Hanyang Med Rev.  2011 Nov;31(4):228-234. 10.7599/hmr.2011.31.4.228.

Nutrition and Chronic Liver Disease

Affiliations
  • 1Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea. noshin@hanyang.ac.kr

Abstract

Malnutrition is very commonly seen in end stage liver disease. More than 65% of patients with chronic liver disease and more than 90% of patients with end-stage liver disease suffer malnutrition. Multiple reports have clearly shown that malnourishment is a relevant factor in complications and mortality due to chronic liver disease. It is essential that all patients with chronic liver disease have a full assessment of nutritional status at presentation. Supplementary enteral nutrition is indicated when chronic liver disease patients are unable to meet their nutritional requirements in their usual daily diet. Non-alcoholic fatty liver disease (NAFLD) is another type of chronic liver condition characterized by overnutrition and ectopic hepatic fat accumulation and/or hepatic inflammation. Patients diagnosed with obesity, insulin resistance, and/or dyslipidemia are at the greatest risk for developing or having NAFLD. A recent hypothesis is that NAFLD is one manifestation of metabolic syndrome or insulin resistance. Unfortunately, there is no consensus as to what dietary approach is most beneficial for preventing the progression of NAFLD. It seems likely that there will not be any single correct dietary plan for all NAFLD patients, so that diet and life-style modifications will best be tailored for the individual needs of the patient.

Keyword

Liver Disease; Liver Cirrhosis; Nutrition Therapy; Fatty Liver

MeSH Terms

Consensus
Diet
Dyslipidemias
End Stage Liver Disease
Enteral Nutrition
Fatty Liver
Humans
Inflammation
Insulin Resistance
Liver
Liver Cirrhosis
Liver Diseases
Malnutrition
Nutrition Therapy
Nutritional Requirements
Nutritional Status
Obesity
Overnutrition
Fatty Liver

Cited by  1 articles

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Joo Ah Lee, Tae Hee Lee, Ji Yeong Kim, Min Gyu Seok, Min Gyu Kang, Ji Hyun Jeong, Hoon Sup Koo, Kyung Ho Song, Yong Seok Kim, Sun Moon Kim, Kyu Chan Huh, Young Woo Choi, Young Woo Kang
Korean J Gastroenterol. 2014;64(5):284-289.    doi: 10.4166/kjg.2014.64.5.284.


