04 May 2020 In Liver Disease

Background/Aims: Multiple meta-analyses and observational studies have reported that alcohol is a risk factor for liver cancer. However, whether there is a safe level of alcohol consumption remains unclear. We performed a systematic review and meta-analysis of the correlation between low-level alcohol consumption and the risk of liver cancer.

Methods: Nested case-control studies and cohort studies involving the general population published prior to July 2019 were searched. In total, 28 publications (31 cohorts) with 4,899 incident cases and 10,859 liver cancer-related deaths were included. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated.

Results: Compared with those with low levels of alcohol consumption, moderate and heavy drinkers (>/=1 drink/day for females and >/=2 drinks/day for males) had pooled ORs of 1.418 (95% CI, 1.192 to 1.687; p<0.001) for liver cancer incidence and 1.167 (95% CI, 1.056 to 1.290; p=0.003) for liver cancer mortality. The pooled OR for liver disease-related mortality for those with more than low levels of alcohol consumption was 3.220 (95% CI, 2.116 to 4.898; p<0.001) and that for all-cause mortality was 1.166 (95% CI, 1.065 to 1.278; p=0.001). The sensitivity analysis showed that none of the studies had a strong effect on the pooled OR. The Egger test, Begg rank correlation test, and the funnel plot showed no overt indication of publication bias.

Conclusions: Continuous consumption of more than a low-level of alcohol (>/=1 drink/day for females and >/=2 drinks/day for males) is related to a higher risk of liver cancer.

24 January 2020 In Liver Disease

OBJECTIVE: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver morbidity. This condition often is accompanied by obesity, diabetes, and metabolic syndrome (MetS). The aim of this study was to evaluate the connection between lifestyle factors and NAFLD in individuals with MetS.

METHODS: A cross-sectional study with 328 participants (55-75 y of age) diagnosed with MetS participating in the PREDIMED-Plus trial was conducted. NAFLD status was evaluated using the non-invasive hepatic steatosis index (HSI). Sociodemographic, clinical, and dietary data were collected. Adherence to the Mediterranean diet (mainly assessed by the consumption of olive oil, nuts, legumes, whole grain foods, fish, vegetables, fruits, and red wine) and physical activity were assessed using validated questionnaires.

RESULTS: Linear regression analyses revealed that HSI values tended to be lower with increasing physical activity tertiles (T2, beta = -1.47; 95% confidence interval [CI], -2.73 to -0.20; T3, beta = -1.93; 95% CI, -3.22 to -0.65 versus T1, Ptrend = 0.001) and adherence to the Mediterranean diet was inversely associated with HSI values: (moderate adherence beta = -0.70; 95% CI, -1.92 to 0.53; high adherence beta = -1.57; 95% CI, -3.01 to -0.13 versus lower, Ptrend = 0.041). Higher tertiles of legume consumption were inversely associated with the highest tertile of HSI (T2, relative risk ratio [RRR], 0.45; 95% CI, 0.22-0.92; P = 0.028; T3, RRR, 0.48; 95% CI, 0.24-0.97; P = 0.041 versus T1).

CONCLUSION: Physical activity, adherence to the Mediterranean diet, and consumption of legumes were inversely associated with a non-invasive marker of NAFLD in individuals with MetS. This data can be useful in implementing precision strategies aimed at the prevention, monitoring, and management of NAFLD.

24 January 2020 In Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is defined by hepatic steatosis in the presence of alcohol intake within safe limits, defined by guidelines of scientific associations (usually 20 g or 2 units/day in women, 30 g or 3 units in men). The diagnosis is usually followed by medical counseling of total abstinence, in order to prevent disease progression.

This policy has been challenged by epidemiological studies, suggesting that the risk of liver disease and disease progression is lower in modest drinkers than in total abstainers. We revised the literature on the effects of modest alcohol intake on disease burden. Epidemiological data may suffer from several potential biases (recall bias for retrospective analyses, difficulties in the calculation of g/day), limiting their validity.

Prospective data suggest that NAFLD patients with regular alcohol intake, although within the safe thresholds, are at higher risk of liver disease progression, including hepatocellular carcinoma; a detrimental effect of modest alcohol drinking is similarly observed in liver disease of viral etiology. Alcohol intake is also a risk factor for extrahepatic cancers, particularly breast, oral, and pharyngeal cancers, with gender difference and no floor effect, which outweigh the possible beneficial effects on cardiovascular system, also derived from retrospective studies.

Finally, the negative effects of the calorie content of alcohol on dietary restriction and weight loss, the pivotal intervention to reduce NAFLD burden, should be considered. In summary, the policy of counseling NAFLD patients for alcohol abstinence should be maintained.

26 November 2019 In Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is the hepatic consequence of metabolic syndrome, which often also includes obesity, diabetes, and dyslipidemia. The connection between gut microbiota (GM) and NAFLD has attracted significant attention in recent years. Data has shown that GM affects hepatic lipid metabolism and influences the balance between pro/anti-inflammatory effectors in the liver. Although studies reveal the association between GM dysbiosis and NAFLD, decoding the mechanisms of gut dysbiosis resulting in NAFLD remains challenging. The potential pathophysiology that links GM dysbiosis to NAFLD can be summarized as: (1) disrupting the balance between energy harvest and expenditure, (2) promoting hepatic inflammation (impairing intestinal integrity, facilitating endotoxemia, and initiating inflammatory cascades with cytokines releasing), and (3) altered biochemistry metabolism and GM-related metabolites (i.e., bile acid, short-chain fatty acids, aromatic amino acid derivatives, branched-chain amino acids, choline, ethanol). Due to the hypothesis that probiotics/synbiotics could normalize GM and reverse dysbiosis, there have been efforts to investigate the therapeutic effect of probiotics/synbiotics in patients with NAFLD. Recent randomized clinical trials suggest that probiotics/synbiotics could improve transaminases, hepatic steatosis, and reduce hepatic inflammation. Despite these promising results, future studies are necessary to understand the full role GM plays in NAFLD development and progression. Additionally, further data is needed to unravel probiotics/synbiotics efficacy, safety, and sustainability as a novel pharmacologic approaches to NAFLD.

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