One of the established emergency room protocols for alcohol poisoning is the intravenous administration of GSH, often combined with B vitamins (so-called “banana bag). Medical school teaching and clinical practice have for decades claimed that alcohol lowers GSH and the drop in GSH is what causes a lot of the damage to internal organs such as the liver as a result of alcohol abuse. I have always wondered what the rationale for this “treatment” was considering the simple biochemical fact that alcohol is a reductant and as such it is expected to shift the redox ratio towards reduction and as such increase relevant redox biomarkers such as the NADH/NAD+, beta-hydroxybutyrate/acetoacetate, lactate/pyruvate and GSH/GSSG ratios, thus making additional supplementation with GSH at best unnecessary and at worst harmful. Yet, the doctors I have been discussing this with as well as many of the already published studies continue to push the narrative that more (not less) GSH is needed, not only for alcohol abuse treatment but for various chronic conditions and aging itself. The study below is one of the few (that I am aware of) that directly shows alcohol raising GSH, depleting GSSG and thus robustly raising the GSH/GSSG ratio. Since a shift in the redox ratio towards reduction has an inhibitory effect on OXPHOS, the regeneration of NAD+ from NADH would also be inhibited, thus directly inhibiting alcohol (and overall) metabolism since alcohol metabolism depends on two enzymes dependent on NAD+ – namely, alcohol dehydrogenase and aldehyde dehydrogenase). Thus, it seems prudent to treat alcohol abuse with NAD+ precursors such as niacinamie and/or oxidizing agents such as quinones, as those shift the redox ratio towards oxidation. On a related note, since now elevated GSH is known to be a driving factor in cancer, this findings suggests that alcohol’s promoting effects on cancer (when consumed in excess) are largely metabolic in origin.
https://microbialcellfactories.biomedcentral.com/articles/10.1186/s12934-025-02864-0
“…Activities of SOD and CAT were subsequently measured after ethanol treatment, revealing that ethanol stress significantly enhanced their activities (Fig. 2A and B). We also measured the contents of GSH and GSSG, and the GSH/GSSG ratio under ethanol stress. As demonstrated in Fig. 2C and E, the GSH content and GSH/GSSG ratio increased significantly, while the GSSG content decreased significantly…”
