Hier beschrijft Dr. Bihari het werkingsmechanisme van naltrexone. Ik ga hier niet uit vertalen omdat dit medisch Engels me te moeilijk is. Maar uw arts en orthomoleculair arts zullen zeker begrijpen wat hier wordt beschreven. 

Mechanisms
The mechanisms involved in the apparent beneficial effect of LDN on cancer have three main elements. The first is the effect of LDN, when taken late at night, in inducing a sharp increase in pituitary and adrenal production of beta-endorphin and metenkephalin, respectively, in the pre-dawn hours, when 90% of the day's manufacture of these hormones occurs. Most studies have shown that naltrexone induces a two to three-fold increase in production of metenkephalin, the endorphin that most specifically activates delta-opioid receptors, the primary endorphin-related anti-growth factor on cancer cells. The low dose of naltrexone, which in higher doses would block endorphin and enkephalin action on the receptor, is gone from the body in about three or four hours — whereas the elevated levels of endorphins and enkephalins persist all day.

The second step involved in the anti-cancer effect of these hormones results from direct activation of opioid receptors of cancer cells by the increased endorphins. If this activation occurs while the cell is dividing, it dies. In fact, relatively small concentrations of metenkephalin, when added to human pancreatic cancer cells or human colon cancer cells growing in the test tube, have been shown to kill both. The apparent mechanism of cell killing is called apoptosis (programmed cell death). This appears to be one of the mechanisms by which endorphins and enkephalins combat cancer.

A third element, which may play a major role in controlling cancer, involves the cells of the immune system, which is regulated/orchestrated to a great extent by endorphins. In particular, endorphins raise the circulating levels of natural killer cells and cytotoxic CD-8 cells, the two immunological cell types that prevent cancer by killing cancer cells as they arise.

It should be emphasized that Dr. Bihari's patients were all treated in a private practice setting without the scientific rigor of a prospective clinical trial. This precludes any scientific claims about the drug's efficacy in treating any of the above-mentioned types of cancer. The results thus far do, however, raise the possibility that the manipulation of opioid receptors on cancer cells as anti-growth factors through the use of endorphins and endorphin-inducing opioid antagonists may eventually prove to have considerable merit, particularly in view of the many years of published, supportive laboratory research findings.

Those cancer cells that have opioid receptors on their cell membranes, and that may, therefore, respond to LDN, include all of those that arise from the gastrointestinal tract. This includes the mouth, esophagus,liver, pancreas, stomach, small intestine, colon and rectum. Lymph glands and the spleen have large numbers of opioid receptors, suggesting that Hodgkin's disease, non-Hodgkin's lymphoma, multiple myeloma and lymphocytic leukemia should respond to LDN. Other malignancies with sizable numbers of opioid receptors on their cell membranes include breast cancer, neuroblastoma, prostate cancer, malignant melanoma, renal cell carcinoma, glioblastoma, astrocytoma, endometrial cancer and small cell and large cell cancers of the lung.


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