Due to the site upgrade, your MY ACCOUNT logins will need to be updated. Please access Forgot Your Password to make this change. If you do not have an account, click here.

Summary of a symposium on how SAMe, Folic Acid and Betaine help alcoholic liver disease

Aug 07, 2007


This is a summary of a symposium on the role of nutrients for treating alcoholic liver disease (ALD). The participants were the National Institute on Alcohol Abuse and Alcoholism in collaboration with various departments from the National Institutes of Health.

Supplementing these patients with SAMe may lessen ALD by decreasing inflammation and free radical damage, by improving Glutathione activity and decreasing the level of the substrate known as s-adenosylhomocysteine or SAH; the direct precursor to homocysteine in the liver. SAMe inhibits the death of healthy liver cells and stimulates the death of liver cancer cells.

Lacking folic acid accelerated liver disease in alcoholics by increasing SAH levels, decreasing SAMe levels and Glutathione, stimulating enzymes that activate carcinogens, and increasing the peroxidation of fatty tissues in the liver, and stimulating the large- stay put immune cells in the liver to cause unnecessary inflammation. A shortage of Folic Acid also decreases the proper activity of DNA increasing the risk of liver cancer. Betaine lessens ALD by improving the creation of SAMe and eventually Glutathione, decreasing the level of SAH and homocysteine. Improving the ratio of SAMe to SAH improves cell function and cellular communication, and decreases the lodging of fats in the liver, Decreasing the level of homocysteine in the liver decreases inflammatory activity by the livers immune cells and decreases liver cell death and fatty acid production. The summation is published in the July 2007 issue of the American Journal of Clinical Nutrition; the journal of the American Society for Nutrition.

In addition to the prestigious group of Scientific Governmental Agencies participating in this symposium, the following institutes also participated;

  • The Division of Gastroenterology/Hepatology, Duke University Medical Center
  • The Department of Medicine, University of Louisville
  • Genome and Biomedical Sciences Facility, UC Davis
  • The Keck School of Medicine, USC
  • The Department of Animal Sciences, University of Wisconsin, Madison