EAP Supplementation Therapy for MS

Until 1984, it was believed that myelin was just a protective insulation on nerves. Now it is understood that myelin also serves as an electrical shunt to the central axis nerve fiber. In order for it to operate properly as an electrical passageway, certain chemical components need to be present in sufficient quantities. 2-amino ethanol phosphate (EAP) is one of these components. EAP greatly impacts electrical conduction at the cell membrane by protecting the membrane from the immune system aggression that is characteristic of MS. Researchers don't know why, but MS patients have less-than-adequate amounts of EAP.

EAP supplementation therapy works by increasing myelin cell membrane polarity and resistance to immune system aggression. This, in turn, increases electrical conduction capabilities.

Research has shown that EAP can be present in lower-than-average levels throughout the body, not just in the myelin cells, in many MS patients. Lower- than-average electrical discharging in urinary tract tissues may account for the recurrent urinary tract infections and symptoms so often experienced by MS patients. Without enough EAP, the electro-static filter that usually protects the urinary tract from infection does not function optimally, giving rise to microbial invasion and subsequent infections.

Ca-EAP (calcium-EAP) was registered in 1965 by the German Federal Health Authority as effective anti-MS medication, and it is used with positive results at the Hachen Sanitarium, the world's largest MS hospital. However, Ca-EAP has been banned by the FDA in the U.S. for unknown reasons. Many Americans travel to Europe for treatments, where IV injections of EAP are one part of a comprehensive MS protocol that also includes diet and lifestyle changes and nutritional supplementation. The documented results are very positive, and most patients who continue with treatment have no further deterioration of their condition.

Publication Review By: Stanley J. Swierzewski, III, M.D.

Published: 31 Dec 1999

Last Modified: 25 Sep 2015