2026/02/17 by Damien Leith, S. D. BARCLAY · 1 voice
Medicine · #Alcohol Consumption and Health Effects #Liver Disease Diagnosis and Treatment #Liver Disease and Transplantation
paper · pdf · doi:10.1111/joim.70076
openalex publication_date 2026/02/17 · openalex created_date 2026/02/18 · openalex updated_date 2026/08/01
Introduced in 2023, the new steatotic liver disease (SLD) nomenclature incorporates a spectrum of conditions causing hepatic steatosis, distinguished by a person's alcohol intake. Metabolic dysfunction–associated steatotic liver disease (MASLD) is the new classification for the condition previously known as non-alcoholic fatty liver disease. This new name addresses stigma associated with the pejorative term ‘fatty’ and allows for a positive definition of the condition—hepatic steatosis in the presence of one or more cardiometabolic risk factors (CMR), in women and men who consume less than 20 and 30 g of alcohol daily, respectively [1]. The SLD nomenclature includes a new category of metabolic dysfunction and alcohol-related liver disease. This encompasses those who otherwise meet the MASLD definition, but who drink to moderate excess (30–60 g alcohol/day in men and 20–50 g in women), but below the thresholds used to define alcohol-related liver disease. At a population level, rising global rates of obesity and Type 2 diabetes (T2D) are mirrored by a growing burden of MASLD-related morbidity and mortality, from cirrhosis and hepatocellular carcinoma [2]. However, at an individual level, only a minority of people with MASLD develop these complications, the risk of which correlates with the development of hepatic fibrosis [3]. The 2024 MASLD Clinical Practice Guideline endorsed by the European Liver, Diabetes and Obesity associations, recommend screening of populations at high-risk of MASLD-related liver fibrosis (those with persistently elevated liver enzyme tests, T2D or obesity and 1 or more CMR), using the Fibrosis-4 (FIB-4) score [3]. Identification of those at risk provides an appropriate context for discussing individualised lifestyle changes with patients, as well as identifying those most likely to benefit from licensed anti-obesity and MASLD-specific pharmacotherapies, proven to aid fibrosis regression. In this issue of Journal of Internal Medicine, Nabi et al. [4] describe the results of MASLD screening amongst a cohort of almost 28,000 middle-aged (50–64 years) adults, enrolled in the Swedish CArdioPulmonary bioImage Study. The authors have demonstrated 18.1% of Swedish adults have hepatic steatosis, based on a non-contrast CT liver attenuation of <48 Hounsfield units. Of participants with MASLD, 24.8% were classified as at risk for advanced liver fibrosis, compared to 6.3% of those without MASLD (p < 0.001), utilising the dynamic aspartate-to-alanine aminotransferase ratio (dAAR). As has been suggested in previous studies [5], using a robust meta-analysis, the authors demonstrate that the risk of fibrosis is shown to increase with cumulative features of the metabolic syndrome. However, less typical, in this study, hypertension is the single biggest predictor of fibrosis (adjusted odds ratio [aOR]: 1.44; 95% confidence interval [CI]: 1.24, 1.66), not T2D (aOR: 1.24; 95% CI: 1.06, 1.46), as would usually be expected [3]. This finding highlights a high-risk group who would potentially be missed by the current MASLD guidelines’ fibrosis screening recommendation. Importantly, this paper provides data from a real-world, general population cohort supporting clear, actionable lifestyle advice that any clinician can give to their patients to prevent or reduce hepatic steatosis. For sedentary patients, any activity is better than none, with even moderate or irregular exercise associated with a reduction in steatosis risk (aOR for MASLD: 0.80; 95% CI: 0.71, 0.89), compared to sedentary individuals. For those already active, more is better—with an increased protective effect of moderate regular exercise (aOR: 0.49; 95% CI: 0.43, 0.56) and regular vigorous exercise (aOR: 0.34; 95% CI: 0.29, 0.41). More than one soda per day is too many (aOR: 1.49; 95% CI: 1.19, 1.88, for two or more sodas compared to no consumption). Even those drinking alcohol at ‘safe levels’ should consider cutting down or stopping, with any alcohol intake likely to increase the risk of MASLD (aOR: 1.02; 95% CI: 1.02, 1.03, for each gram of alcohol/day). The deleterious effect of alcohol is reinforced by the added significant risk of fibrosis (defined as dAAR >1.5708) associated with alcohol within ‘safe limits’ (aOR of fibrosis 1.02; 95% CI: 1.01, 1.03, for each gram/day of alcohol consumed). However, although increased exercise and reduced soda intake showed a trend towards reduced fibrosis risk, this does not meet statistical significance. This highlights the importance of ensuring individuals identified at high risk of advanced fibrosis are referred to appropriate specialist services for further fibrosis assessment and consideration of anti-obesity or newer anti-fibrotic agents, alongside being offered targeted lifestyle advice and support. More surprisingly, and contrary to previous meta-analyses [6, 7], the data here do not support high coffee intake as being protective against MASLD. In fact, the authors demonstrate an increased risk of MASLD associated with coffee intake of one or more cups daily and a dose-dependent increasing risk up to four or more cups per day (aOR: 1.73; 95% CI: 1.41, 2.13). In addition, a non-significant trend towards increased fibrosis risk with coffee consumption was also seen (aOR: 1.37, 95% CI: 0.97, 1.90; p 0.065) for those drinking four or more cups of coffee daily compared to non-coffee drinkers. This study has a number of notable limitations, acknowledged by the authors. A relatively insensitive CT threshold of <48 Hounsfield units to define steatosis is likely to have underestimated the prevalence of steatosis in the study population and led to misclassification of some MASLD patients as non-MASLD. In addition, the absence of platelet counts meant FIB-4, the guideline-recommended fibrosis screening tool, could not be calculated, necessitating the choice of the dAAR to define those at risk of fibrosis. This has a relatively modest positive predictive value compared to FIB-4 and other non-invasive modalities such as transient elastography. Self-reporting of alcohol consumption, as opposed to objective biomarkers such as phosphatidylethanol, has been demonstrated to risk underestimation of alcohol intake and possible misclassification of MASLD [8]. As alcohol is a risk factor for both fibrosis and hypertension, alcohol underreporting is a potential explanation for the higher risk of fibrosis encountered in people with hypertension in this cohort. In addition, at least in some populations, coffee drinkers are more likely to consume alcohol than non-coffee drinkers [9], which could also be an explanation for some of the excess MASLD and fibrosis risk associated with coffee drinking demonstrated in the study. Despite these limitations, Nabi O., Spaak J. and Bergström G. et al. provide an important indicator of the potential prevalence of MASLD and those at risk of MASLD fibrosis in a large population sample. The study adds to the evidence base of risk factors for, and lifestyle changes protective against, MASLD and fibrosis, allowing clinicians to make clear, actionable recommendations to patients. Finally, the higher risk of fibrosis associated with hypertension compared to T2D and the possible harmful effect of coffee are significant novel findings and should prompt further investigation. In the meantime, clinicians can confidently tell their patients, if they wish to avoid MASLD and its complications, ‘put down your soda, get off the couch and walk past the bar’. The authors declare no conflicts of interest.