Insulin Potentiation Therapy

• How It Works

  Insulin Potentiation Therapy has not been shown to treat or prevent cancer.

  Insulin potentiation therapy involves administering insulin at the same time as chemotherapy drugs, with the idea that lower chemotherapy doses are then needed because insulin lets more of the drug enter cells. However, this has not been proven experimentally.

  In general, insulin should not been taken by non-diabetics because it can decrease blood sugar to dangerously low levels, causing symptoms such as headache and delirium.

• Purported Uses
  • To treat cancer
    Evidence is lacking to support this claim.
• Do Not Take If
  • You are taking hypoglycemic agents: IPT can have additive effects.
• Side Effects
  • Low blood sugar
• Clinical Summary

  Insulin Potentiation Therapy (IPT) is an alternative cancer therapy that uses insulin to potentiate the effects of chemotherapy and other medications. This therapy was developed in Mexico by Dr. Donato Perez Garcia in the 1930s and has been used together with other unconventional therapies for many years ⁽¹⁾. Advocates of IPT believe that cancer cells consume more sugar than healthy cells and are therefore more sensitive to insulin and insulin-like growth factor (IGF) ^(2) (7). Insulin is also believed to increase the permeability of cell membranes, increasing the intracellular concentration and cytotoxic effect of anticancer drugs ⁽¹⁾. According to the theory underlying this therapy, if cancer cells can be activated by exogenous insulin, a reduced dose (up to one-tenth the normal dose) of a chemotherapy drug can provide the same cytotoxic effects with less severe adverse reactions. The pharmacokinetic profiles on concurrent use of insulin and chemotherapy drugs are lacking and it is unclear whether insulin also potentiates toxic effects of chemotherapy on healthy cells. Exploratory studies suggest some benefit with a combination of chemotherapy and IPT ^(9) (10), but well-designed clinical trials have not been conducted.

  Many of the medications used in IPT, such as insulin and other chemotherapy drugs, are FDA-approved but IPT clinics administer them “off-label.” Furthermore, some clinics that administer IPT are not operated or staffed by oncologists. Side effects of IPT include hypoglycemic reaction. A systematic review of 21 studies showed a correlation between circulating levels of IGF-I, IGFBP3 (IGF-binding protein) and an increased risk of common cancers ⁽⁸⁾.

• Purported Uses
  • Cancer treatment
• Mechanism of Action

  IPT is a treatment strategy that utilizes the physiological activities of insulin. It is based on the theory that insulin and insulin-like growth factor (IGF) play an important role in the cell cycle. IGF has been shown to affect proliferation, adhesion, and migration of normal as well as cancerous cells ⁽²⁾ and certain IGF receptors are found to be overexpressed in many forms of cancer. Therefore, cancer cells may be selectively more sensitive than normal cells to IGF ^(1) (7).

  IGF receptors can be activated by exogenous insulin. Insulin is also believed to increase the permeability of cell membranes, leading to the increased intracellular concentrations and cytotoxic effects of anticancer drugs.

  Proponents argue that insulin synergistically enhances the efficacy of anticancer drugs so that a reduced dose can be used with similar cytotoxic effects ^(5) (6). However, the role of IGF receptors in cancer treatment appears to be more complex. At least one study has demonstrated that IGF receptor inhibition can also increase the effects of anticancer drugs ⁽³⁾.

• Adverse Reactions
  • Hypoglycemia
• Herb-Drug Interactions
  • Hypoglycemic agents: IPT may potentiate their effects.
• References

  1. Ayre SG, et al. Insulin, chemotherapy, and the mechanisms of malignancy: the design and the demise of cancer. Med Hypotheses. 2000;55(4):330-4.

  2. Leroith D, Roberts C. The insulin-like growth factor system and cancer. Cancer Lett. 2003;195(2):127-37.

  3. Benini S, et al. Inhibition of insulin-like growth factor I receptor increases the antitumor activity of doxorubicin and vincristine against Ewing sarcoma cells. Clin Cancer Res. 2001;7(6):1790-7.

  4. Ayre SG, et al. Insulin potentiation therapy: a new concept in the management of chronic degenerative disease. Med Hypotheses. 1986;20(2):199-210.

  5. Ayre SG, et al. Neoadjuvant low-dose chemotherapy with insulin in breast carcinomas. Eur J Cancer. 1990;26(11-12):1262-3.

  6. Albaster O, et al. Metabolic modification by insulin enhances methotrexate cytotoxicity in MCF-7 human breast cancer cells. Eur J Cancer Clin Oncol. 1981;(11):1223-8.

  7. Holdaway IM, Friesen HG. Hormone binding by human mammary carcinoma. Cancer Res. 1977;37(7 Pt 1):1946-52.

  8. Renehan AG, et al. Insulin-like growth factor (IGF)-I, IGF binding protein-3, and cancer risk: systematic review and meta-regression analysis. Lancet. 2004;263:1346-53.

  9. Damyanov C, Gerasimova D, Maslev I, Gavrilov V. Low-dose chemotherapy with insulin (insulin potentiation therapy) in combination with hormone therapy for treatment of castration-resistant prostate cancer. ISRN Urol. 2012;2012:140182.

  10. Lasalvia-Prisco E, Cucchi S, Vázquez J, Lasalvia-Galante E, Golomar W, Gordon W. Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients. Cancer Chemother Pharmacol. 2004 Mar;53(3):220-4.