Mechanism of Magnesium Sulphate

A frequently asked question concerns the function of magnesium sulphate ( Epsom Salts ) in the Liver Flush protocol. It is often considered that it only value is as a laxative or purgative. It gets a lot of bad press because of the bitter taste that many people find difficult to tolerate. I have been ask many times and very loudly; WHERE IS THE MEDICAL EVIDENCE. I have recently found a number of interesting papers that show the results of taking magnesium sulphate on the biliary system and the blood.

The most interesting and up-to-date paper was presented in 1981 and published in 1982 by a research scientist at The University of Texas Medical Branch, Galveston, Texas.

First of all a little revision:

It is important to know that the name of the hormone that causes the gallbladder to contract is called cholecystokinin. The bile flows into the duodenum though a nipple called the Ampular of Vater. In fact both bile and pancreatic fluid flow through this nipple which is surround by a muscle that form the control valve. This muscular arrangement is known as the Sphincter of Oddi. When there is a demand for bile the gallbladder contracts, which increases the pressure in the biliary system and expands the bile ducts and the Sphincter then allows bile into the duodenum as a number of pulses.



When certain foods, mainly fats reach the first part of the intestines called the duodenum they cause the release of the hormone cholecystokinin and this causes the gallbladder to contract, the bile ducts to expand and the sphincter to relax.

The fact that Magnesium Sulphate contracted the gallbladder had been known for a long time but there was no hard evidence. With modern measuring apparatus it was possible to see inside the body and take accurate measurements.

The experiment at the University of Texas involved given people a 25g solution of magnesium sulphate in 100 mL of distilled water. Blood plasma samples were collected and gallbladder volumes were determined from. Cholecystokinin increased significantly at 20 minutes after oral magnesium sulphate and reached a maximal value at 50 minutes. A maximum reduction of gallbladder volume (to one third of original) was achieved at 50 minutes after ingestion of magnesium sulphate. The study provides direct evidence that the mechanism of magnesium sulphate stimulated gallbladder contraction occurs through the release of CCK, and shows a close correlation between CCK release and contraction of the gallbladder.

There was no significant change in serum magnesium concentrations indicating that very little of the magnesium finds its way into the blood and casts doubts on the claims that Epson salts is harsh on kidney function.

All the volunteers in the experiment noted hyper intestinal activity and had increased bowel movements, an average of three, from 30 minutes to 24 hours after oral ingestion of magnesium sulphate.

The stimulatory effect of magnesium sulphate on gallbladder contraction has been demonstrated by measuring bile flow. It also relaxes the sphincter of Oddi. In 1943 it had been reported that magnesium sulphate acts to produce gallbladder emptying for the same length of time as egg yolk and differs merely in the degree to which it affects the gallbladder contraction or the relaxation of the sphincter of Oddi.

References:

Boyden EA, Bergh GS, Layne JA. An analysis of the reaction of the human gall bladder and sphincter of Oddi to magnesium sulfate. Surgery 1943; 13:723-733.

Malagelada J-R, Holtermuller KH, Go VLW. Relative potencies of magnesium (Mg++), calcium (Ca++) and oleic acid (C18) on pancreatic, gallbladder and intestinal function in man. Gastroenterology 1974; 66:A-83/737.

Malagelada J-R, Holtermuller KH, McCall JT, Go VLW. Pancreatic, gallbladder, and intestinal responses to intraluminal magnesium salts in man. Dig Dis 1978; 23:481-485.

Correlation Between Gallbladder Size and Release of Cholecystokinin After Oral Magnesium Sulfate in Man KAZUTOMO INOUE, M.D., ISIDORO WIENER, M.D., CHARLES J. FAGAN, M.D., LARRY C. WATSON, M.D., JAMES C. THOMPSON, M.D.
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