Biography:

Dr. Van Dyke is a Professor of Biochemistry and Molecular Pharmacology at West Virginia University Medical School with 50 years of research experience. He developed the first effective screening system for antimalarial drugs by measuring the effects of drugs on synthesis of malarial parasite DNA and RNA. He screened more than 10,000 drugs and found mefloquine and halofantrine which were developed commercially. Prof. Knox Van Dyke began to study diabetes 1 and 2 and found the actual cause of these diseases originates from a toxic peroxide called peroxynitrite. The first observation of him was that all the drugs developed to treat diabetes essentially only control blood glucose (sugar). Excessive sugar is not the cause of diabetes nor is it lack of weight control. These problems increase peroxynitrite, but they do not destroy excessive peroxynitrite per se, so the disease and its 6 major pathological consequences continue. He has developed a combination of non-toxic substances which will control these diseases effectively and prevent its many devastating pathologies. He has over 300 publications and 150 patents.

Abstract:

The fundamental basis of diabetes continues unrecognized and mostly untreated. Depending on the type of diabetes 1 or 2-treatment generally consists of insulin injections or anti-diabetic drugs that lower excessive blood glucose and/or hemoglobin A1C. Often patients are asked to lose weight and exercise more frequently. Blood glucose can be tightly controlled and still diabetic pathologies continue. Using a diabetic Streptozotocin (STZ) rat model, we demonstrated that diabetes and cataracts could be completely prevented with carboxy-PTIO which oxidizes nitric oxide and a nitration target Acetaminophen (Tylenol). This indicated that the action of STZ could be destroyed without harm to the animals. How does STZ cause diabetes in the first place? STZ is a molecule of 2-deoxyglucose (2-DG) linked to methyl nitrosourea (MNU). STZ enters the blood stream and to the pancreatic-Beta cells where it enters Glut-2 receptors. Once inside the cell, the molecule splits into its two pieces i.e., 2DG and MNU. MNU begins generating a peroxide known as peroxynitrite (OON=O-). The peroxynitrite attacks DNA, protein and lipids of the cell and damages mitochondria which kill the cell via apoptosis or necrosis. When beta cells die, alpha cells replaced them, producing excessive glucagon and increasing blood glucose thereby creating a diabetic state. When STZ is injected intra-articularly in the brain of normal mice, they develop decreased brain glucose metabolism and insulin resistance in a few days and in a few months Alzheimer’s disease with plaques and tangles. We have developed a reaction with peroxynitrite and L-012 to produce blue luminescence via oxidation. Now we demonstrate that STZ generates peroxynitrite based luminescence which is inhibited by the same substances that inhibit peroxynitrite-based luminescence itself. We show that STZ nicks plasmid DNA similarly to peroxynitrite, which we believe initiates both Alzheimer’s disease and diabetes.