Non-alcoholic Fatty Liver Disease and Alcohol-Related Liver Disease: Two Intertwined Entities
Open accessAbstract
Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide, with a prevalence of 25-30%. Since its first description in 1980, NAFLD has been conceived as a different entity from alcohol-related fatty liver disease (ALD), despite that, both diseases have an overlap in the pathophysiology, share genetic-epigenetic factors, and frequently coexist. Both entities are characterized by a broad spectrum of histological features ranging from isolated steatosis to steatohepatitis and cirrhosis. Distinction between NAFLD and ALD is based on the amount of consumed alcohol, which has been arbitrarily established. In this context, a proposal of positive criteria for NAFLD diagnosis not considering exclusion of alcohol consumption as a prerequisite criterion for diagnosis had emerged, recognizing the possibility of a dual etiology of fatty liver in some individuals. The impact of moderate alcohol use on the severity of NAFLD is ill-defined. Some studies suggest protective effects in moderate doses, but current evidence shows that there is no safe threshold for alcohol consumption for NAFLD. In fact, given the synergistic effect between alcohol consumption, obesity, and metabolic dysfunction, it is likely that alcohol use serves as a significant risk factor for the progression of liver disease in NAFLD and metabolic syndrome. This also affects the incidence of hepatocellular carcinoma. In this review, we summarize the overlapping pathophysiology of NAFLD and ALD, the current data on alcohol consumption in patients with NAFLD, and the effects of metabolic dysfunction and overweight in ALD.
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Aberrant lipid handling causes the intracellular accumulation of potentially toxic bioactive lipid species in hepatocytes, an essential phenomenon in both MASH and ASH.
“Aberrant lipid handling causes the intracellular accumulation of potentially toxic bioactive lipid species in hepatocytes; an essential phenomenon in both MASH and ASH(201).”
From The liver as a central "hub" of the immune system: pathophysiological implications (2025) · cites this paper as [201]
The ‘Hepatic Fat Accumulation and Lipotoxicity’ section says dysregulated hepatic lipid flux leads to accumulation of triglycerides and other lipids in both NAFLD and ALD, and identifies harmful lipid species involved in lipotoxicity. It calls lipotoxicity important in NAFLD/NASH, but says the phenomenon is not well characterized in ALD and evidence about intrahepatic lipid species and their effects is scarce. Thus, it does not establish the claimed essential role in both MASH and ASH. (LLM, conf=0.88)
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Alcoholic Liver Disease and Apoptosis
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The Role of Autophagy in Liver Diseases: Mechanisms and Potential Therapeutic Targets
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Self-citationRESPONSE TO ALCOHOL IN CHRONIC ALCOHOLICS WITH LIVER DISEASE
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Nonalcoholic Fatty Liver Disease versus Alcohol-related Liver Disease: Is it Really so Different?
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Alcoholic Liver Disease and Apoptosis
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Oxidative Stress in Liver Pathophysiology and Disease
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Alcohol consumption and metabolic syndrome: clinical and epidemiological impact on liver disease
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Self-citationDiet and exercise in NAFLD/NASH: Beyond the obvious
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Insights into Nonalcoholic Fatty-Liver Disease Heterogeneity
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PNPLA3 as a therapeutic target for fatty liver disease: the evidence to date
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The liver as a central "hub" of the immune system: pathophysiological implications
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Epidemiology of Alcohol-Associated Liver Disease
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Effect of Probiotics Therapy on Nonalcoholic Fatty Liver Disease
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Metabolic and alcohol-associated liver disease (MetALD): a representation of duality
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Alcohol-Associated Liver Disease: Evolving Concepts and Treatments
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Global epidemiology of alcohol‐associated liver disease in adolescents and young adults
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Self-citationEfficacy and safety of obeticholic acid in liver disease—A systematic review and meta-analysis
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Self-citationManagement of Portal Hypertension
