Insulin Potentiation Therapy

Insulin Potentiation Therapy

Insulin potentiation therapy (IPT) is an unconventional cancer treatment method that utilizes insulin to administer low-dose chemotherapy or mandelonitrile (B17).

This therapeutic approach capitalizes on the inherent molecular biology of cancer cells, particularly their secretion of insulin and insulin-like growth factor, and the interaction of these substances with their respective receptors.

By combining insulin with chemotherapy drugs, significantly lower doses (about 10-15% of the standard dose) can be targeted more precisely and effectively to cancerous cell populations. This approach nearly eradicates dose-related side effects while purportedly enhancing the antineoplastic effects.

Advocates of IPT provide the following explanation of cancer biology to elucidate the mechanisms behind IPT. Insulin, the central component of IPT, exerts three significant actions on cancer cells, in addition to lowering blood sugar levels and consequently depriving cancer cells of their energy source. Reduced blood glucose levels (below 60 mg/dl) also trigger the secretion of growth hormone, which presumably fortifies the immune system.

Insulin differentiates cancer cells from normal cells biologically based on insulin receptor density. Insulin, a hormone naturally produced in the pancreas, facilitates the transport of nutrients from the bloodstream into cells. It attaches to cell receptors, allowing nutrients to enter. Insulin can discern and distinguish cancer cells from healthy ones in several ways. While insulin is secreted in the pancreas to regulate blood glucose levels, it activates a glucose transport protein in all cells, cancerous or healthy, facilitating glucose entry and reducing blood glucose levels. One key distinction between cancer and normal cells is the markedly higher concentration of insulin receptors, or docking sites for insulin, in cancer cells.

Cancer cells, driven by their rapid growth and proliferation, exhibit heightened glucose uptake to sustain their voracious appetite compared to normal cells. When nutrients are introduced into the body, they are preferentially consumed by cancer cells, further weakening the patient.

Moreover, cancer cells possess the ability to produce insulin and insulin-like growth factor (IGF), allowing them to autonomously enhance their glucose uptake.

The capacity to self-produce insulin sets cancer cells apart from normal cells. Additionally, insulin underscores a second abnormality: the higher concentration of insulin receptors on cancer cells. For instance, breast cancer cells have six times more insulin receptors and ten times more IGF receptors per cell than normal cells. Furthermore, insulin can cross-react with and activate IGF receptors on cancer cells, intensifying its impact on cancer cells compared to normal tissues. The ligand effect, a function of receptor concentration, dictates that the greater the number of receptors for a specific ligand—such as insulin—the stronger the ligand's effect on the tissue.

By stimulating insulin and IGF receptors on cancer cells through insulin administration during IPT, the biological disparities of cancer cells—greater insulin reception and voracious appetite—render them more receptive to chemotherapy and infusion therapies used in biological cancer treatments.