Steatotic liver disease: what role does alcohol consumption play?

Metabolic-dysfunction associated steatotic liver disease (MASLD) includes diagnostic criteria such as overweight/ obesity, metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM). MASLD is a subtype of steatotic liver disease (SLD). MASLD is characterized by SLD plus one or more cardiovascular disease (CVD) risks. Metabolic and alcohol-related liver disease (MetALD) is characterized by an alcohol consumption between 20-40 g/day for females and 30-50 gr/day for males and alcohol related liver disease (ALD) is characterized by an alcohol consumption >40 g/day for females and >50 g/day for males. Synergism or a supra-additive interaction between alcohol consumption (AC) and metabolic factors is well known. The aim of this narrative review is to explore the following points: 1) it is mandatory early identification of AC and it is necessary to also identify low dosage of AC; 2) all SLD subtypes increase cardiovascular and oncologic risk; 3) fibrosis is the most important predictor of long term survival. For this reason early liver fibrosis (LF) detection is crucial to reduce hepatic and extra hepatic pathology and motivate the patient to change lifestyle. This narrative review is based on a detailed analysis of the scientific literature published before December 31, 2024 and examining the most recent guidelines on SLD (PubMed, Web of Science, Scopus, Google Scholar). From the data reported in the present narrative review, the following emerges: 1) due to the significant synergistic effect between SLD and alcohol, the cut-off to distinguish MASLD and MetALD should be reduced to 10 g/day for women and 20 g/day for men; 2) it is useful to identify even low doses of consumption. The most appropriate suggestion is total alcohol abstinence (especially in cases with high oncological risk) and even light AC increases the risk of morbidity and mortality expecially in young people; 3) it is necessary to identify LF early and improve lifestyle; 4) cardiometabolic risk factors are present in >90% of subjects with all subtypes of SLD (mainly ALD) and therefore, cardiologists and hepatologists must cooperate; 5) all subjects who come to our attention for the first time (altered liver function, MS, T2DM, CVDs) must undergo ultrasonography with elastography. Subsequent oncologic surveillance beyond rigid schemes must be decided on a case-by-case basis. In cirrhotic patients and in non-cirrhotic patients at high clinical risk, in our opinion surveillance is semi-annual (especially in the presence of T2DM and/or AC). In light of epidemiological data, in medium-low risk cases, for prudence, surveillance can be annual. It is appropriate to raise awareness among health-care professionals and the broader public that SLD is a major risk factor for liver and non-liver disease. It is necessary to combat SLD with prevention and early detection. Early detection of steatosis and fibrosis is a motivating factor for lifestyle correction. The latter represents both primary prevention and therapy in the case of early pathology. This leads to a reduction in cases of decompensated liver disease, cardiovascular and oncologic pathologies with better management of economic resources.