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{{Expert-subject|Medicine|date=November 2008}}
{{Expert-subject|Medicine|date=November 2008}}


'''Insulin potentiation therapy (IPT)''' is an [[alternative cancer treatment]] using [[insulin]] to administer [[low-dose chemotherapy]].<ref name="pmid3526099">{{cite journal |author=Ayre SG, Perez Garcia y Bellon D, Perez Garcia D |title=Insulin potentiation therapy: a new concept in the management of chronic degenerative disease |journal=Med. Hypotheses |volume=20 |issue=2 |pages=199–210 |year=1986 |pmid=3526099| doi = 10.1016/0306-9877(86)90126-X}}</ref>. It was developed by [[Donato Perez Garcia ,MD]] back in 1930 as a targeted therapy for chronic degenerative diseases and some types of cancer.
'''Insulin potentiation therapy (IPT)''' is an [[alternative cancer treatment]] using [[insulin]] to administer [[low-dose chemotherapy]].<ref name="pmid3526099">{{cite journal |author=Ayre SG, Perez Garcia y Bellon D, Perez Garcia D |title=Insulin potentiation therapy: a new concept in the management of chronic degenerative disease |journal=Med. Hypotheses |volume=20 |issue=2 |pages=199–210 |year=1986 |pmid=3526099| doi = 10.1016/0306-9877(86)90126-X}}</ref>. It was developed by [[Donato Perez Garcia]],MD back in 1930 as a targeted therapy for chronic degenerative diseases and some types of cancer.
The therapeutic approach is said to take advantage of the endogenous molecular biology of cancer cells, specifically the secretion of [[insulin]] and insulin-like growth factor, and the interaction of these biochemicals with their specific receptors. By using insulin in conjunction with chemotherapy drugs, significantly less drugs (about 10-15 % of a standard dose) can be targeted more specifically and more effectively to cancer cell populations, thus virtually eliminating dose-related side-effects while claiming enhancing antineoplastic effects.
The therapeutic approach is said to take advantage of the endogenous molecular biology of cancer cells, specifically the secretion of [[insulin]] and insulin-like growth factor, and the interaction of these biochemicals with their specific receptors. By using insulin in conjunction with chemotherapy drugs, significantly less drugs (about 10-15 % of a standard dose) can be targeted more specifically and more effectively to cancer cell populations, thus virtually eliminating dose-related side-effects while claiming enhancing antineoplastic effects.


Revision as of 01:24, 23 July 2012

Insulin potentiation therapy (IPT) is an alternative cancer treatment using insulin to administer low-dose chemotherapy.[1]. It was developed by Donato Perez Garcia,MD back in 1930 as a targeted therapy for chronic degenerative diseases and some types of cancer. The therapeutic approach is said to take advantage of the endogenous molecular biology of cancer cells, specifically the secretion of insulin and insulin-like growth factor, and the interaction of these biochemicals with their specific receptors. By using insulin in conjunction with chemotherapy drugs, significantly less drugs (about 10-15 % of a standard dose) can be targeted more specifically and more effectively to cancer cell populations, thus virtually eliminating dose-related side-effects while claiming enhancing antineoplastic effects.

Claimed explanatory molecular biology

The proponents of IPT give the following explanation of the biology of cancer and its cells in order to understand the mechanisms of IPT, which relies upon insulin, the most integral component of IPT, having three significant actions upon cancer cells described below, as well as also dropping blood sugar levels and thus the energy source for cancer. Low blood glucose (below 60 mg/dl) also stimulates secretion of growth hormone, and growth hormone, it is presumed, helps to strengthen the immune system.

Differentiation between cancer and normal cells

Insulin biologically differentiates cancer cells from normal cells based on insulin receptor concentration. The body’s own hormone insulin is produced in the pancreas and is responsible for transporting nutrients from the blood into the cells. Insulin docks onto the cell and opens it so that these nutrients can enter. Insulin can serve to distinguish and differentiate cancer cells from healthy cells in several ways. Insulin is produced in the pancreas, one of whose many functions is the regulation of blood glucose levels. Insulin activates a glucose transport protein within all cells – whether they be cancerous or healthy - which allows glucose, the energy source, to enter, thus lowering the blood glucose level. One of the differences between normal cells and cancer cells is that the cancer cells have considerably more insulin receptors, i.e. docking points for insulin, than normal cells.[2]

The growth of cancer is abnormally rapid, its sole purpose being to spread, therefore it has a voracious appetite compared to normal cells. When food is introduced into the organism, this goes as a matter of priority to the cancer cells, which gobble it up greedily. Thus they eat up more and more of the food for the organism, which leads to the patient becoming weaker and weaker and more feeble.[3]

Cancer cells have developed the ability to produce insulin and insulin-like growth factor (IGF) themselves; this way they can autonomously increase their glucose uptake.[4][5][6][7][8][9][10][11][12][13]

