Until recently, the most common cause of cirrhosis of the liver in the United States was attributed to alcohol abuse. Hepatitis C is now the number one cause of liver cirrhosis (26%), followed closely by alcohol abuse at 21% (NIDDK 2000). A cofactor such as the hepatitis C virus can increase the risk of cirrhosis in those who also consume alcohol in excess (NIDA 2002).
In the United States, a type of cancer known as hepatocellular carcinoma is observed in 10-20% of patients who have cirrhosis (Wolf 2001). As with other cancers, early detection and number and size of tumors influence survival. Treatment for HCC ranges from surgical removal of the HCC if the patient has good liver function to transplantation (NIDDK 2000; Columbo 2001; Wolf 2001). If the patient cannot have surgery (because of advanced age, other health conditions, poor liver function, large tumors, or tumors in strategic locations), possible treatment includes ultrasound-guided injection of solutions that cause necrosis of tumor cells in the cancerous area; using a catheter to eliminate blood supply to the tumor; injecting antitumor agents directly into the tumor; systemic chemotherapy; and radiation (Columbo 2001).
Because the liver can often continue to perform essential functions in spite of serious damage, it is important to eat foods and take proper nutrients to retain its regeneration and detoxification abilities.
Phosphatidylcholine (PC) is one of the most important substances for liver protection and health and is a primary constituent of the cell membrane. As such, PC is necessary for integrity of liver cells. In studies in rats, PC has prolonged the survival of rat liver cells in culture by stabilizing the cell membrane (Miyazak et al. 1991). Liver cells that have been damaged by alcohol or cirrhosis are unable to meet the ongoing demands of the liver for phospholipid synthesis. Adding phospholipids such as PC via oral intake played an important role in regeneration of damaged liver cells (Horejsova et al. 1994). In an early study, Neuberger (1983) stated: "It has been shown that orally administered polyunsaturated PC can be incorporated into the liver cell membrane."
Other studies have shown the antifibrotic effect of PC. Not only does PC inhibit the development of hepatic fibrosis, it actually accelerates the regression of existing fibrosis (Ma et al. 1996). Part of this effect is probably due to PC promoting the breakdown of collagen (Lieber 1999), but it may also be due to an inhibitory effect on the stellate cell (Poniachik et al. 1999). In experimental studies, PC was also found to protect against alcoholic cirrhosis in baboons and against carbon tetrachloride-induced cirrhosis in rats (Aleynik et al. 1997). In another study (Navder et al. 1997), PC was shown to prevent earlier changes induced in the alcoholic liver before cirrhosis even develops.