Good Day All,
I have had alcoholic liver disease for several years now, and wanted to spread the word on a supplement I have found to be very helpful to me.
I work as a healthcare professional, and when I found out alcohol use had damaged my liver, I researched the best way to stop the progression of my disease.
Aside from the well known beneficial effects of SAM-e, B-Complex vitamins, Silymarin/Silibinin, magnesium and zinc; a concentrated form of the active component of simple Lecithin (Phosphatidylcholine) called Polyenylphosphatidylcholine or "PPC" (brand names PhosChol and HepatoPro) have been showing remarkable results in preventing, halting progression, and even reducing existing fibrosis in liver disease studies done by a Dr Charles Lieber, and colleagues at the Alcohol Research and Treatment Center, V.A. Medical Center, Bronx, N.Y
"Chronic administration of a soybean-derived polyenylphosphatidylcholine (PPC) extract prevents the development of cirrhosis in alcohol-fed baboons".
If you, or someone you know is having liver problems of any kind, I beg you explore the possiblities of supplementing PPC. If you are unable to obtain PPC, simple Lecithin may be of some help. You would need to take six to nine lecithin capsules per day to equal the benifit of two or three PPC per day.
Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin
Charles S. Lieber, M.D. *, Leonore M. Decarli, Ki M. Mak, Cho-Il Kim, Maria A. Leo
Section of Liver Disease and Nutrition, Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine (CUNY), New York, New York
Correspondence to Charles S. Lieber, (151/G), Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center, Bronx, NY 10468
Presented in part at the International Symposium on Phospholipids held December 4, 1989, in Cologne, FRG.
Department of Health and Human Services; Grant Number: AA03508, DK 32810
Department of Veterans Affairs
Characteristic features of alcoholic liver injury include fibrosis and striking membrane alterations, with associated phospholipid changes. To offset some of these abnormalities, a 10-yr study was conducted in baboons: 12 animals (eight females, four males) were fed a liquid diet supplemented with polyunsaturated lecithin (4.1 mg/kcal) for up to 8 yr, with either ethanol (50% of total energy) or isocaloric carbohydrate. They were compared with another group of 18 baboons fed an equivalent amount of the same diet (with or without ethanol), but devoid of lecithin. In the two groups, comparable increases in lipids developed in the ethanol-fed animals, but striking differences in the degree of fibrosis were seen. Whereas at least septal fibrosis (with cirrhosis in two) and transformation of their lipocytes into transitional cells developed in seven of the nine baboons fed the regular diet with ethanol, septal fibrosis did not develop in any animals fed lecithin (p < 0.005). They did not progress beyond the stage of perivenular fibrosis (sometimes associated with pericellular and perisinusoidal fibrosis) and had a significantly lesser activation of lipocytes to transitional cells. Furthermore, when three of these animals were taken off lecithin, but continued on the same amount of the ethanol-containing diet, they rapidly (within 18 to 21 mo) progressed to cirrhosis, accompanied by an increased transformation of their lipocytes to transitional cells. These results indicate that some component of lecithin exerts a protective action against the fibrogenic effects of ethanol. Because we had previously found that choline, in amounts present in lecithin, has no comparable action, the polyunsaturated phospholipids themselves might be responsible for the protective effect. (HEPATOLOGY 1990;12:1390-1398).
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