Being able to produce its own insulin makes cancer different from normal cells, but there is a second abnormality that insulin highlights. Every cell in the body has insulin receptors on the outer surface of its membrane, from 100-100,000 receptors per cell. But cancer cells have a much higher concentration of receptors. Breast cancer cells, for example, have six times more insulin receptors and ten times more IGF receptors per cell than normal cells. As an added boost, insulin is able to react with its own receptors and is also able to cross-react with and activate the IGF receptors on cancer cells. This means that insulin will affect cancer cells sixteen times as strongly as it affects normal tissues.[14][15][16][17][18][19][20][21][22][23][24][25] Something else to take into consideration is that ligand effect is a function of receptor concentration. In a particular tissue, the more receptors there are for a certain ligand – such as insulin – the greater the effect of that ligand on that tissue.

By activating the insulin and IGF receptors on cancer cells through the administration of insulin during an IPT treatment, the biological differences of cancer cells - higher reception of insulin, voracious appetite compared to normal cells - make them more receptive to chemotherapy and infusion therapies applied during biological cancer therapies (see mandelonitrile(B17).

Modification of cancer cell metabolism

Not only does insulin provide cancer cells with the means to grow it has also been proven that IGFs are the most potent mitogen - promoter of cell division - for cancer growth.[citation needed]

The favorable effect in a treatment that is trying to kill cancer is in the killing mechanism of chemotherapy medications. The standard pharmacologic treatment for cancer involves drugs, which are designed to attack cells that are dividing, cell division being the means by which tissue "grows." Cancer cells are rapidly dividing cells, and are constantly going through cell division. There are several phases to cell division, the one called the S-Phase being when cells replicate DNA. There are some chemotherapy agents that are S-Phase-dependent: They attack cells that are in the S-phase of cell division, not cells in the resting phase.

However, hair cells, red and white blood cells, and cells found in the digestive tract also fall into this category of rapidly dividing cells - the reason why the side-effects related to standard chemotherapy are associated with these areas. In order to get a tumoral response in conventional chemotherapy, a high dose of drugs has to be used, causing healthy cells to be affected, as well. The chemotherapy drugs by themselves cannot differentiate between rapidly dividing cancer cells and rapidly dividing healthy cells. By implementing insulin in conjunction with chemotherapy drugs, the cancer cells are highlighted as being different based on receptor concentration and are promoted to grow, which makes it likely that more of them will be in the S-phase cycle. These effects allow for the powerful chemo agents to target the cancer cells more specifically, sparing healthy cells and, therefore, chemo-related side-effects.

Increase in cell membrane permeability

The third effect that insulin has on cancer cells is to activate enzyme activity in the cell membrane, making them more permeable.[citation needed]

Cell membranes are largely made up of triglycerides, which are built of fatty acids. The more saturated a fatty acid is the higher the melting point (example: butter [a saturated fat with a higher melting point] is solid at room temperature, whereas olive oil [an unsaturated fat with a lower melting point] is a liquid). The enzyme that insulin activates is called delta-9 desaturase, and the action of this enzyme is to de-saturate - to make a saturated fat into an unsaturated fat. Delta-9 desaturase - once it has been activated by insulin - de-saturates the fatty acids that make up the cell membrane of cancer cells.[citation needed] This fatty acid – saturated stearic acid – has a melting point of 65 °C. Stearic acid, once it has been de-saturated, becomes mono-unsaturated oleic acid, which has a melting point of 5 °C. At physiologic temperatures (the temperature of the body, about 37.5 °C), tristearin – triglyceride with three stearic acids attached that composes the cancer cell membrane - is going to be more "waxy" than "oily" because of its higher melting point. This makes for a less permeable cell membrane. On the other hand, once the insulin has activated the enzyme delta-9 desaturase, the cell membrane of cancer cells is composed of triolein – the triglyceride with three oleic acids attached – with a melting point of 5 °C. This cell membrane will be more permeable at physiologic temperatures. The chemotherapy drugs are, thus, able to enter the cancer cells more easily because of the increased cell membrane permeability, providing the required intracellular dose intensity to kill the cancer.