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MetALD : New Perspectives on an Old Overlooked Disease
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Self-citationHepatoprotection of capsaicin in alcoholic and non-alcoholic fatty liver diseases
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Nutritional Approaches in Children with Overweight or Obesity and Hepatic Steatosis
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Managing cirrhosis with limited resources: perspectives from sub-Saharan Africa
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Subclinical versus advanced forms of alcohol-related liver disease: Need for early detection
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Regulation of Cytochrome c Oxidase by Natural Compounds Resveratrol, (–)-Epicatechin, and Betaine
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The Tumor Microenvironment of Hepatocellular Carcinoma: Untying an Intricate Immunological Network
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Concomitant western diet and chronic-binge alcohol dysregulate hepatic metabolism
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Plasticity of monocytes and macrophages in cirrhosis of the liver
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Liquid Liver Biopsy for Disease Diagnosis and Prognosis
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Type I and II interferon signaling in colorectal cancer liver metastasis
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Mineralocorticoid receptor modulation by dietary sodium influences NAFLD development in mice
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Self-citationThe bidirectional impacts of alcohol consumption and MAFLD for progressive fatty liver disease
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Self-citationAnti-miR-873-5p improves alcohol-related liver disease by enhancing hepatic deacetylation via SIRT1
Agudo, R. R., González‐Recio, I., Serrano‐Maciá, M., Bravo, M., Petrov, P., Blaya, D., Herranz, J. M., Mercado-Gómez, M., Rejano-Gordillo, C. M., Lachiondo‐Ortega, S., et al. (2023) · JHEP Reports · doi:10.1016/j.jhepr.2023.100918 · Cited by 13 · see citing works
An update on the genetics of alcoholic liver disease
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Self-citationHigh prevalence of liver fibrosis among general population: a Romanian population-based study
Trifan, A. V., Muzica, C. M., Năstasă, R., Zenovia, S., Stratina, E., Stafie, R., Rotaru, A., Sîngeap, A.-M., Cojocariu, C., Sfarti, C. V., et al. (2023) · Hepatology Communications · doi:10.1097/hc9.0000000000000032 · Cited by 13 · see citing works
Intensive Care Unit Care of a Patient with Cirrhosis
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Self-citationLean MASLD and Cardiovascular Disease: A Review
Lebovics, N., Heering, G., Frishman, W. H., & Lebovics, E. (2025) · Cardiology in Review · doi:10.1097/crd.0000000000000893 · Cited by 11 · see citing works
Liver Transplantation in Acute-on-Chronic Liver Failure
Kulkarni, A. V., & Reddy, K. R. (2023) · Clinics in Liver Disease · doi:10.1016/j.cld.2023.03.015 · Cited by 11 · see citing works
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cAMP–PKA/EPAC signaling pathways: crucial regulators of lipid homeostasis
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Kulkarni, A. V., Wall, A. E., Reddy, K. R., & Bittermann, T. (2024) · Liver Transplantation · doi:10.1097/lvt.0000000000000448 · Cited by 6 · see citing works
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Terlipressin in the management of adults with hepatorenal syndrome-acute kidney injury (HRS-AKI)
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Kupffer cells are protective in alcoholic steatosis
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- Authors
- Idalsoaga, F., Kulkarni, A. V., Mousa, O. Y., Arrese, M., & Arab, J. P.
- Affiliations
- Pontificia Universidad Católica de Chile (CL)
- Asian Institute of Gastroenterology (IN)
- Mayo Clinic (US)
- Corresponding author
- Arab, Juan Pablo
- Venue
- Frontiers in Medicine
- Publisher
- Frontiers Media SA
- Published
- 2020-08-20
- Volume
- 7
- Pages
- 448-448
- ISSN
- 2296-858X (ISSN-L)
- PMC
- PMC7468507
- OpenAlex
- W3080530345
- Cited by
- 136
- References
- 206
- Citations by year
- 2026: 14 · 2025: 23 · 2024: 23 · 2023: 26 · 2022: 32 · 2021: 17
- FWCI
- 2.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Fondo Nacional de Desarrollo Científico y Tecnológico (1191145, 1200227)
- Consejo Nacional de Innovación, Ciencia y Tecnología (AFB170005)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- non-alcoholic fatty liver disease, alcoholic liver disease, alcohol consumption, steatohepatitis, liver cirrhosis, metabolic dysfunction, obesity, metabolic syndrome, hepatocellular carcinoma, pathophysiology, disease progression
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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