Caffeine is Protective in Patients With Non-alcoholic Fatty Liver Disease

A. Birerdinc; M. Stepanova; L. Pawloski; Z. M. Younossi

Disclosures

Aliment Pharmacol Ther. 2012;35(1):76-82. 

In This Article

Abstract and Introduction

Abstract

Background Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, is the most common cause of primary liver disease. Although recent studies have found that coffee drinking is protective against end stage chronic liver disease, there are scarce caffeine intake data in NAFLD specifically.
Aim To investigate the effects of dietary behaviour in NAFLD patients, using four continuous cycles of the National Health and Nutrition Examination Surveys (NHANES 2001–2008).
Methods Using data from four continuous cycles of NHANES, dietary intake questionnaires that list 62 nutrition components. Logistic regression was used to identify independent predictors of NAFLD among nutrition components after adjustment for potential clinical confounders. All analyses were run using SAS 9.1 and SUDAAN 10.0 (SAS Institute Inc., Cary, NC, USA).
Results Of the 62 nutrient components used for the univariate analysis, 38% were significant (P-value <0.05) in NAFLD with caffeine consumption being higher in the control group (P-value <0.001). The multivariate analysis using demographics, clinical parameters and nutritional components found five factors independently associated with NAFLD [African American Race P-value <0.001); Male gender P-value <0.001); Obesity (BMI ≥ 30) P-value <0.001); Caffeine intake (mg) P-value <0.001) and total plain water consumption (g) P-value ≤0.02)].
Conclusions Our analysis shows that caffeine intake is independently associated with a lower risk for NAFLD suggesting a potential protective effect. These data necessitate further research to elucidate the mechanism by which caffeine can protect against NAFLD.

Introduction

Non-alcoholic fatty liver disease is currently one of the most common causes of elevated liver enzymes and chronic liver disease in the Western world.[1–5] Attributed to the rapidly increasing rate of obesity, along with other components of metabolic syndrome, such as Type II diabetes, the prevalence of NAFLD is growing at an alarming rate in both adults and children.[5–7] In the United States, it is estimated that 25–30% of the population is afflicted with NAFLD, 2–3% have NASH and of these, 10–15% develop cirrhosis.[8–12]

The general consensus is that obesity in the United States population is an important contributing factor in the increased incidence of NAFLD.[4,5] According to the National Health and Nutrition Examination Survey (NHANES) conducted between 2007 and 2008, the prevalence of obesity in adults reached 32.2% among men and 35.5% among women.[13] Based on projected obesity rates, it is predicted that by the year 2025, 45–50% of the adult population will be obese, resulting in NAFLD related liver disease in over 25 million Americans.[14]

Despite the well established link between NAFLD and BMI,[15] obese and overweight people are not the only ones who are at risk of developing NAFLD and NASH.[16] The propensity of NAFLD to be a progressive disease suggests that early interventions could potentially prevent the more serious latter stage manifestations of this disease. These observations indicate that the development of NAFLD is indeed multi-factorial and other factors, such as dietary habits may play an important role in the development of NAFLD.

Although a number of nutritional studies have been performed to assess the interaction between diet and liver disease, caffeine intake has garnered a lot of attention. Studies done in the United States have shown that increased coffee intake is associated with a lower incidence of abnormal alanine aminotransferase (ALT) activity.[17] In addition, studies from Europe and Japan have indicated an inverse relationship between coffee and levels of g-glutamyltransferase and aminotransferases in serum.[18–24]

Assessing end stage liver-specific outcomes, a large population based study in Norway found an inverse association between coffee consumption and liver cirrhosis.[25] Furthermore, a study using the first National Health and Nutrition Examination Survey (1971–1975) found that coffee and tea drinking decreases the risk of clinically significant chronic liver disease as defined by death or hospitalisation due to CLD.[17] Caffeine has also been implicated in hepatic fibrosis, as recently demonstrated by a study showing that regular coffee consumption, above a threshold of approximately two coffee-cup equivalents per day, was associated with less severe hepatic fibrosis.[26] Recent studies have also suggested that coffee consumption may reduce the risk of developing hepatocellular carcinoma (HCC) in high-risk populations.[27] In addition, research in the field of hepatitis C and treatment with peginterferon plus ribavirin found that high-level consumption of coffee (more than three cups per day) to be an independent predictor of improved virological response.[28] Despite the increasing focus on the effects of coffee in the aetiology of severe liver disease, there is little data assessing the relationship between coffee consumption and NAFLD specifically.

Using recent U.S. population data, the aim of this study is to investigate the effects of dietary behaviour, specifically the nutrition components measured for NHANES participants, on the prevalence of NAFLD.

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