Insulin is used in IPT to enhance anticancer drug cytoxicity and safety, via 1) an effect of biological differentiation based on insulin receptor concentration, 2) an effect of metabolic modification to increase the S-phase fraction in cancer cells, enhancing their susceptibility to cell-cycle phase-specific agents, and 3) a membrane permeability effect to increase the intracellular dose intensity of the drugs. Significantly less drug can, thus, be targeted more specifically and more effectively to cancer cells, all this occurring with a virtual elimination of the dose-related side-effects.[26][27]

Supportive research

In-vitro studies [28][29] have shown how IPT works supporting the informal clinical work that has been conducted on hundreds of patients worldwide.[citation needed]

A clinical trial of IPT for treating breast cancer was done in Uruguay and concluded that "The group treated with insulin + methotrexate responded most frequently with stable disease" compared to being treated with methotrexate alone or insulin alone.[30]

In 2000, the National Cancer Institute's Cancer Advisory Panel on Complementary and Alternative Medicine (CAPCAM) invited Drs. Perez Garcia and Ayre to present IPT to them as part of the National Cancer Institute's (NCI's) Best Case Series program.[31][32] However CAPCAM have not in the time since undertaken any further research into IPT.[citation needed]

Footnotes

  1. ^ Ayre SG, Perez Garcia y Bellon D, Perez Garcia D (1986). "Insulin potentiation therapy: a new concept in the management of chronic degenerative disease". Med. Hypotheses. 20 (2): 199–210. doi:10.1016/0306-9877(86)90126-X. PMID 3526099.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ Dr med Peter Wolf (2008). Innovations in biological cancer therapy, a guide for patientes and their relatives. Hannover: Naturasanitas. pp. 42–43. ISBN 978-3-9812416-1-7.
  3. ^ Dr med Peter Wolf (2008). Innovations in biological cancer therapy, a guide for patientes and their relatives. Hannover: Naturasanitas. p. 44. ISBN 978-3-9812416-1-7.
  4. ^ Zapf J., Froesch E.R. (1986). "Insulin-like growth factors/somatomedins: structure, secretion, biological actions and physiological role". Hormone Research. 24 (2–3): 121–130. doi:10.1159/000180551. PMID 3530937.
  5. ^ Gross G.E., Boldt D.H., Osborne C.K. (1984). "Pertubation by insulin of human breast cancer cell kinetics". Cancer Research. 44 (8): 3570–3575. PMID 6378371.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Cullen J.K, Yee, Sly W.S; et al. (1990). "Insulin-like growth factor receptor expression and function in human breast cancer". Cancer Research. 50 (1): 48–53. PMID 2152773. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  7. ^ Hilf R. (1981). "The actions of insulin as a hormonal factor in breast cancer. In: Pike M.C., Siiteri P.K., Welsh C.W.,eds. Hormones and Breast Cancer, Cold Spring Harbor Laboratory": 317–337. {{cite journal}}: Cite journal requires |journal= (help)
  8. ^ Goustin A.S., Leof E.B., Shipley G.D., Moses H.L. (1986). "Growth Factors and Cancer". Cancer Research. 46 (3): 1015–1029. PMID 3002607.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Rasmussen A.A., Cullen K.J. (1998). "Paracrine/autocrine regulation of breast cancer by the insulin-like growth factors". Breast Cancer Res Treat. 47 (47(3)): 219–33. doi:10.1023/A:1005903000777.
  10. ^ Holdaway I.M., Freisen H.G. (1977). "Hormone binding by human mammary carcinoma". Cancer Research. 37 (7 Pt 1): 1946–1952. PMID 193630.
  11. ^ Pap V., Pezzino V., Constantino A.; et al. (1990). "Elevated insulin receptor content in human breast cancer". J Clin Invest. 86 (5): 1503–1510. doi:10.1172/JCI114868. PMC 296896. PMID 2243127. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  12. ^ Yee D. (1998). "The insulin-like growth factors and breast cancer - revisited". Breast Cancer Res Treat. 47 (47(3)): 197–199. doi:10.1023/A:1005938615798.
  13. ^ Quinn K.A., Treston A.M., Unsworth E.J.; et al. (1996). "Insulin-like growth factor expression in human cancer cell lines". J Biol Chem. 271 (19): 11477–83. doi:10.1074/jbc.271.19.11477. PMID 8626706. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  14. ^ Pavelik L., Pavelik K., Vuk-Pavlovic S. (1984). "Human mammary and bronchial carcinomas: in vivo and in vitro secretion of substances immunologically cross-reactive with insulin". Cancer. 53 (11): 2467–2471. doi:10.1002/1097-0142(19840601)53:11<2467::AID-CNCR2820531117>3.0.CO;2-#. PMID 6370415.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Shames J.M., Dhurandhar N.R., Blackard W.G. (1968). "Insulin-secreting bronchial carcinoid tumor with widespread metastases". American Journal of Medicine. 44 (4): 632–637. doi:10.1016/0002-9343(68)90065-X. PMID 4296076.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Jaques G., Rotsch M, Wegmann C.; et al. (1988). "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 (2): 336–343. doi:10.1016/0014-4827(88)90335-7. PMID 2837402. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  17. ^ Nakanishi Y., Mulshine J.L., Kaspryzk P.G.; et al. (1988). "Insulin-like growth factor-1 can mediate autocrine proliferation of human small cell cancer cell lines in vitro". J Clin Invest. 82 (1): 354–359. doi:10.1172/JCI113594. PMC 303516. PMID 2839551. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  18. ^ Wong M., Holdaway I.M. (1985). "Insulin binding by normal and neoplastic colon tissue". Int J Cancer. 35 (3): 335–341. doi:10.1002/ijc.2910350309. PMID 3882582.
