Malnutrition in Liver Disease

The liver is responsible for the metabolism of many hormones that have discordant effects on protein, carbohydrate, and lipid metabolism, including insulin, the sex hormones, insulin-like growth factors, and glucagon. It is thus not surprising that chronic and acute liver disease can profoundly alter nutritional status and amino acid metabolism.

The prevalence of malnutrition in patients with liver disease varies from 10% to 100%, depending largely on the method of nutritional assessment performed and the population studied. Protein-calorie malnutrition (PCM)⁵ can be observed in all clinical stages but is more frequently seen in advanced stages of liver disease (1). Alcoholic liver disease is the form of liver disease most frequently associated with PCM. Reported prevalences of PCM are between 20% for patients with compensated alcoholic liver disease in the community and 100% in hospitalized patients with acute alcoholic hepatitis (2). Reliable data based on a detailed nutritional assessment of the prevalence of PCM in patients with nonalcoholic liver disease are relatively scant. In a study by Morgan et al. (3), 40% of patients with primarybiliary cirrhosis were found to have evidence of PCM vs. 12% of patients with chronic hepatitis.

The pathophysiology of malnutrition in liver disease is complex and multifactorial. Contributing factors include diminished intake, increased requirements (e.g., due to ascites formation and maldigestion), altered substrate utilization (characterized by lowered respiratory quotients), and altered protein and amino acid metabolism.

When the liver fails acutely, it is the loss of hepatic regulation of protein metabolism that results rapidly in death. The alterations in amino acid metabolism associated with liver disease are characterized by low levels of circulating BCAAs (leucine, isoleucine and valine), elevated levels of circulating aromatic amino acids(phenylalanine, tryptophan and tyrosine), and methionine (4). It is widely believed that the changes in amino acid metabolism play a role in the pathogenesis of many of the complications of cirrhosis, such as portosystemic encephalopathy. Cirrhosis is often associated with a) increased endogenous leucine flux, an indicator of protein breakdown and leucine oxidation; and b) decreased protein synthesis response to a meal.

The presence of malnutrition has been variably associated with increased short- and long-term mortality in patients with acute and chronic liver diseases (5,6). Preoperative malnutrition has also been reported to be associated with increased operative blood loss, longer lengths of stay in intensive care units, increased mortality, and higher total hospital charges after liver transplantation (7). Furthermore, malnutrition is associated with its own morbidity in patients with acute and chronic liver disease, for example, cognitive dysfunction and dermatological manifestations of zinc deficiency. In this setting, nutritional therapy, particularly BCAA supplementation, is an attractive concept in the prevention and treatment of complications.

 

Hepatic Encephalopathy

What Is Hepatic Encephalopathy?

Hepatic encephalopathy refers to the changes in the brain that occur in patients with advanced acute or chronic liver disease. If liver cells are damaged, certain substances that are normally cleansed from the blood by the healthy liver are not removed (ammonia mainly, and other toxins). A patient with chronic hepatic encephalopathy may develop progressive loss of memory, disorientation, untidiness, and muscular tremors, leading to a form of chronic dementia. The ingestion of protein invariably aggravates these symptoms.

The treatment of hepatic encephalopathy involves, first, the removal of all drugs that require detoxification in the liver and, second, the reduction of the intake of protein. Restricting the amount of protein in the diet will generally lower the levels of amino acids and ammonia in the bloodstream and brain. Most physicians advise their patients with this condition to eat only about 40 grams of protein a day, and will prescribe lactulose or neomycin to lower amino acid production. Non-meat proteins, such as those found in vegetables and milk, are preferred. Certain amino acids are used in treatment, since they are considered less likely to cause mental impairment. A dietary supplement rich in these amino acids is used at many liver treatment centers.

http://hepatitis-central.com/hcv/whatis/encephalopathy.html

Hepamin and Your Liver

Liver is an interesting organ with high regenerative capacity and complex functions (Michalopoulos and DeFrances, 1997; Taub, 2004; Michalopoulos and Khan, 2005c;Fausto et al., 2006). Liver receives all exiting circulation from the small and most of the large intestine, as well as spleen and pancreas, through the portal vein. Its “strategic” location in relation to the food supply via the portal vein, and the unique gene-and protein-expression patterns of hepatocytes (the main functional cells of the liver) allow it to function as a biochemical defense against toxic chemicals entering through the food and as a re-processor of absorbed food ingredients. Nutrients entering the liver are transformed into secreted proteins (albumin, most coagulation factors, several plasma carrier proteins etc. in the peripheral blood), lipids sent as lipoproteins into the other tissues, carbohydrates stored in the liver as glycogen (the main glucose reserve used for stabilization of glucose levels in the blood). Synthesis of bile is essential for absorption of fat and lipophilic nutrients. As a major regulator of plasma glucose and ammonia levels, liver is essential for optimal function of the brain. Loss of liver function leads to chronic “hepatic encephalopathy” and eventually coma. The wide array of functions performed by liver towards the rest of the body has been safeguarded by evolutionary events which imparted to liver a phenomenal capacity to regenerate. This process allows liver to recover lost mass without jeopardizing viability of the entire organism. The phenomenon of liver regeneration following loss of liver mass is seen in all vertebrate organisms, from humans to fish. It is also triggered when livers from small animals (e.g., dogs) are transplanted to large recipients of the same species. It has been recorded and mythologized in ancient times from the myth of Prometheus and libraries of clay tables picturing scarred livers of sacrificial animals, used to foretell the future in ancient Babylon and Rome (Michalopoulos and DeFrances, 1997).