity (an insulin-like growth factor) using antibodies to the insulin receptor. J Clin Invest 66:130-140, 1980
20) Jacobs S, Cook S, Svoboda M, Van Wyk JJ. Interaction of the monoclonal antibodies alpha-IR-1 and alpha-IR3 with insulin and somatomedin-C receptors. Endocrinol 118:223-226, 1986
21) Goustin AS, Leof EB, Shipley GD, Moses HL. Growth factors and cancer. Cancer Res 46:1015-1029, 1986
22) Unterburger P, Sinop A, Noder w, et al. Diabetes mellitus and breast cancer: a retrospective follow-up study. Onkologie 13:17-20, 1990
23) Yee D, Palk S, Lebovic GS, et al. Analysis of insulin-like growth-factor I gene expression: evidence for a paracrine role in human breast cancer. Mol Endocrinol 3:509-517, 1990
24) Hilf R. Primary and permissive actions of insulin in breast cancer. In: Leung BS, ed. Hormonal regulation of mammary tumors. Montreal, Eden Press, 1982, Vol. 2, 123-137
25) Alabaster O, Vonderhaar BK, Shafie SM. Metabolic modification by insulin enhances methotrexate cytotoxicity in MCF-7 human breast cancer cells. Eur J Cancer Clin Oncol 17:1223-1228, 1981
26) Oster JB, Creasey WA. Enhancement of cellular uptake of ellipticine by insulin preincubation. Eur J Cancer Clin Oncol 17:1097-1103, 1981
27) Schilsky RL, Bailey BD, Chabner BA. Characteristics of membrane transport of methotrexate by cultured human breast cancer cells. Biochem Pharmacol 30:1537-1542, 1981
28) Shinitzky M, Henkart P. Fluidity of cell membranes – current concepts and trends. Int Rev Cytol 60:121-147, 1971
29) Jeffcoat R. The biosynthesis of unsaturated fatty acids and its control in mammalian liver. Essays Biochem 15:1-36, 1979
30) Gasparro FP, Knobler RM, Yemul SS, Bisaccia E, Edelson RL. Receptor mediated photo-cytotoxicity: synthesis of a photoactivatable psoralen derivative conjugated to insulin. Biochem Biophys Res Comm 141:502-209, 1986
31) Poznansky MJ, Singh R, Singh B. Insulin: carrier potential for enzyme and drug therapy. Science 223:1304-1306, 1984
32) Ayre SG. New approaches to the delivery of drugs to the brain. Med Hypotheses 29:283-291, 1989
33) Gross GE, Boldt DH, Osborne CK. Perturbation by insulin of human breast cancer cell kinetics. Cancer Res 44:3570-3575, 1984
34) Paridaens R, Klijn JGM, Julien JP, et al. Chemotherapy with estrogenic recruitment in breast cancer: experimental background and clinical studies conducted by the EORTC breast cancer cooperative group. Eur J Cancer Clin Oncol 22:728, 1986
35) Van der Burg B, de Laat SW, van Zoelen EJJ. Mitogenic stimulation of human breast cancer cells in a growth-factor defined medium: synergistic action of insulin and estrogens. In: Brescani F, King RGB, Lippman ME, Raynaud JP, eds. Progress in Cancer Research and Therapy, vol. 35: Hormones and Cancer 3. New York, Raven Press, Ltd. 1988, 231-233.
36) Goldfine ID, Purello F, Vigneri R, and Clawson GA. Direct regulation of nuclear functions by insulin: relationship to mRNA metabolism. In: Czech MP, ed. Molecular Basic of Insulin Action. New York, Plenum Press, 1985, 329-345.
37)Blood Brain Barrier Passage of Azidothyumidine in Rats: Effects of Insulin
Steven G. Ayre (1), Brian Skaletski (2) and Aron D. Mosnaim( 2).
Research Communications in Chemical Pathology and Pharmacology JANUARY 1989 VOL.63, NO. 1. Departments of Family Medicine and Pharmacology and Molecular Biology , University of Health Sciences/The Chicago Medical School, North Chicago, IL 60064.
38)New Approaches to Delivery of Drugs to the Brain. S.G. Ayre. Medical Hypotheses 29:283-291, 1989
39)Insulin, chemotherapy, and the mechanisms of malignancy: the design and the demise of cancer. S.G. Ayre, M.D., D. P. Garcia Bellon, M.D., D. P. Garcia, Jr., M.D. Medical hypotheses 55.4 (2000): 330-334.
