Description
In Insulin Potentiation Therapy (IPT) insulin is used alongside conventional chemotherapy. It is claimed that insulin enhances the effects of chemotherapy, enabling a 75–90% reduction in the usual doses of anticancer drugs and thus reducing the risk of adverse effects.
Efficacy
Only two very small clinical trials have been published in peer-reviewed journals. While these studies reported promising preliminary findings regarding tumour growth, they had significant methodological shortcomings and do not allow any conclusion about the impact on disease progression or survival.
Safety
IPT is associated with risks such as hypoglycaemia and reduced anticancer effects of lower doses of chemotherapeutic drugs, which could lead to drug resistance. Concerns have been raised that IPT might even promote tumour growth.
Description
Insulin Potentiation Therapy (IPT) uses insulin alongside conventional chemotherapy. It is claimed that insulin potentiates the effects of chemotherapy, allowing lower doses to be used (Ayre 1986).
The therapy was developed by the Mexican doctor Donato Pérez García in the 1930s for the treatment of syphilis. He later used IPT to treat other diseases, including arthritis, asthma, colitis and eventually cancer. (Ayre 1986) However, the therapy has remained controversial.
Ingredients
Insulin is a peptide hormone used as a conventional therapy for diabetes. Several medical preparations of insulin are available and sold under different brand names.
Application and dosage
In IPT, insulin is usually given subcutaneously prior to chemotherapy. Chemotherapeutic agents are administered as in standard anticancer therapy, although at lower concentrations (Ayre 2000).
In the only two clinical trials of IPT published in a peer-reviewed journal (Damyanov 2012; Lasalvia 2004) cancer patients were given 0.3 to 0.4 units intravenous insulin per kg body weight followed by chemotherapy at lower doses than usual, starting 20 minutes after insulin administration or sooner if symptoms of hypoglycaemia were observed.
Alleged indications
In conventional care, insulin is used to treat diabetes. In IPT, it is claimed that insulin enhances the effects of chemotherapy, enabling a 75–90% reduction in the standard doses of anticancer drugs and thus reducing the risk of adverse effects. (Ayre 1986).
Mechanism of action
The proposed mechanism of action involves increased uptake of chemotherapeutic agents by cancer cells through insulin and IGF receptor-mediated pathways resulting in increased effects of these chemotherapeutic agents. (Ayre 1086; Ayre 2000; Alabaster 1981; Oster 1981; Zou 2009) However, this mechanism remains theoretical and is not supported by strong clinical evidence.
The postulated underlying processes based on preclinical studies include (Sissung 2019):
- Cell cycle modulation: In vitro and small preclinical studies suggest that insulin pretreatment promotes cancer cells to enter into the S-phase, where cells are more vulnerable to chemotherapeutic agents. (Ayre 2000).
- Enhanced insulin/IGF receptor signalling: Insulin activates glucose transporters and cellular uptake via IR/IGF-R pathways. Changes to cancer cell membranes may improve drug penetration, though the older idea of nonspecific permeability has been disproven (Sissung 2019; MSKCC 2025).
Concerns have been raised based on in vitro studies that insulin and high glucose levels may rather promote tumour proliferation (Kern 1984), angiogenesis (Escudero 2017); and chemoresistance. (Sissung 2019); see also Is it safe.
Legal issues
IPT is not approved by the FDA or EMA for the treatment of cancer or any other condition.
Description of included studies
- Insulin-potentiation therapy (IPT) inventor Perez and his successors claimed that several cancer patients were successfully treated with IPT, (Ayre 1986; Ayre 2000) though case reports or clinical trials to substantiate these claims have not been published in peer-reviewed journals.
- Two small clinical studies have explored the use of IPT in cancer therapy. One uncontrolled study (n=16) in patients with castration-resistant tumours and one RCT (n=30) in women with metastatic breast cancer. The trials are described in table 1.
Limitations
- The evidence is very preliminary and limited by methodological weaknesses.
- Sample sizes are small (n=16, n=30); high dropout rates.
- Lack of (robust) controls.
Results for efficacy
- Disease progression and QoL: Both studies suggest potential benefits of IPT in stabilizing disease and improving QoL with minimal toxicity but results are very preliminary.
Adverse events
- Data on IPT-specific adverse events are lacking. Most safety concerns are extrapolated from known risks of insulin and chemotherapy individually.
- Hypoglycaemia is the most commonly reported adverse event of insulin administration, especially in non-diabetic patients.
Contraindications
- Contraindications for IPT are not well established. However, standard contraindications for insulin and chemotherapy apply, including administration during pregnancy, lactation, and in paediatric patients. (WHO 2002)
Interactions
- IPT can potentiate the effects of hypoglycaemic agents.
- Data on interactions with specifically the insulin-chemotherapy combinations used in IPT are not available but the respective interactions with insulin and chemotherapy need to be considered.
