Are soft drink consumption and fatty liver in any way connected?

Peer-reviewed | Manuscript received: January 17, 2013 | Revision accepted: March 08, 2013

Introduction

The increase in overweight, type-2 diabetes mellitus and dyslipidemia has reached epidemic proportions. Closely associated with it is the development of non-alcoholic fatty liver disease (NAFLD) [1]. NAFLD is increasingly being recognized as a serious health problem, especially in Western industrial nations [1–3]. The spectrum of NAFLD extends from simple deposits of fat in the liver to non-alcoholic steatohepatitis (NASH), fibrosis and, ultimately, cirrhosis [1–3]. In simple steatosis, histology reveals triglyceride-containing fat vesicles within the hepatic parenchyma; NASH, by contrast, is characterized by inflammatory infiltrates and cell destruction. In cirrhosis, scar tissue replaces the degenerated hepatic parenchyma [2].

Soft drinks are defined as non-alcoholic carbonated beverages sweetened either with non-caloric sweeteners such as aspartame (“diet soft drinks”) or with sugar, especially fructose (“regular soft drinks”). Since the 1960s, high-fructose corn syrup (HFCS) which contains a high percentage of fructose (HFCS-42 and HCFS-55 with 42 % and 55 % of fructose, respectively), has been used as a sweetener [4]. Because it is inexpensive to produce, HFCS is widely used in manufacturing soft drinks [5, 6]. It is, therefore, not surprising that the consumption of fructose has climbed by 25–30 % over the past three decades [5]. Over the past fifty years, the per capita consumption of soft drinks has grown by nearly 500 % in the USA [7].

Summary

Objective of the present study was to elucidate the effects of soft drink consumption on the prevalence of hepatic steatosis in a randomly selected populationbased collective. A total of 1,435 subjects (54.6 % women, 45.4 % men) underwent upper abdominal sonographic examination and were questioned regarding their soft drink consumption and their body-mass index (BMI), waist-to-hip ratio (WHR); laboratory parameters and anthropometric data were documented. The prevalence of hepatic steatosis in the overall collective stood at 26.1 % (n = 374; women 39.0 %; men 61.0 %). Consumption of soft drinks was reported by 20.8 % of subjects (n = 298); hepatic steatosis was diagnosed in 23.2 % (n = 69). The prevalence stood at 26.8 % among non-consumers. Male sex, greater age, higher BMI and WHR increased the risk of developing hepatic steatosis. A higher prevalence of hepatic steatosis could not be demonstrated for consumers of soft drinks (p = 0.3715).

Keywords: Fatty liver, NAFLD, soft drinks, ultrasound

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