Author information
1 Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA.
2 Department of Medicine, Santa Clara Valley Medical Center, San Jose, CA.
3 Department of Medicine, Stanford University School of Medicine, Stanford, CA.
4 Division of Gastroenterology and Hepatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul Metropolitan Government Boramae Medical Center, Seoul, Korea.
5 Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Abstract
BACKGROUND AND AIMS:
The relationship between bisphenol A (BPA) and non-alcoholic fatty liver disease(NAFLD) is undefined. We studied the impact of BPA on NAFLD.
METHODS:
We performed a cross-sectional analysis of data from the National Health and Nutrition Examination Survey (NHANES) 2005-2014 among adults in the United States (US). NAFLD was diagnosed using the hepatic steatosis index (HSI) and the US fatty liver index (USFLI) in the absence of other causes of chronic liver diseases. The first sample using HSI consisted of 7605 adults. The second sample using USFLI consisted of 3631 participants with availability of fasting data.
RESULTS:
Of the first 7605 participants (mean age 47 years, 48.4% male), the prevalence of NAFLD and abnormally elevated alanine aminotransferase (ALT) levels was correlated with urinary BPA levels (P < 0.05). Compared to the reference group with lowest quartile of urinary BPA levels, those with the third and fourth quartiles were 81% and 53% more likely to develop NAFLD defined by HSI. In a multivariate model, the ORs for NAFLD in the third and fourth quartiles were 1.69 (95% CI 1.39-2.04) and 1.44 (95% CI 1.19-1.76) respectively (P for trend <0.001). In the second sample using USFLI, high BPA levels (fourth quartile) remained an independent predictor of NAFLD (OR 1.44, 95% CI 1.05-1.98, P for trend = 0.012).
CONCLUSIONS:
High levels of urinary BPA were associated with NAFLD in a nationally representative sample of adults in the US. The pathophysiology remains unclear and warrants further investigation.