Low Protein Diet Liver Disease – John V Logomarsino, PhD, RD, LD/N, Central Michigan University, Department of Human Environmental Studies, Mt. Pleasant, MI 48859, United States of America
Protein intake plays an important role in cirrhosis of the liver in adults. However, the type and amount of protein taken in cirrhosis has been controversial. The purpose of this paper is to investigate the optimal protein intake for the management of cirrhosis and prevention of hepatic encephalopathy in adults. Protein restriction of 0.6 g/kg/d has traditionally been used as therapeutic nutritional therapy for cirrhosis of the liver. However, recent evidence has shown that protein restriction leads to many negative outcomes for adults with cirrhosis. Current research suggests a protein intake of 1.2-1.5 g/kg/d in liver cirrhosis; however, most older adults do not eat this much. Strategies to help increase protein intake and manage cirrhosis include ensuring there is enough protein at each meal through regular or supplemental intake, protein supplements before bed or overnight, and branched chain amino acid supplements. An emphasis on vegetable protein versus animal protein is probably not a beneficial treatment option due to a lack of sufficient evidence regarding potential benefits and negative effects.
Low Protein Diet Liver Disease
Iiames J, Logomarsino JV. Protein Recommendations for Older Adults with Cirrhosis: A Review. Journal of Gastroenterology and Hepatology Research 2015; 4(4): 1546-1556 Available from: URL: http:///index.php/joghr/article/view/1014
Ways To Reverse A Fatty Liver
Nutritional management is an important part of managing cirrhosis. Poor nutritional status in cirrhosis is strongly associated with life-threatening complications, decline in liver function, and reduced survival[1, 2]. This is particularly true for adults who are already at high risk of malnutrition, poor living conditions, and increased morbidity and mortality[3-5]. Due to the fact that nutrition plays a very important role in cirrhosis and adults, it seems that protein intake would be encouraged. However, this has not always been the case.
The type and amount of protein intake in cirrhosis has long been debated with various recommendations. A review completed in 2013 by Bauer et al  addressed specific protein requirements for healthy adults with acute and chronic diseases; however cirrhosis was not addressed. The purpose of this paper is to review different protein recommendations for the management of cirrhosis and the prevention of hepatic encephalopathy in adults. A literature search was conducted in PubMed and CINAHL using the search terms dietary protein, older adults, liver disease, hepatic encephalopathy, sarcopenia, nutrition, and age 65+. Studies were considered for inclusion if they were written in English and had relevant applications for adults with cirrhosis. Additional publications were identified by searching the reference lists of retrieved articles.
In 2010, chronic liver disease was the fifth leading cause of death in men of all age groups in the United States; in 1989 it was the ninth leading cause of death, suggesting a general increase in incidence. In addition, the fastest growing number of patients with cirrhosis is over 50. This is not surprising because many features of aging lend themselves to the development and progression of chronic liver disease and cirrhosis.
There are a number of different factors that often occur in adults that contribute to the development of chronic liver disease and cirrhosis. After reaching a maximum size in early adulthood, the liver gradually decreases in size and the amount of blood flow it receives, leading to a decrease in function and efficiency over time. Also, increased ammonia production and bacterial overgrowth are common in adults, both of which are thought to play an important role in the development of hepatic encephalopathy. Older adults tend to have chronic constipation, intestinal dysmotility, and increased colonic length, which puts them at risk for increased ammonia production. Finally, adulthood is associated with a higher incidence of diabetes, which is strongly associated with the progression of liver cirrhosis .
Fatty Liver Disease Diet: What To Eat And Avoid
It is estimated that 20% of patients with cirrhosis and 60% of patients with less cirrhosis are malnourished. In adults, protein-energy malnutrition is associated with high health care costs, frequent increases in bed sores and infections, increased morbidity and mortality, and poor physical performance [4, 5]. In dog experiments, poor nutritional status has been shown to promote the development of hepatic encephalopathy . In addition, malnutrition in cirrhosis is positively associated with aging. Many factors contribute to the development of malnutrition in adults with cirrhosis, including poor nutrition, altered absorption, sarcopenia, and altered metabolism. All factors must be investigated and considered when developing treatment and prevention strategies.
