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Here, we propose a hypothesis of how early mitochondrial adaptations for alcohol metabolism lead to<jats:styled-content style=\"fixed-case\">ALD<\/jats:styled-content>pathogenesis. Acutely, ethanol (EtOH) feeding causes a near doubling of hepatic EtOH metabolism and oxygen consumption within 2 to 3\u00a0hours. This swift increase in alcohol metabolism (<jats:styled-content style=\"fixed-case\">SIAM<\/jats:styled-content>) is an adaptive response to hasten metabolic elimination of both EtOH and its more toxic metabolite, acetaldehyde (AcAld). In association with<jats:styled-content style=\"fixed-case\">SIAM<\/jats:styled-content>, EtOH causes widespread hepatic mitochondrial depolarization (mtDepo), which stimulates oxygen consumption. In parallel, voltage\u2010dependent anion channels (<jats:styled-content style=\"fixed-case\">VDAC<\/jats:styled-content>) in the mitochondrial outer membrane close. Together,<jats:styled-content style=\"fixed-case\">VDAC<\/jats:styled-content>closure and respiratory stimulation promote selective and more rapid oxidation of EtOH first to AcAld in the cytosol and then to nontoxic acetate in mitochondria, since membrane\u2010permeant AcAld does not require<jats:styled-content style=\"fixed-case\">VDAC<\/jats:styled-content>to enter mitochondria.<jats:styled-content style=\"fixed-case\">VDAC<\/jats:styled-content>closure also inhibits mitochondrial fatty acid oxidation and<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>release, promoting steatosis and a decrease in cytosolic<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>. After acute EtOH, these changes revert as EtOH is eliminated with little hepatocellular cytolethality. mtDepo also stimulates mitochondrial autophagy (mitophagy). After chronic high EtOH exposure, the capacity to process depolarized mitochondria by mitophagy becomes compromised, leading to intra\u2010 and extracellular release of damaged mitochondria, mitophagosomes, and\/or autolysosomes containing mitochondrial damage\u2013associated molecular pattern (mt<jats:styled-content style=\"fixed-case\">DAMP<\/jats:styled-content>) molecules. mt<jats:styled-content style=\"fixed-case\">DAMP<\/jats:styled-content>s cause inflammasome activation and promote inflammatory and profibrogenic responses, causing hepatitis and fibrosis. We propose that persistence of mitochondrial responses to EtOH metabolism becomes a tipping point, which links initial adaptive EtOH metabolism to maladaptive changes initiating onset and progression of<jats:styled-content style=\"fixed-case\">ALD<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/acer.13877","type":"journal-article","created":{"date-parts":[[2018,8,22]],"date-time":"2018-08-22T15:57:01Z","timestamp":1534953421000},"page":"2072-2089","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":55,"title":["A Unifying Hypothesis Linking Hepatic Adaptations for Ethanol Metabolism to the Proinflammatory and Profibrotic Events of Alcoholic Liver Disease"],"prefix":"10.1111","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2377-0070","authenticated-orcid":false,"given":"Zhi","family":"Zhong","sequence":"first","affiliation":[{"name":"Department of Drug Discovery and Biomedical Sciences Medical University of 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