©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Biol Chem. Dec 5, 2025; 16(4): 111831
Published online Dec 5, 2025. doi: 10.4331/wjbc.v16.i4.111831
Published online Dec 5, 2025. doi: 10.4331/wjbc.v16.i4.111831
Fatty liver reexamined choline and mitochondrial toxin amelioration
Joseph Mercola, Independent Researcher, Midwestern University, Downers Grove, IL 60515, United States
Author contributions: Mercola J was the sole author responsible for study conception and design, data acquisition and interpretation, manuscript preparation and revision, final approval of the version to be published, and agrees to be accountable for the integrity of the work in all respects.
Conflict-of-interest statement: I have no conflicts of interests.
Corresponding author: Joseph Mercola, Researcher, Independent Researcher, Midwestern University, 555 31 Street, Downers Grove, IL 60515, United States. drm@mercola.com
Received: July 10, 2025
Revised: July 22, 2025
Accepted: October 27, 2025
Published online: December 5, 2025
Processing time: 147 Days and 12.4 Hours
Revised: July 22, 2025
Accepted: October 27, 2025
Published online: December 5, 2025
Processing time: 147 Days and 12.4 Hours
Core Tip
Core Tip: This review recasts fatty liver disease as a reversible mitochondrial toxicosis driven by linoleic acid (LA) and ethanol when choline intake is inadequate. It collates pre-clinical and pilot clinical evidence showing that bioavailable, gutmicrobial trimethylamineNoxide-sparing choline carriers (citicoline, αglycerophosphocholine), together with LA restriction or alcohol abstinence, restore phosphatidylcholine/phosphatidylethanolamine balance, revive hepatic respiration and shrink intrahepatic fat. This dual nutrition-first approach targets the root bioenergetic defect, offering a low-risk route to halt steatosis progression and warrants large, randomized trials.