40)Low dose chemotherapy in combination with insulin for the treatment of metastatic tumors: C. Damyanov, M. Radoslavova, V. Gavrilov, D. Stoeva. Medical Center of Integrative Medicine, Sofia, Bulgaria. Journal of BUON 14: 711-15, 2009.
41)Insulin Potentiation Therapy in the treatment of malignant neoplastic diseases: a three year study. Damyanov C, Gherasimova DM, Avramov LA, Masley IK (2012). J Cancer Sci Ther 4: 088-091. doi:10.4172/1948-5956.1000117
42)Low-Dose Chemotherapy with insulin (Insulin Potentiation Therapy) in combination with hormone therapy for treatment of castration-resistant prostate cancer. Damyanov, Christo, et al. ISRN urology 2012 (2012).
43)Metabolic Modification by Insulin Enhances Methotrexate Cytotoxicity in MCF-7 Human Breast Cells. Alabaster, O. Vonderhaar, B. and Shafie, S. Eur J Cancer Clin Oncol. Vol 17, No. 11, pp 1223-1228. 1961.
44)Insulin treatment in cancer cachexia: effects on survival, metabolism, and physical functioning. Lundholm K, Körner U, Gunnebo L, Sixt-Ammilon P, Fouladiun M, Daneryd P, Bosaeus I. Clin Cancer Res. 2007 May 1;13(9):2699 706.
45)Long-Term Effect of Diabetes and Its Treatment on Cognitive Function. Jacobson, Alan, et.al. N Engl J Med 2007; 356:1842-52.
46)Preclinical safety and antitumor efficacy of insulin combined with irradiation. Bénédicte F. Jordan, Nelson Beghein, Nathalie Crokart, Christine Baudelet, Vincent Gregoire, Bernard Gallez. Radiotherapy and Oncology 81 (2006) 112–117.
47)Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients. Lasalvio-Prisco, Eduardo, et.al. Cancer Chemother Pharmacol (2004) 53: 220–224.
48)The effect of insulin on chemotherapeutic drug sensitivity in human esophageal and lung cancer cells. Zhonghua Yi Xue Za Zhi. 2003 Feb 10;83(3):195-7.
49)Pretreatment with insulin enhances anticancer functions of 5-fluorouracil in human esophageal and colonic cancer cells. Zou K, Ju JH, Xie H. Acta Pharmacol Sin. 2007 May; 28(5):721-30.
50)A pilot study of Auron Misheil Therapy (AMT) in patients with advanced cervical cancer: tumor response and its correlation with clinical benefit response, and preliminary quality of life data.” Scheele, Jürgen, et al. Oncology reports 22.4 (2009): 877-883.
51)Insulin in endometrial carcinoma chemotherapy: A beneficial addition and not a problem. Sha, Huilan, et al. Journal of Huazhong University of Science and Technology [Medical Sciences] 30 (2010): 631-637.
52) Insulin for Everything. TIME magazine April 10, 1944
53)Long-Term Outcomes of the Treatment of Unresectable (Stage III - IV)Ductal Pancreatic Adenocarcinoma Using Metabolically Supported Chemotherapy (MSCT): A Retrospective Study
Mehmet Salih Iyikesici1, Ayshe Slocum2*, Engin Turkmen3, Ovunc Akdemir4, Abdul Kadir Slocum5, Turgut Ipek6, Erhun Eyuboglu6, Ferhan Bulent Berkarda7.
How to get in touch with Donato Perez Garcia, MD.
Mobil phone: 664-228-3367
Assistant Email: firstname.lastname@example.org
Consultorio #505. Hospital Angeles Tijuana
Phone: +52-1-(664) 616-4878
Phone: +51-(664) 635-1827
Skype Phone USA: (619) 798-8017
IPT E-Booklet: http://issuu.com/iptldmd/docs/ipt_ebooklet/1
YouTube: Patient Testimonials and Educational videos about IPT/IPTLD
Blogs: “IPTLD for Cancer and Chronic Degenerative Diseases Treatment by Donato Perez Garcia, M.D.”
Donato Perez Garcia, MD.