  19. ^ Kiang D.T., Bauer G.E., Kennedy B.J. (1973). "Immunoassayable insulin in carcinoma of the cervix associated with hypoglycemia". Cancer. 31 (4): 801–804. doi:10.1002/1097-0142(197304)31:4<801::AID-CNCR2820310407>3.0.CO;2-J. PMID 4706048.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  20. ^ Pavelik K., Bolanca M., Vecek N.; et al. (1992). "Carcinomas of the cervix and corpus uteri in humans:stage- dependent blood levels of substance(s) immunologically cross-reactive with insulin". J Nat Cancer Inst. 68 (6): 891–894. PMID 7045486. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  21. ^ Pavelic K., Popovic M. (1981). "Insulin and glucagon secretion by renal adenocarcinoma". Cancer. 48 (1): 98–100. doi:10.1002/1097-0142(19810701)48:1<98::AID-CNCR2820480119>3.0.CO;2-A. PMID 7016301.
  22. ^ Oleesky S., Bailey I., Samos S., Bilkus D. (1962). "A fibrosarcoma with hypoglycemia and a high serum insulin level". Lancet. 280 (2): 378–380. doi:10.1016/S0140-6736(62)90231-3. PMID 14481722.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ Pavelic K., Odavic M., Pekic B. (1982). "Correlation of substance(s) immunologically cross-reactive with insulin, glucose and growth hormone in Hodgkin's lymphoma patients". Cancer Letter. 17 (17): 81–86. doi:10.1016/0304-3835(82)90112-4.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Colman P.G., Harrison L.C. (1984). "Structure of insulin/insulin-like growth factor-1 receptors on the insulinoma cell, RIM-m5F". Biochem. Biophys. Res. Commun. 124 (2): 657–662. doi:10.1016/0006-291X(84)91605-X. PMID 6093809.
  25. ^ Lee P.D.K., Rosenfeld R.G., Hintz R.L., Smith S.D. (1986). "Characterization of insulin, insulin-like growth factors I and II, and growth hormone receptors on human leukemic lymphoblasts". L Clin Endocr Metab. 62 (1): 28–35. doi:10.1210/jcem-62-1-28. PMID 2999181.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ^ Alabaster O., Vonderharr B.K., Shafie S.M. (1981). "Metabolic modification by insulin enhances methotrexate cytoxicity in MCF-7 human breast cancer cells". Eur J Cancer Clin Oncol. 17 (11): 1223–1228. doi:10.1016/S0277-5379(81)80027-2. PMID 7037424.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ Oster J.B., Creasey W.A. (1981). "Enhancement of cellular uptake of ellipticine by insulin preincuabation". Eur J Cancer Clin. 17 (17): 1097–1103. doi:10.1016/0014-2964(81)90294-2.
  28. ^ Hug V, Johnston D, Finders M, Hortobagyi G. (1986). "Use of growth-stimulatory hormones to improve the in vitro therapeutic index of doxorubicin for human breast tumors" (PDF). Cancer Res. 46 (1): 147–52. PMID 3509991.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  29. ^ Alabaster O, Vonderhaar B, Shafie S (1981). "Metabolic modification by insulin enhances methotrexate cytotoxicity in MCF-7 human breast cancer cells". Eur J Cancer Clin Oncol. 17 (11): 1223–8. doi:10.1016/S0277-5379(81)80027-2. PMID 7037424.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  30. ^ Lasalvia-Prisco E, Cucchi S, Vázquez J, Lasalvia-Galante E, Golomar W, Gordon W (2004). "Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients". Cancer Chemother Pharmacol. 53 (3): 220–4. doi:10.1007/s00280-003-0716-7. PMID 14655024. The group treated with insulin + methotrexate responded most frequently with stable disease{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ "Minutes of the Third Meeting". Cancer Advisory Panel for Complementary and Alternative Medicine (CAPCAM). September 18, 2000 [dead link]. Archived from the original on October 29, 2007. Retrieved 2008-01-28. {{cite web}}: Check date values in: |date= (help)
  32. ^ "NCI CAM News - OCCAM to Reissue Program Announcement but Adds New Priorities". NCI Office of Complementary and Alternative Medicine. Spring 2009. Retrieved 2010-06-28. These collaborations are particularly relevant to CAM practices that have been identified through the NCI Best Case Series Program and warrant NCI-initiated research but have not ascertained enough data for a larger project. Examples of such therapeutic regimens include ... insulin potentiation therapy...
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