07 February 2023 In Liver Disease

Alcohol use and metabolic syndrome are highly prevalent in the population and frequently co-exist. Both are implicated in a large range of health problems, including chronic liver disease, hepatocellular carcinoma, and liver-related outcomes (i.e. decompensation or liver transplantation). Studies have yielded mixed results regarding the effects of mild-moderate alcohol consumption on the risk of metabolic syndrome and fatty liver disease, possibly due to methodological differences.

The few available prospective studies have indicated that mild-moderate alcohol use is associated with an increase in liver-related outcomes.

This conclusion was substantiated by systems biology analyses suggesting that alcohol and metabolic syndrome may play a similar role in fatty liver disease, potentiating an already existing dysregulation of common vital homeostatic pathways. Alcohol and metabolic factors are independently and jointly associated with liver-related outcomes. Indeed, metabolic syndrome increases the risk of liver-related outcomes, regardless of alcohol intake. Moreover, the components of metabolic syndrome appear to have additive effects when it comes to the risk of liver-related outcomes. A number of population studies have implied that measures of central/abdominal obesity, such as the waist-to-hip ratio, can predict liver-related outcomes more accurately than BMI, including in individuals who consume harmful quantities of alcohol.

Many studies even point to synergistic interactions between harmful alcohol use and many metabolic components. This accumulating evidence showing independent, combined, and modifying effects of alcohol and metabolic factors on the onset and progression of chronic liver disease highlights the multifactorial background of liver disease in the population. The available evidence suggests that more holistic approaches could be useful for risk prediction, diagnostics and treatment planning.

26 August 2022 In Liver Disease
The role of moderate alcohol consumption in the evolution of NAFLD is still debated. The aim of this study is to evaluate the impact of current and lifelong alcohol consumption in patients with NAFLD. From 2015 to 2020, we enrolled 276 consecutive patients fulfilling criteria of NAFLD (alcohol consumption up to 140 g/week for women and 210 g/week for men). According to their current alcohol intake per week, patients were divided in: abstainers, very low consumers (C1:
26 August 2022 In General Health

BACKGROUND: Gamma-glutamyltransferase (GGT) levels in the blood can be a sensitive marker of liver injury but the extent to which they give insight into risk across multiple outcomes in a clinically useful way remains uncertain.

METHODS: Using data from 293,667 UK Biobank participants, the relationship of GGT concentrations to self-reported alcohol intake and adiposity markers were investigated. We next investigated whether GGT predicted liver-related, cardiovascular (CV) or all-cause mortality, and potentially improved CV risk prediction.

FINDINGS: Higher alcohol intake and greater waist circumference (WC) were associated with higher GGT; the association was stronger for alcohol with evidence of a synergistic effect of WC. Higher GGT concentrations were associated with multiple outcomes. Compared to a GGT of 14.5 U/L (lowest decile), values of 48 U/L for women and 60 U/L for men (common upper limits of 'normal') had hazard ratios (HRs) for liver-related mortality of 1.83 (95% CI 1.60-2.11) and 3.25 (95% CI 2.38-4.42) respectively, for CV mortality of 1.21 (95% CI 1.14-1.28) and 1.43 (95% CI 1.27-1.60) and for all-cause mortality of 1.15 (95% CI 1.12-1.18) and 1.31 (95% CI 1.24-1.38). Adding GGT to a risk algorithm for CV mortality reclassified an additional 1.24% (95% CI 0.14-2.34) of participants across a binary 5% 10-year risk threshold.

INTERPRETATION: Our study suggests that a modest elevation in GGT levels should trigger a discussion with the individual to review diet and lifestyle including alcohol intake and consideration of formal liver disease and CV risk assessment if not previously done.

FUNDING: British Heart Foundation Centre of Research Excellence Grant (grant number RE/18/6/34217), NHS Research Scotland (grant number SCAF/15/02), the Medical Research Council (grant number MC_UU_00022/2); and the Scottish Government Chief Scientist Office (grant number SPHSU17).

23 September 2021 In Liver Disease

BACKGROUND AND OBJECTIVE: There is no consensus regarding modest alcohol consumption in patients with non-alcoholic fatty liver disease (NAFLD) due to conflicting results. The aim of this meta-analysis was to examine the effects of modest alcohol consumption on histological severity, histological course, hepatocellular carcinoma, and long-term clinical outcomes in NAFLD patients.

METHODS: We searched MEDLINE and EMBASE databases from inception to October 2020 for studies evaluating the effects of modest alcohol consumption among patients with NAFLD. A random-effects meta-analysis using pooled odds ratio (OR) and hazard ratio (HR) was calculated with 95% confidence interval (CI). Study quality was assessed with the Newcastle-Ottawa Scale.

RESULTS: Fourteen cross-sectional or cohort studies with aggregate data on 14,435 patients were included in the analysis. Modest alcohol consumption resulted in lower risks for steatohepatitis (OR 0.59; 95% CI 0.45-0.78; I (2) = 12%) and advanced fibrosis (OR 0.59, 95% CI 0.36-0.95; I (2) = 75%). Histological follow-up data showed that modest alcohol use was associated significantly with less steatohepatitis resolution but not with fibrosis progression. The HR for developing hepatocellular carcinoma was 3.77 (95% CI 1.75-8.15; I (2) = 0%). NAFLD patients with modest alcohol intake had a lower mortality risk than lifelong abstainers (HR 0.85; 95% CI 0.75-0.95; I (2) = 64%).

CONCLUSION: This meta-analysis suggests that medical advice for modest alcohol drinking should be made cautiously in caring for an individual patient based on the clinical context. Practically, patients with steatohepatitis or advanced fibrosis should avoid alcohol use, whereas patients with low fibrosis risk may be allowed for modest and safe drinking.

Page 1 of 2

Contact us

We love your feedback. Get in touch with us.

  • Tel: +32 (0)2 230 99 70
  • Email: This email address is being protected from spambots. You need JavaScript enabled to view it.

Disclaimer

The authors have taken reasonable care in ensuring the accuracy of the information herein at the time of publication and are not responsible for any errors or omissions. Read more on our disclaimer and Privacy Policy.