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Insulin Potentiation Therapy

How It Works

Bottom Line: Insulin Potentiation Therapy is a questionable cancer therapy that is not effective in treating cancer.

Insulin potentiation therapy involves administering insulin at the same time as chemotherapy drugs, with the idea that lower doses of chemo are needed because insulin lets more of the drugs enter cells. However, this has never actually been proven experimentally. If it is true, then it is also possible that insulin will increase the toxic effects of chemotherapy drugs on human cells such as bone marrow and the lining of the intestine, which is not a desirable effect. 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. There is no proof from clinical trials that insulin potentiation therapy works.

Purported Uses

  • To treat cancer
    There is no proof from clinical trials that insulin potentiation therapy is safe or effective in treating cancer.

  • Research Evidence

    No clinical trials have tested the safety or effectiveness of insulin potentiation therapy.

    Warnings

  • This therapy may cause the excessive lowering of blood sugar.
  • The drugs used in insulin potentiation therapy are all approved by the F.D.A., but for other uses.
  • Clinics where insulin potentiation therapy is given may not be staffed with trained oncologists.

  • Side Effects

  • Low blood sugar

  • Common Name

    IPT

    Clinical Summary

    Insulin Potentiation Therapy (IPT) is a questionable cancer therapy that uses insulin as an adjunct agent to potentiate the effect of chemotherapy and other medications. This therapy was developed in Mexico by Dr. Donato Perez Garcia in the 1930's 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 therefore cancer cells are 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 behind the therapy, if cancer cells can be activated by exogenous insulin, a reduced dose (up to one-tenth the normal dose) of a chemo drug can provide the same cytotoxic effects with less severe adverse reactions. No clinical trials have been performed to validate these claims. In addition, the pharmacokinetic profiles on concurrent use of insulin and chemo drugs are lacking and it is unclear whether the insulin also potentiates the toxic effects of chemotherapy on healthy cells. Although proponents have cited many anecdotal case reports suggest that IPT may be effective, currently there is no data comparing the efficacy of IPT to conventional chemotherapy. Most of the medications used, such as insulin and other chemo drugs, are approved by the FDA, but the IPT clinics administer them 'off-label.' 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). IPT remains an unproven cancer therapy until there are more studies available to validate its benefit.

    Purported uses

    • Cancer treatment

    Constituents

    Insulin, chemotherapy agents.

    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 the proliferation, adhesion and migration of normal as well as cancerous cells (2). 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 increase in intracellular concentration and cytotoxic effect of anticancer drugs. Proponents argue that insulin synergistically enhances the efficacy of anticancer drug so that a reduced dose can be used with similar cytotoxic effects (5) (6). The mechanism of IGF receptor's role in cancer treatment appears to be more complex. At least one study has demonstrated the inhibition of IGF receptors can also increase the effects of anticancer drugs (3).

    Pharmacokinetics

    Insulin is believed to increase the permeability of cell membrane, leading to the increase in intracellular concentration and cytotoxicity of anticancer drugs (1).

    Warnings

    May cause hypoglycemic reactions.

    Adverse Reactions

  • Hypoglycemia

  • Herb-Drug Interactions

    Hypoglycemic agents.

    References

    1. Ayre SG, et al. Insulin, chemotherapy, and the mechanisms of malignancy: the design and the demise of cancer. Med Hypotheses. 2000 Oct;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's 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.

    Last Updated: Dec. 19, 2007
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