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Dietary and Lifestyle Management

Abstain From Alcohol

Alcoholism is the second most common cause of cirrhosis in the United States (NIDDK 2014a; Orman 2013; Perz 2006). Five-year survival amongst all cirrhotic patients is 70%, but is only 30% in drinkers with decompensated cirrhosis. In contrast, prognosis improves with abstinence; after alcohol cessation, the 5-year survival of patients with compensated and decompensated cirrhosis can climb as high as 90% and 60%, respectively (Schwartz 2012).

Avoid Tobacco Use

In one population-based study, smoking >10 g tobacco/day nearly quadrupled the risk of alcoholic cirrhosis and more than doubled the risk of other types of cirrhosis in women. In men, the corresponding increases were 60% and 40%, though the latter results fell just shy of statistical significance. Tobacco smoke contains chemical substances with cytotoxic properties that can activate stellate cells and induce fibrosis. In addition, smoking increases pro-inflammatory chemical messengers (eg, TNF-α, IL-1, IL-6) and decreases anti-inflammatory messengers (eg, IL-10) (Dam, Flensborg-Madsen 2013).

Adjust Prescription Drug Doses

Many drugs depend on the liver for metabolism, or require albumin, synthesized by the liver, for their pharmacokinetics and distribution. Cirrhosis alters these processes, making reduced dosages, or in some cases, avoidance, necessary. Recommendations for safe prescribing include (Lewis 2013):

  • Reduce medication dosages in general (consult your healthcare professional before making a change)
  • Opioid analgesics, anxiolytics, and sedatives can cause or worsen hepatic encephalopathy symptoms and should be used cautiously
  • Non-steroidal anti-inflammatory drugs (NSAIDs) can more readily cause renal failure and gastrointestinal bleeding in patients with cirrhosis and should generally be avoided
  • Anticancer and immunomodulating drugs; lower doses are recommended for some agents
  • Antimicrobials; some types (macrolides, tetracyclines, aminoglycosides) should generally be avoided
  • Proton pump inhibitors and histamine blockers can lead to serious infections
  • Antidepressants; half-lives and clearances may be altered
  • Cardiovascular drugs; dose adjustments may be needed for anti-arrhythmic drugs and beta-blockers


Coffee consumption has been associated with a lower incidence of cirrhosis in several observational studies (Muriel 2010). In one study, 4 or more cups of coffee per day reduced the risk of alcoholic cirrhosis by 80% compared to non-coffee drinkers. For one to three cups, the associated protection was 40%. The same study found that for non-alcoholic cirrhosis, 4 or more cups per day conferred a 30% reduced risk of cirrhosis (Klatsky 2006). Coffee may reduce the risk of fibrosis by lowering blood levels of growth factors associated with liver damage and fibrosis (Arauz 2013). Coffee consumption has also been associated with reduced risk of liver cancer in several European and Japanese studies, especially among heavy drinkers (consumption of over 3 cups of coffee per day reduced hepatocellular carcinoma risk by an average of 55% over 12 observational studies) (Bravi 2007; Larsson 2007).

Some benefit of coffee may be due to its antioxidant content (Arauz 2013). There is no definitive indication of exactly which coffee compounds are responsible for its health benefits. However, chlorogenic acids (a member of the group of antioxidant compounds known as polyphenols) have been shown in animal models to reduce liver inflammation and fibrosis (Shi 2009; Shi 2013).

Maintain Adequate Nutrient Intake

Liver disease in general, and cirrhosis especially, increases the likelihood of malnutrition, which is not surprising given the vital role of the liver in maintaining nutrient levels and energy balance (Purnak 2013). The European Society for Clinical Nutrition and Metabolism (ESPEN), the International Society for Hepatic Encephalopathy and Nitrogen Metabolism Consensus, and other groups have developed recommendations for avoiding malnutrition in individuals with cirrhosis or hepatic encephalopathy (Plauth 2006; Amodio 2013; Purnak 2013):

  • Calories. Patients should strive for an energy intake of 35-40 kcal/kg/day (Plauth 2006; Amodio 2013). Moderate, gradual weight loss is indicated for many individuals with NAFLD or NASH. Dietary fructose has been associated with metabolic syndrome and diabetes, two conditions associated with NAFLD and NASH (Purnak 2013).
  • Protein. Restriction of dietary protein is not recommended, unless it is not tolerated due to hepatic encephalopathy. The diet should include 1.2-1.5 g/kg/day of whole protein to avoid muscle wasting (Plauth 2006).
  • Vitamins. Patients with both alcohol and non-alcohol-related cirrhosis may be deficient in water-soluble vitamins, especially thiamine, and supplementation is warranted in patients with decompensated cirrhosis (Amodio 2013). Vitamin B12 and folate deficiencies have been reported in HBV and HCV infection (Purnak 2013); folate deficiency was present in one study of obese patients with NAFLD (Hirsch 2005). Low folate concentrations were associated with elevated levels of the vasculotoxic compound homocysteine in cirrhosis patients in an observational study (Kazimierska 2003). Patients with cholestatic liver disease may have reduced absorption of fat-soluble vitamins (A, D, E, and K) (Purnak 2013; Jaurigue 2014). Vitamin A deficiency is also a common problem in HCV infection (Purnak 2013), and vitamin K may be useful in the treatment of bone loss in patients with cirrhosis and chronic liver disease (Shiomi 2002; Lipkin 2002).
  • Minerals. Tissue zinc levels are decreased in patients with cirrhosis and hepatic encephalopathy, though trials of zinc supplementation have had conflicting results (Amodio 2013). Hepatic osteodystrophy, a common consequence of cirrhosis, can lead to calcium/magnesium imbalances. One study found that untreated hepatitis C patients presented with lower levels of plasma and red blood cell zinc and selenium than did healthy control subjects (Ko 2005).