How can I reduce my risk of getting nonalcoholic fatty liver disease?

Answer: Try increasing your intake of caffeine.

Aliment Pharmacol Ther. 2012 Jan;35(1):76-82. doi: 10.1111/j.1365-2036.2011.04916.x.

Caffeine is protective in patients with non-alcoholic fatty liver disease.

Birerdinc A, Stepanova M, Pawloski L, Younossi ZM.

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.

Here’s another study reporting the protective powers of coffee (caffeine?) for the liver:

Hepatology. 2011 Oct 10. doi: 10.1002/hep.24731. [Epub ahead of print]

Association of coffee and caffeine consumption with fatty liver disease, nonalcoholic steatohepatitis, and degree of hepatic fibrosis.

Molloy JW, Calcagno CJ, Williams CD, Jones FJ, Torres DM, Harrison SA.

Abstract

Coffee caffeine consumption (CC) is associated with reduced hepatic fibrosis in patients with chronic liver diseases, such as hepatitis C. The association of CC with nonalcoholic fatty liver disease (NAFLD) has not been established. The aim of this study was to correlate CC with the prevalence and severity of NAFLD. Patients involved in a previously published NAFLD prevalence study, as well as additional NASH patients identified in the Brooke Army Medical Center Hepatology clinic, were queried about their caffeine intake. A validated questionnaire for CC was utilized to assess for a relationship between caffeine and four groups: ultrasound negative (controls), bland steatosis/not-NASH*, NASH stage 0-1, and NASH stage 2-4. A total of 306 patients responded to the CC questionnaire. Average milligrams of total caffeine/coffee CC per day in controls, bland steatosis/not-NASH, NASH stage 0-1, and NASH stage 2-4 were 307/228, 229/160, 351/255, and 252/152, respectively. When comparing patients with bland steatosis/not-NASH to those with NASH stage 0-1, there was a significant difference in CC between the two groups (P = 0.005). Additionally, when comparing patients with NASH stage 0-1 to those with NASH stage 2-4, there was a significant difference in coffee CC (P = 0.016). Spearman’s rank correlation analysis further supported a negative relationship between coffee CC and hepatic fibrosis (r = -0.215; P = 0.035). Conclusion: Coffee CC is associated with a significant reduction in risk of fibrosis among NASH patients. (Hepatology 2011).

*  Translation:  NASH = Non-alcoholic steatohepatitis; steatohepatitis = fatty liver. Therefore NASH = Non-alcoholic fatty liver disease = NAFLD!)

Here’s an interesting summing up of where non-alcoholic fatty liver fits into metabolic syndrome:

Ned Tijdschr Geneeskd. 2011;155:A3181.

Treatment of non-alcoholic fatty liver disease

[Article in Dutch]
Koek GH.

Abstract

Non-alcoholic fatty liver disease (NAFLD) comprises benign steatosis and steatohepatitis (NASH) and may lead to liver fibrosis, cirrhosis and hepatocellular carcinoma. Its prevalence is estimated to be 20% in the general population and 50-100% in patients with overweight and obesity. In about 15-30% of patients steatosis evolves to NASH which can only be diagnosed by means of a liver biopsy. NAFLD may be described as the hepatic component of the metabolic syndrome and is a consequence of the Western lifestyle. The pathogenesis is multifactorial; oxidative stress plays a crucial role in maintaining inflammation and progressive fibrosis. Lifestyle modification with weight loss and increased physical activity is the cornerstone of the treatment, which should take place in a multidisciplinary setting. To date, no specific registered drug for NAFLD treatment is available. Supportive drug therapy is mainly focused on aspects of the metabolic syndrome and chronic inflammation.