Consumption of Sugar-Sweetened Beverages Has a Dose-Dependent Effect on the Risk of Non-Alcoholic Fatty Liver Disease: An Updated Systematic Review and Dose-Response Meta-Analysis

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) is a serious health problem, but the dose-response relationship between sugar-sweetened beverages (SSBs) and NAFLD remains uncertain. Methods: A systematic review and dose-response meta-analysis were conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Review Manager 5.3 and Stata 14.0 were used to combine trials and analyze data. The dose-response meta-analysis was performed by non-linear trend regression. Results: Twelve studies recruiting a total of 35,705 participants were included. The results showed that the consumption of SSBs was associated with 1.39-fold increased odds of NAFLD (95% CI: 1.29–1.50, p < 0.00001). The risk of NAFLD rose with an increased consumption of SSBs, while the consumptions of low doses (<1 cup/week), middle doses (1–6 cups/week) and high doses (≥7 cups/week) of SSBs increased the relative risk of NAFLD by 14%, 26% and 53%, respectively (p = 0.01, p < 0.00001, p = 0.03, respectively). Conclusions: This study demonstrates that consumers of SSBs are at significantly increased risk of NAFLD, and the consumption of SSBs has a dose-dependent effect on the risk of NAFLD. The findings of this study strengthen the evidence base for healthy dietary patterns and are meaningful for the primary prevention of NAFLD.

Clinical spectrum of non-alcoholic fatty liver disease in patients with diabetes mellitus

“…risk of NAFLD increased at least 26%, and up to 53% in patients who drank at least 1 cup per day [27]. This reiterates the importance of educating and fostering of healthy dietary patterns in the primary prevention of NAFLD.…”

“…Indeed, a recent systematic review and meta-analysis demonstrated that sugar-sweetened beverage consumption significantly increased the risk of NAFLD in a dose-dependent fashion. At a quantity of at least 1 cup per week (moderate-high dose), the relative risk of NAFLD increased at least 26%, and up to 53% in patients who drank at least 1 cup per day [ 27 ]. This reiterates the importance of educating and fostering of healthy dietary patterns in the primary prevention of NAFLD.…”

Chronic high dietary sucrose induces sexually dimorphic metabolic adaptations in liver and adipose tissue

“…The preservation of systemic insulin responsiveness (and glucose tolerance; Supplementary Figure 2) in our model demonstrate a clear decoupling of the mechanisms responsible for steatosis and those responsible for impairments in insulin sensitivity following chronic sucrose intake and, in the case of female mice, overt obesity ( Figure 1A). In humans, sugar sweetened beverage consumption is strongly associated with NAFLD (Arenaza et al, 2019;Asgari-Taee et al, 2019;Assy et al, 2008;Cahlin et al, 1973;Chen et al, 2019;Ma et al, 2015) but not always with obesity (Te Morenga et al, 2014).…”

“…Findings from observational studies and meta analyses indicate that excessive sugar intake or compromised sugar metabolism may be an initiating factor for NAFLD in humans (Arenaza et al, 2019;Asgari-Taee et al, 2019;Assy et al, 2008;Cahlin et al, 1973;Chen et al, 2019;Ma et al, 2015).…”

“…Although dietary sugars have been used extensively to induce cardiometabolic abnormalities in animal models (Bacon et al, 1984;Bukowiecki et al, 1983;Burke et al, 2018;Chen et al, 2019;Kawasaki et al, 2009;Oliveira et al, 2014;Ritze et al, 2014;Softic et al, 2019;Togo et al, 2019), the molecular mechanisms underlying sugar-induced hepatic lipid accumulation remain poorly understood in a context that is translational to human dietary practices (Choo and Sievenpiper, 2015). Most preclinical studies rely upon use of supraphysiologic concentrations of sucrose, glucose or fructose to induce steatosis and other metabolic comorbidities (Chen et al, 2011;Choo and Sievenpiper, 2015;Softic et al, 2019;Soria et al, 2001), often with the confounding addition of excess dietary lipid (Chen et al, 2011;Oliveira et al, 2014;Softic et al, 2019).…”