Protein requirements are affected by alcohol intake as well as the degree of malnutrition and liver disease. Alcohol ingestion impairs hepatic amino acid uptake and protein synthesis, reduces protein secretion from the liver and increases catabolism in the gut [2]. Patients with Child's A cirrhosis have been found to have normal protein catabolism with increased protein synthesis when a high-protein diet was fed [38]. A follow-up study was done to evaluate protein synthesis in patients with more severe liver disease. Six patients with Child's B or C cirrhosis were analyzed with a 15N-glycine kinetic study and were also found to have higher protein catabolism while fasting than did controls [39]. In the patients with cirrhosis, a high-calorie (46 kcal/kg), high-protein (1.6g/kg) diet reduced protein catabolism slightly (although not significantly) compared with fasting.

Protein is necessary to help the liver regenerate and recover from hepatitis. A moderate protein intake (0.8-1 g/kg) is probably adequate for uncomplicated hepatitis or cirrhosis. However, protein needs are increased to about 1.2-1.3 g/kg to promote nitrogen balance [40]. If alcoholic hepatitis, decompensated liver disease and/or malnutrition is present, protein needs may be as high as 1.5 g/kg [13].

For many years, the idea that protein should be restricted in the presence of hepatic encephalopathy was promoted. The basis for this recommendation was that protein intake increased serum ammonia levels, which in turn increased encephalopathy. This theory has never been proven in a controlled study. Moreover, a study published in 2004 showed that there was no benefit of a low-protein diet on serum ammonia levels or encephalopathy [41]. In this landmark study, 30 encephalopathic patients admitted to an emergency department were randomized to receive either a normal protein diet (1.2 g/kg) or a low-protein diet with a slow progression to a normal diet. Encephalopathy was not different between the two groups. Although protein synthesis was equal between the two groups, the low-protein group had increased protein breakdown.

Branched-chain amino acid (BCAA)-enriched formulas have been touted as beneficial for patients with hepatic encephalopathy. The literature is equivocal in regards to their true benefit. In a large study, Marchesini et al. [42] randomized 174 patients with liver disease to receive either a BCAA, lactoalbumin or maltodextrin supplement for a year. Those who received the BCAA formula had reduced event outcomes (death and deterioration to exclusion criteria) compared to the lactoalbumin group (p = 0.039). In addition, the average hospital admission rate was lower in the BCAA group vs. the lactoalbumin group (p = 0.006) and the maltodextrin group (p = 0.003). Those who received BCAA had stable or improved nutritional parameters, liver function tests, anorexia and heath-related quality of life scores. In addition, those patients also had a reduction in their mean Child-Pugh score.

On the other hand, a Cochrane review evaluating the effectiveness of BCAA in liver failure published in the same year found no significant improvements associated with BCAA when high methodological quality studies were evaluated [43]. The BCAA studies are difficult to evaluate as a whole because they vary in study design, study and control groups, composition of formulas, type of disease, level of encephalopathy and duration of therapy.

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Good Carb Diet

Good Carb Diet

WHAT IT IS A three-phase plan that has been likened to the low-carbohydrate Atkins program because during the first two weeks, South Beach eliminates most carbs, including bread, pasta, potatoes, fruit and most dairy products. In PHASE 2, healthy carbs, including most fruits, whole grains and dairy products are gradually reintroduced, but processed carbs such as bagels, cookies, cornflakes, regular pasta and rice cakes remain on the list of foods to avoid or eat rarely.

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