The Impact of Diet on Liver Fibrosis and on Response to Interferon Therapy in Patients With HCV-Related Chronic Hepatitis

Carmela Loguercio, MD; Alessandro Federico, MD; Mario Masarone, MD; Roberto Torella, MD; Marcello Persico, MD


Am J Gastroenterol. 2008;103(12):3159-3166. 

In This Article


Dietary components have been implicated in deranged liver function in physiological conditions[36,37] and in patients with liver diseases.[20,22,26,38] Our study, carried out on a large number of HCV patients and controls, demonstrates that dietary intake affects liver histology, and indirectly, response to treatment. In fact, at univariate and multivariate analysis, a high intake of calories, carbohydrates, and lipids was associated with more severe fibrosis. This finding illustrates that diet is an important factor in the management of patients affected by HCV. Interestingly, HCV patients did not seem to adhere to a so-called healthy diet. Indeed, both patients and controls exceeded the daily recommended doses of total proteins, carbohydrates, and lipids. Even more surprisingly, both groups consumed a similar amount of alcohol. Moreover, the number of heavy drinkers (> 40 g/day) was similar in the two groups.

Alcohol affects HCV by enhancing oxidative stress and HCV replication[38] and increases insulin resistance in obese individuals by interfering with the traffic of lipids between adipose tissue and liver.[39] It stimulates the production of inflammatory cytokines that in turn affect and are affected by insulin resistance in a vicious circle, and finally, by activating transcriptional factors, alcohol accelerates the progression to fibrosis in HCV-infected patients.[40,41,42]

We found that a high intake of PUFA was associated with a higher degree of steatosis, and that a higher intake of lipids and carbohydrates was associated with fibrosis. Similar associations were found in animals with alcohol-induced liver damage and/or experimental NASH,[43,44,45,46] and in patients with NAFLD[47,48]. It is noteworthy that obesity[49] and diabetes[50] have been found to be risk factors for hepatocellular carcinoma in case-controlled studies. Taken together, the foregoing data suggest a synergistic mechanism whereby alcohol, diet and HCV alter the metabolism of lipids and carbohydrates, which in turn, results in liver damage.

The viral characteristics (RNA, viremia, genotype) are important in determining the outcome of treatment with IFN and ribavirin in HCV-positive patients.[51] Also host characteristics seem to be important in establishing the clinical management of patients with HCV-related chronic hepatitis.[1,2,3,4,52] Furthermore, weight reduction has been shown to reduce steatosis and abnormal liver enzymes and improve fibrosis in patients with chronic hepatitis C.[53] Here we report the novel finding that, in a large population of HCV-positive patients, several dietary components were related to the severity of liver damage, and that BMI and staging negatively affected the response to therapy in patients affected by hepatitis C. This suggests that educational programs aimed at correcting the overall lifestyle of liver disease patients should be part of the therapeutic strategy of these patients. The simple recommendation of a low calorie, low fat diet may not be effective in an era in which attention is focused on natural products, including such foods as complementary or chemopreventive drugs.[36]

Our finding that alcohol intake was similar in patients and controls might indicate that physicians, including hepatologists, do not consider this aspect sufficiently important, and consequently do not advise their patients to abstain from drinking. Because frequent contacts with medical professionals during treatment has been associated with reduced alcohol intake,[54] we suggest the HCV patients undergo regular counseling about this issue in order to improve their awareness of alcohol-related problems.

Globalization of dietary habits, which has been well discussed in recent years,[55] seems to be related to the emerging problem of obesity[56] also in our regions, formerly taken as an example of a correct diet. Besides being a cardiovascular risk,[57] obesity is also an important factor of liver damage in hepatitis C.[23,41,49,53]

In conclusion, we show that, besides alcohol consumption, an unbalanced diet is an important factor of hepatitis C evolution and nonresponse to antiviral treatment. Specific nutritional education and severe alcohol restrictions might, synergistically, improve the response to antiviral therapy.

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