Reference

1. Ritter L, Gazzola J. Nutritional evaluation of the cirrhotic patient: an objective, subjective or multicompartmental approach? Arq Gastroenterol. 2006. 43:66–70.
2. Campillo B, Richardet JP, Scherman E, Bories PN. Evaluation of nutritional practice in hospitalized cirrhotic patients: results of a prospective study. Nutrition. 2003. 19:515–521.
Article
3. Shanbhogue RL, Bistrian BR, Jenkins RL, Jones C, Benotti P, Blackburn GL. Resting energy expenditure in patients with end-stage liver disease and in normal population. JPEN J Parenter Enteral Nutr. 1987. 11:305–308.
Article
4. Muller MJ, Bottcher J, Selberg O, Weselmann S, Boker KH, Schwarze M, et al. Hypermetabolism in clinically stable patients with liver cirrhosis. Am J Clin Nutr. 1999. 69:1194–1201.
Article
5. Meng QH, Wang JH, Yu HW, Li J, Feng YM, Hou W, et al. Resting energy expenditure and substrate metabolism in Chinese patients with acute or chronic hepatitis B or liver cirrhosis. Intern Med. 2010. 49:2085–2091.
Article
6. Verboeket-van de Venne WP, Westerterp KR, van Hoek B, Swart GR. Energy expenditure and substrate metabolism in patients with cirrhosis of the liver: effects of the pattern of food intake. Gut. 1995. 36:110–116.
Article
7. Matos C, Porayko MK, Francisco-Ziller N, DiCecco S. Nutrition and chronic liver disease. J Clin Gastroenterol. 2002. 35:391–397.
Article
8. Shintani Y, Fujie H, Miyoshi H, Tsutsumi T, Tsukamoto K, Kimura S, et al. Hepatitis C virus infection and diabetes: direct involvement of the virus in the development of insulin resistance. Gastroenterology. 2004. 126:840–848.
Article
9. Nagy I, Hajnal F, Mohacsi G, Nemeth J, Laszik Z, Pap A. Pancreatic trophism in experimental liver cirrhosis. Int J Pancreatol. 1993. 14:157–166.
Article
10. Figueiredo FA, Dickson ER, Pasha TM, Porayko MK, Therneau TM, Malinchoc M, et al. Utility of standard nutritional parameters in detecting body cell mass depletion in patients with end-stage liver disease. Liver Transpl. 2000. 6:575–581.
Article
11. Koo BK, Chung JM, Lee HS. Biochemical evaluation of nutritional status of vitamins and minerals in patients with alcoholic liver disease. J Korean Soc Food Sci Nutr. 1998. 27:1244–1252.
12. Mendenhall CL, Moritz TE, Roselle GA, Morgan TR, Nemchausky BA, Tamburro CH, et al. A study of oral nutritional support with oxandrolone in malnourished patients with alcoholic hepatitis: results of a Department of Veterans Af fairs cooperative study. Hepatology. 1993. 17:564–576.
Article
13. Mendenhall CL, Moritz TE, Roselle GA, Morgan TR, Nemchausky BA, Tamburro CH, et al. The VA Cooperative Study Group #275. Protein energy malnutrition in severe alcoholic hepatitis: diagnosis and response to treatment. JPEN J Parenter Enteral Nutr. 1995. 19:258–265.
Article
14. Plauth M, Cabre E, Riggio O, Assis-Camilo M, Pirlich M, Kondrup J, et al. ESPEN Guidelines on Enteral Nutrition: Liver disease. Clin Nutr. 2006. 25:285–294.
Article
15. Deems RO, Friedman MI. Macronutrient selection in an animal model of cholestatic liver disease. Appetite. 1988. 11:73–80.
Article
16. Muller MJ, Rieger A, Willmann O, Lautz HU, Balks HJ, Von Zur Muhlen A, et al. Metabolic responses to lipid infusions in patients with liver cirrhosis. Clin Nutr. 1992. 11:193–206.
Article
17. Nompleggi DJ, Bonkovsky HL. Nutritional supplementation in chronic liver disease: an analytical review. Hepatology. 1994. 19:518–533.
Article
18. Huang MA, Greenson JK, Chao C, Anderson L, Peterman D, Jacobson J, et al. One-year intense nutritional counseling results in histological improvement in patients with non-alcoholic steatohepatitis: a pilot study. Am J Gastroenterol. 2005. 100:1072–1081.
Article
19. Kechagias S, Ernersson A, Dahlqvist O, Lundberg P, Lindstrom T, Nystrom FH. Fast-food-based hyper-alimentation can induce rapid and profound elevation of serum alanine aminotransferase in healthy subjects. Gut. 2008. 57:649–654.
Article
20. van der Meer RW, Hammer S, Lamb HJ, Frolich M, Diamant M, Rijzewijk LJ, et al. Effects of short-term high-fat, high-energy diet on hepatic and myocardial triglyceride content in healthy men. J Clin Endocrinol Metab. 2008. 93:2702–2708.
Article
21. Hollingsworth KG, Abubacker MZ, Joubert I, Allison ME, Lomas DJ. Low-carbohydrate diet induced reduction of hepatic lipid content observed with a rapid non-invasive MRI technique. Br J Radiol. 2006. 79:712–715.
Article
22. Tendler D, Lin S, Yancy WS Jr, Mavropoulos J, Sylvestre P, Rockey DC, et al. The effect of a low-carbohydrate, ketogenic diet on nonalcoholic fatty liver disease: a pilot study. Dig Dis Sci. 2007. 52:589–593.
Article
23. Maioli MA, Alves LC, Perandin D, Garcia AF, Pereira FT, Mingatto FE. Cytotoxicity of monocrotaline in isolated rat hepatocytes: effects of dithiothreitol and fructose. Toxicon. 2011. 57:1057–1064.
Article
24. Pivato LS, Constantin RP, Ishii-Iwamoto EL, Kelmer-Bracht AM, Yamamoto NS, Constantin J, et al. Metabolic effects of carbenoxolone in rat liver. J Biochem Mol Toxicol. 2006. 20:230–240.
Article
25. Assy N, Nasser G, Kamayse I, Nseir W, Beniashvili Z, Djibre A, et al. Soft drink consumption linked with fatty liver in the absence of traditional risk factors. Can J Gastroenterol. 2008. 22:811–816.
Article
26. Ouyang X, Cirillo P, Sautin Y, McCall S, Bruchette JL, Diehl AM, et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol. 2008. 48:993–999.
Article
27. Le KA, Ith M, Kreis R, Faeh D, Bortolotti M, Tran C, et al. Fructose overconsumption causes dyslipidemia and ectopic lipid deposition in healthy subjects with and without a family history of type 2 diabetes. Am J Clin Nutr. 2009. 89:1760–1765.
Article
28. Rodriguez-Calvo R, Barroso E, Serrano L, Coll T, Sanchez RM, Merlos M, et al. Atorvastatin prevents carbohydrate response element binding protein activation in the fructose-fed rat by activating protein kinase A. Hepatology. 2009. 49:106–115.
Article
29. Ahmed U, Redgrave TG, Oates PS. Effect of dietary fat to produce non-alcoholic fatty liver in the rat. J Gastroenterol Hepatol. 2009. 24:1463–1471.
Article
30. Vilar L, Oliveira CP, Faintuch J, Mello ES, Nogueira MA, Santos TE, et al. High-fat diet: a trigger of non-alcoholic steatohepatitis? Preliminary findings in obese subjects. Nutrition. 2008. 24:1097–1102.
Article
31. Tetri LH, Basaranoglu M, Brunt EM, Yerian LM, Neuschwander-Tetri BA. Severe NAFLD with hepatic necroinflammatory changes in mice fed trans fats and a high-fructose corn syrup equivalent. Am J Physiol Gastrointest Liver Physiol. 2008. 295:G987–G995.
Article
32. Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med. 2003. 348:2082–2090.
Article
33. Esposito K, Marfella R, Ciotola M, Di Palo C, Giugliano F, Giugliano G, et al. Effect of a mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA. 2004. 292:1440–1446.
Article
34. Ventegodt S, Merrick E, Merrick J. Clinical holistic medicine: the Dean Ornish program ("opening the heart") in cardiovascular disease. ScientificWorldJournal. 2006. 6:1977–1984.
Article
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