Studies and bibliographical references
Medicine is an empirical science. The overemphasis of the scientific nature of medicine and the downgrading of everything that has happened and happens for thousands of years in medicine without any double-blind studies is a result of the fact that science has become an instrument of marketing. Medical science is not at all unbiased - i.e. without monetary aspects.
Medicine is an empirical medicine: the technical development in all aspects of our life cannot deny this. Science should not obscure, although this may happen, as medicine is reigned by fear and hope. Also physicians are subject to self-deception, unless they do not analyse what they do self-critically. They should be aware of the anachronism they live with: after all, there is no clear explanation for life according to natural-scientific criteria. The high order which requires life is diametrically opposed to the principles of entropy. If they cannot accept this self-critical attitude for whatever reasons - either for reasons of narcissism or insecurity with which they are confronted every day in their job -, they adapt their behaviour to the majority which hardly accepts protest.
The following statements and some statements on other sites of this website are supported by studies. Please consider the study about patients with advanced breast cancer at the university hospital Montevideo, as it is the only one that meets the scientific requirements of medical science nearly completely.
Bibliographical references of scientific nature on the IPT are the following:
"The metabolic modification provoked by insulin enhances the cytotoxicity of methotrexate in the human MCF-7 breast-cancer cells up to the factor 10,000"
Metabolic Modification by Insulin Enhances Methotrexate Cytotoxicity in MCF-7 Human Breast Cancer Cells - Alabaster O, Vonderhaar BK, Shafie SM. Eur J Cancer Clin Oncol 17:1223-1228, 1981 Georg Washington Universität (1981) (read whole study here (alabaster)
The human breast-cancer cells have six times more insulin receptors (1) and ten times more IGF-I receptors (2) than the normal tissue in the body. (IGF = Insulin-Growth-Factor) Hormone binding by human mammary carcinoma Holdaway IM, Freisen HG.Cancer Res 37:1946-1952, 1977und IGF-I receptor expression and function in HBCC Cullen JK et al.Cancer Res 50:48-53, 1990
"A reversible metabolic promoter (mediator, catalyst), i.e. insulin, enhances the ability to destroy of chemotherapeutic medicine. It is possible to promote the growth and metabolism of cancer cells and increase the sensitivity of the chemotherapy, while administering the chemotherapeutic medicine and improving its therapeutic effect."
Zhonghua Yi Xue Za Zhi. 2003 Feb 10;83(3):195-7. Article in Chinese, PMID: 12812659 Abstract from PubMed
(Read more).
The following authors present the secretion of insulin and IGF-1, and the production of specific receptors for insulin in human breast-cancer cells:
Hormone binding by human mammary carcinoma - Holdaway I.M., Freisen H.G.. Cancer Res 37:1946-1952, 1977
Insulin-like growth factor receptor expression and function in human breast cancer - Cullen J.K., Yee D., Sly W.S., et al. . Cancer Res 50:48-53, 1990 Elevated insulin receptor content in human breast cancer - Papa V., Pezzino V., Costantino A., et al. J Clin Invest 86:1503-1510, 1990
Supraphysiological concentrations of insulin can replace the need for IGF-1 in a defined medium by a cross reaction with an IGF-1 receptor. Growth factors and cancer. - Goustin et al. Cancer Res 46:1015-1029, 1986. "INS, IGF-I, EGF, TGF-alpha & TGF-beta are autocrine growth factors in human breast-cancer cells. The unreasonable and late distribution of autocrine growth factors which are usually needed by cells during the normal embryogenesis is responsible for the malignant transformation. Due to this autonomous self-stimulation, the cells overcome the blockade of the normal cell cycle and become cancer cells." Autocrine secretion and malignant transformation of cells - Sporn MB, Todaro GJ. NEJM, 308:487-490, 1980
The combination of insulin and IGF-1 acts autonomously at the cellular level within tumours, independent from any control. They work together in an autocrine and/or a paracrine and complementary way, whereas the IGF-I is a more important anabolic hormone, as it is responsible for the transmission of information regarding tumour growth, and the insulin provides and regulates the energy for these processes. (translated) Insulin-like growth factors/somatomedins: structure, secretion, biological actions and physiological role - Zapf J., Froesch E.R. . Hormone Res 24:121-130, 1986. After the introduction of insulin into the asynchronous population of breast-cancer cells, the S-phase division in vitro was 66 %, compared with 37% during control.
Perturbation by insulin of human breast cancer cell kinetics - Gross GE, Boldt DH, Osborne CK . Cancer Res 44:3570-3575, 1984
The university hospital in Montevideo carried out a scientific study with patients with advanced breast cancer (translated):
"In case of breast cancer with metastases resistent to medicine (multi drug resistent), methotrexate plus insulin provoked a strong anti-tumour reaction, which could not be observed with methotrexate or insulin alone."
"For this reason, our results support the hypothesis that insulin can potentiate the anti-cancer effect of methotrexate (2). And they support "in vivo" the previously-mentioned "in vitro" results (10). "Our results confirm that insulin potentiates methotrexate, while insulin alone did not lead to tumour growth (group 3). This effect matches previous results of in-vitro models: the enhancement of cytotoxic substances caused by insulin, was not a direct consequence of the insulin-related rise of the growth rate of tumour cells." Cancer Chemotherapy and Pharmacology, ©Springer-Verlag 2003 10.1007/s00280-003-0716-7 - [online publication on 4 December 2003; original article]
Insulin-induced Enhancement of Antitumoral Response to Methotrexate in Breast Cancer Patients Eduardo Lasalvia-Prisco 1,2,3,5, Silvia Cucchi 2,4, Jesus Vazquez 2,3, Eduardo Lasalvia-Galante 2,3, Wilson Golomar 2,3, and William Gordon 4 Lasalvia-Prisco E,Cucchi S, Vazquez J, Lasalvia-Galante E, Golomar W, Gordon W.:
Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients. Cancer Chemotherapy and Pharmacology. - © Springer-Verlag 2003 10.1001/s00280-0030716-7. (Published online December 4,2003) (Read whole study here).
