Insulin potentiation therapy (IPT) is an experimental alternative cancer treatment using insulin as an adjunct to low-dose chemotherapy. IPT is closely related to Insulin Potentiation Targeted Low Dose (IPTLD). However, IPTLD is used specifically to treat cancer with 10-25% of the traditional dose of chemotherapy drugs. IPT is used to treat a variety of other chronic degenerative diseases in addition to cancer.
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History
IPT was invented by Donato Perez Garcia in 1932. It was developed and continued by his son, Donato Perez Garcia Bellon, as well as his grandson, Donator Perez Garcia, Jr.
Originally, Garcia targeted syphilis, and later tried the treatment for chronic degenerative diseases and some types of cancer.
In 1939, the Mexican Secretary General of the Department of Health recommended that insulin shock therapy receive comprehensive scientific investigation as a treatment for neurosyphilis, in response to Donato Perez Garcia's documented success in using IPT to treat patients with neurosyphilis, both Mexico and the U.S.
In 1940, high Mexican officials produced and signed a document certifying the success of Donato Perez Garcia's treatment in an army experimental field clinic established the previous year. The document attests: "That said therapy was 100 percent effective. That its application proved innocuous even in many cases where accepted methods were dangerous. That it was applied without danger to patients of all ages. That it did not require special equipment or locale. That this therapy obtains positive permanent results in an amazingly short time.} That from an economic standpoint there is absolutely no comparison between this therapy and those to this day accepted since its cost is insignificant. That this method proved not only applicable to neurosyphilis but also to many other diseases of a bacterial nature, as was proven in treating members of the family of military personnel at this clinic for different ailments."
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Method
IPT uses insulin to increase the permeability of cell membranes in diseased cells in order to increase the absorbance of therapeutic agents. When used to treat cancer in conjunction with chemotherapy in IPTLD treatments, a dose of insulin is injected into a vein followed by a low dose of chemotherapy drugs when the insulin has been absorbed. The chemotherapy dose is usually 10% to 25% of the traditionally prescribed dose. Then sugar water is injected to stop the hypoglycemia (low blood sugar) caused by the insulin injection.
Efficacy
According to one 1981 study, "Insulin, which activates and modifies metabolic pathways in MCF-1 human breast cancer cells, is shown to increase the cytotoxic effect of methotrexate up to ten thousand-fold in vitro." In 2003, Chinese researchers conducted an experiment in which human esophageal cancer cells and human lung adenocarcinoma cells were treated with combinations of insulin and several chemotherapeutic drugs, concluding, "A reversible metabolic promoter, insulin enhances the cytotoxity of the chemotherapeutic agents. It is possible to increase the growth and metabolism of cancer cells first so as to enhance the chemosensibility, and then administer chemotherapeutic agents, thus improving their therapeutic effects."
Another medical study has shown that in multidrug- resistant metastatic breast cancer, methotrexate administered with insulin produced a significant antitumoral response that was not seen with either methotrexate or insulin used separately. Practitioners using IPT alongside hormone therapy to treat castration- resistant prostate cancer reported that, "In spite of the small number of the treated patients with castration-resistant prostate tumors, the preliminary results are promising and this gives us hope and expectations for future serious multicenter research over the possibilities for routine implementation of IPTLD."
Anecdotal reports from practitioners of IPT suggest that IPT has been implemented successfully as part of an IPTLD program in the treatment of forms of several forms of cancer in multiple patients. A 1989 report published on the use of IPT in conjunction with low dose chemotherapy to treat breast carcinoma in four patients states that, "Significant improvements were seen in the clinical course of each patient through reduction in size or disappearance of the primary, regression of metastases, changes in laboratory and radiologic parameters, and improvements in Karnofsky scores. The regimen was tolerated by all four patients, without dose-related side effects."
IPT has not been proven to work. Long-term outcomes, such as survival, have never been published. Four individual case studies, one small, uncontrolled clinical trial and one small prospective, randomized controlled trial have shown temporary reductions in the size of tumors for some patients.
Adverse effects
The immediate risk is hypoglycemia.
The use of lower than normal doses of chemotherapy can has been alleged to cause drug resistance, which could make future treatment at standard, proven doses ineffective. For some cancers, especially breast and colon cancers, insulin may promote tumor growth.
Mechanism of action
IPT works by increasing the cytotoxicity of chemotherapeutic agents. It has been proposed that insulin potentiates chemotherapeutic drugs in two ways: by increasing the permeability of tumor cancer cell membranes so that they may absorb a greater quantity of cytotoxic drugs, and by modifying the metabolic function of cancer cells so as to render them more sensitive to the cytotoxic effects of the drugs. One hypothesis for the mechanism of insulin's membrane effect is that the hormone activates delta- 9 desaturase enzyme activity in cancer cells, altering cellular lipid synthesis so that saturated stearic acid is transformed to the unsaturated compound oleic acid, which increases cell membrane fluidity, and thus, permeability, at physiological temperatures of 20 degrees Celsius. Other hypotheses for insulin's membrane effect propose that drugs are absorbed onto glucose molecules, with transmembrane transport then occurring via the insulin-activated glucose transport protein, or suggest a similar adsorption of drug molecules onto insulin with the resulting chimeric drug-insulin complex being internalized into the cell by a process of receptor-mediated endocytosis.
With respect to its metabolic effect, the cross- reaction of insulin with insulin growth factor (IGF) receptors, on cancer cell membranes increases the S- phase fraction in tumors, promoting cellular growth and thus increasing the cancer cells' vulnerability to cytotoxic drugs.
Cost
Costs run up to US $2,000 per treatment session. Multiple sessions are normal. Patients often pay the full cost out of pocket, because it is an unproven therapy that is not covered by health insurance.
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