Warnings
- The use of chemotherapeutic drugs at only 10%-25% of the recommended dose is a concern (MSKCC 2025). There is no evidence that such low doses of chemotherapy in combination with insulin can produce the same anticancer effect as the recommended doses.
- The use of lower doses of chemotherapeutic drugs may promote drug resistance.
- Insulin and IGF-1 signalling have been implicated in promoting tumour growth. (Giovannucci 2010; Vigneri 2009; Goodwin 2002; Gallagher 2020; Wolpin 2009). Elevated insulin levels may stimulate cancer cell proliferation, especially in cancers with high insulin receptor expression. Preliminary data from a long-term observational studies reported that insulin glargine increased the risk of developing pancreatic cancer and medullary thyroid cancer in humans (Wang 2025).
Alabaster O, Vonderhaar BK, Shafie SM. Metabolic modification by insulin enhances methotrexate cytotoxicity in MCF-7 human breast cancer cells. Eur. J. Cancer Clin. Oncol. 1981 Nov;17(11):1223-228.
Ayre SG, Garcia y Bellon DP, Garcia DP Jr. Insulin, chemotherapy, and the mechanisms of malignancy: the design and the demise of cancer. Med. Hypotheses. 2000 Oct;55(4):330-334.
Ayre SG, Perez Garcia y Bellon D, Perez Garcia D Jr. Insulin potentiation therapy: a new concept in the management of chronic degenerative disease. Med. Hypotheses. 1986 Jun;20(2):199-210.
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.
Escudero CA, Herlitz K, Troncoso F, et al. Pro-angiogenic Role of Insulin: From Physiology to Pathology. Front Physiol. 2017 Apr 5;8:204. doi: 10.3389/fphys.2017.00204.
Gallagher EJ, LeRoith D. Hyperinsulinaemia in cancer. Nat Rev Cancer. 2020 Nov;20(11):629-644. doi: 10.1038/s41568-020-0295-5. Epub 2020 Sep 9.
Giovannucci E, Harlan DM, Archer MC, Bergenstal RM, Gapstur SM, Habel LA, Pollak M, Regensteiner JG, Yee D. Diabetes and cancer: a consensus report. CA Cancer J. Clin. 2010 July-August;60(4):207-221. Accessed 8th of September 2020.
Goodwin PJ, Ennis M, Pritchard KI, Trudeau ME, Koo J, Madarnas Y, Hartwick W, Hoffman B, Hood N. Fasting insulin and outcome in early-stage breast cancer: results of a prospective cohort study. J. Clin. Oncol. 2002 January 1;20(1):42-51. Accessed 8th of September 2020.
Kern DH, Chien FW, Morton DL. Selective effects of insulin and hydrocortisone on colony formation and chemosensitivity of human tumors in soft agar. Int. J. Cancer. 1984 Jun 15;33(6):807-812. Accessed 8th of September 2020.
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):220-224.
Memorial Sloan Kettering Cancer Center. Insulin Potentiation Therapy. 2025, accessed June 2025.
Oster JB, Creasey WA. Enhancement of cellular uptake of ellipticine by insulin preincubation. Eur. J. Cancer Clin. Oncol. 1981 Oct;17(10):1097-1103.
Peacock JL, Gorschboth CM, Norton JA. Impact of insulin on doxorubicin-induced rat host toxicity and tumor regression. Cancer Res. 1987 Aug 15;47(16):4318-4322.
Sissung T M, Schmidt K T, Figg W D. Insulin potentiation therapy for cancer? Lancet Oncol 2019; 20: 191–92.
Vigneri P, Frasca F, Sciacca L, Pandini G, Vigneri R. Diabetes and cancer. Endocr. Relat. Cancer. 2009 December;16(4):1103-1123. Accessed 8th of September 2020.
Wang T, He G, Xiong W, Huang J. Adverse drug events associated with insulin glargine: a real-world pharmacovigilance study based on the FAERS database. Front Pharmacol. 2025 Apr 28;16:1563238.
World Health Organization. (2002). Breastfeeding and maternal medication: Recommendations for drugs in the eleventh WHO Model List of Essential Drugs (WHO Reference No. 55732). World Health Organization.
Zou K, Ju JH, Xie H. Pretreatment with insulin enhances anticancer functions of 5-fluorouracil in human esophageal and colonic cancer cells. Acta Pharmacol. Sin. 2007 May;28(5):721-730.
Citation
CAM Cancer Consortium. Insulin potentiation therapy, October 2025.
Document history
Updated in July 2025 by Lisa Dal Pozzo and Barbara Wider. Updated literature search in October 2025. Assessed as up to date in January 2023, August 2020, January 2019, June 2017, April 2016 by Barbara Wider. Updated and revised in January 2013 by Luc Geeraert, first published in August 2011 authored by Luc Geeraert.
