br Relationship of Fatty Liver with the Metabolic Syndrome T

Relationship of Fatty Liver with the Metabolic Syndrome Traditionally deemed to be the “hepatic manifestation of the metabolic syndrome”, NAFLD is more correctly deemed to be bi-directionally linked with either the Metabolic Syndrome (MetS) or its individual components. Indeed, on the one hand metabolic derangements are a strong predictor of all the individual histological components of NAFLD (Ballestri et al., 2016b). On the other hand, NAFLD assessed with either liver nobiletin or ultrasonography will predict the risk of incident MetS and type 2 diabetes (T2D) over 5 years (Ballestri et al., 2016a).
Relationship of Alcohol with MetS Alcohol consumption exerts a complex effect on the MetS with light alcohol consumption reducing and heavy alcohol consumption increasing the risk of MetS (Sun et al., 2014). Consistently, a randomized controlled trial in 224 individuals reported that initiating moderate consumption of alcohol (particularly red wine) modestly decreased cardiometabolic risk in patients with well controlled T2D (Gepner et al., 2015).
How Little Alcohol Is Safe? A consensus report concluded that the threshold of acceptability in healthy adults/elderly was ≤30g ethanol daily for men and ≤15g daily for women (Poli et al., 2013). Such a modest amount of alcohol does not necessitate any medical action (Poli et al., 2013). This study confirms that, irrespective of sex, alcohol <20g daily is probably safe. In men the threshold of safety may even be higher, whereas women are more vulnerable and develop more severe toxicity for lower amounts of alcohol. This is of interest given that the drinking of moderate amounts of red wine regularly is probably associated with a relative health benefit thanks to antioxidants such as polyphenols, particularly resveratrol.
Japan vs. Other Countries: Reasons for the Discrepancy Interestingly, findings from this study would suggest that the beneficial effect of modest alcohol consumption is restricted to Japan, and is not extended to other countries (the Japanese paradox). This conclusion may, though, be spurious given that quantity and quality of data vary across countries and are probably non-comparable. Alternatively, types of alcoholic beverages and pattern of alcohol consumption in Japan or interaction of host\'s metabolic factors (notably including obesity) may account for this discrepancy (Askgaard et al., 2015). Of note, binge drinking was consistently associated with increased risk of fatty liver across countries, suggesting that this pattern of alcohol consumption is universally harmful.
Conclusions To sum up, the study by Roerecke et al. (2016) confirms, in Japanese individuals, that modest alcohol consumption does not exert any detrimental effects in healthy individuals. In this specific setting, bioluminescent may even have beneficial effects by decreasing incidence and prevalence of steatosis. Future studies should evaluate the reasons why such benefits are not reproducible outside Japan, namely the Japanese paradox.
Acknowledgements
We thank for their comments on our meta-analysis on the relationship between alcohol consumption and hepatic steatosis (). We would like to clarify our position on overall risk associated with alcohol consumption and specifically on the risk of hepatic steatosis. First, as we have stated in our paper, we are in agreement with Lonardo et al. that a distinction between alcoholic and non-alcoholic hepatic steatosis has little meaning because alcohol is only one of the risk factors for liver disease, including non-alcoholic fatty liver disease. Different dimensions of alcohol consumption should be distinguished in this regard as non-regular binge drinking among moderate drinkers seems to increase the risk for hepatic steatosis. However, other risk factors also play a role, and the interactions among all risk factors determine the overall risk for liver injury. The large heterogeneity we observed in countries other than Japan underlines that risk factors other than alcohol play a substantial role in risk for hepatic steatosis and precludes us from clearly identifying the role alcohol plays in the development of hepatic steatosis. Thus, categorizing the etiology of liver injury based on one risk factor does not make much sense.