In adults, food intake naturally decreases over time, which contributes to the development of malnutrition. Other causes of reduced food intake in adults and patients with cirrhosis include anorexia, early satiety after ascites or elevated leptin, altered mental status, unpleasant meals, physical dependence, polypharmacy, altered taste perceptions, and nutrient intake poor during treatment or tests [3 , 4, 16-18].
Altered absorption is another factor that encourages the development of malnutrition. In cirrhosis, it is caused by small intestinal bacterial overgrowth, intestinal microflora imbalance, pancreatic allocrine function, portosystemic shunt, bile acid deficiency, and competition with drugs[19-21]. One study that looked at the stool contents of patients with cirrhosis and healthy controls found evidence of impaired fatty acid metabolism, which may further contribute to malabsorption . Furthermore, reduced gastric acid and atrophic gastritis are common in adults and may further contribute to malabsorption, especially if caused by bacterial overgrowth.
Altered metabolism is another important factor contributing to the development of malnutrition in cirrhosis. One of the main characteristics of cirrhosis is insulin resistance. Insulin resistance leads to a reduction in glucose disposal and glycogen formation and thus a general reduction in liver and muscle glycogen stores. This leads to increased fat oxidation and gluconeogenesis and muscle protein catabolism for energy use. Total protein loss is also due to reduced synthesis of urea and liver proteins, as well as increased urinary nitrogen excretion[20, 22-27]. Furthermore, it has been shown that healthy patients need 3 days of fasting to enter the starvation state, while patients with cirrhosis will switch to gluconeogenesis from amino acids after only one fast .
Low Protein Diet
Sarcopenia, or the loss of skeletal muscle, is the most common complication in cirrhosis and is believed to be a major contributor to the development of malnutrition in cirrhosis. The development of sarcopenia is accelerated by physical inactivity and poor protein intake, which is common in cirrhosis and older adults. It has been shown that 7.2-8.6% of elderly women consume a protein level of less than 0.66 g/kg/d and that approximately 10-25% of adults consume less than the recommended dietary allowance of 0.8 g/kg/d[ 31 ] . After the age of 50 there is a reduction of 1% in muscle mass per year. Furthermore, reduced physical activity and bed rest associated with hospitalization are very common in older adults with cirrhosis and contribute to loss of muscle mass. Lean tissue loss in healthy adults during bed rest is much greater than that in young adults. In cirrhosis as in older adults, skeletal muscle protein synthesis is reduced and impaired compared to healthy young adults, while total muscle protein breakdown is increased, further contributing to a reduction in muscle mass[14 , 16].
Hypermetabolism does not occur in all cases of cirrhosis, but has been shown to occur in 16-34% of cases, further contributing to malnutrition[17, 18]. Moreover, more protein is required to respond to the inflammatory and catabolic states associated with chronic and acute diseases, and inflammation has been noted in patients with mild hepatic encephalopathy. Experts currently recommend a protein intake of 1.2-1.5 g/kg/day to maintain muscle mass and physical performance in adults. However, these recommendations contradict the protein restrictions that have become common in the treatment of cirrhosis and hepatic encephalopathy.
Protein restriction in cirrhosis to prevent and manage hepatic encephalopathy (HE) has been common for more than half a century. In 1893, dogs with porto-caval shunts were found to develop neurological symptoms after eating meat. In the 1930s, the same types of dogs were found to improve when fed bread and milk instead of meat. In the mid-20th century, protein restriction was found to reduce HE in patients who underwent portosystemic shunt surgery. The hypothesis was that a reduction in protein intake led to a reduction in ammonia production and therefore a reduction in HE. The exercise was then extended to all patients with cirrhosis, with or without HE. A 2006 study showed that 58% of dietitians continued to restrict dietary protein and 64% accepted requests for inappropriate protein restriction in patients with HE. Although there is much observational data to support the hypothesis that protein is harmful in HE, results from experimental data showed that this is not the case. In fact, since the 1970s, a great deal of research has shown that protein restriction can be harmful in HE, especially in older adults.
Since the 1970s, many studies have been conducted that have proven that protein restriction is not beneficial in HE; a summary of these studies can be found in table 1[24, 36-45]. In 1977, Greenberger et al  described a case of a woman with chronic HE who tolerated up to 90 g of vegetables.
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