DHM (dihydromyricetin / ampelopsin)
Detox · Flavonoid / α1-GABA-A modulator
Tier C+
Bottom line
Read Off Label grades DHM (dihydromyricetin / ampelopsin) as C+ (5.3/10) based on preclinical evidence, unclear benefit magnitude, and a low-risk safety profile.
Dihydromyricetin (DHM) is a flavonoid most concentrated in Hovenia dulcis (Japanese raisin tree) and Ampelopsis grossedentata (vine tea) — both used in traditional East Asian medicine for alcohol-related complaints.
Studied, labeled, or reported-use context: 300-500 mg PO with first drink and/or before bed; typical biohacker protocols 300-1000 mg total/day;… — OTC dietary supplement (US/EU/Asia); not FDA-approved for any indication; sold as the active ingredient in branded "anti-hangover" products including Cheers, Flyby, NeverLate; not individualized guidance.
What the evidence says
Dihydromyricetin (DHM) is a flavonoid most concentrated in Hovenia dulcis (Japanese raisin tree) and Ampelopsis grossedentata (vine tea) — both used in traditional East Asian medicine for alcohol-related complaints. Modern interest dates to Shen 2012 (J Neurosci) which demonstrated DHM as a positive allosteric modulator at α1-containing GABA-A receptors that competes with ethanol — explaining the rodent reduction in voluntary intake, intoxication, and withdrawal severity. **Human translation gap is the central decision input**: a peer-reviewed double-blind placebo-controlled hangover RCT found NO significant effect on hangover severity, and a separate pharmacokinetic study found no effect on alcohol metabolism. Despite this, multiple supplement brands (Cheers, Flyby, NeverLate) market DHM-based products with strong claims. A 2021 PubMed review of 82 commercial hangover products found NONE had peer-reviewed human data supporting their claims. **Evidence summary**: preclinical pharmacology supports a plausible mechanism involving ALDH2; human trials did not show reliable hangover prevention and short-term safety data remain limited. Distinct from the broader Hovenia dulcis tradition — DHM is a single purified flavonoid, while traditional Hovenia preparations contain multiple constituents. A 2026 systematic review of DHM across alcohol-attributed conditions is the clearest available statement of where this evidence actually sits: **22 studies, of which 8 were in vitro, 17 in vivo, and only 2 clinical**. Across models DHM consistently attenuated ethanol-induced cytotoxicity, oxidative stress, inflammation and hepatic steatosis, improved AST/ALT, and modulated Nrf2 and AMPK. The review was unregistered with no prior protocol and performed no meta-analysis because heterogeneity precluded it. For a compound sold largely as a hangover product, the operative fact is the 2-out-of-22 clinical share — this row's `Preclinical` rating is exactly right and this review is the citation that demonstrates it rather than asserting it.
Mechanism
Flavonoid (ampelopsin) from Hovenia dulcis (Japanese raisin tree) and Ampelopsis grossedentata (Chinese vine tea); positive allosteric modulator at α1-containing GABA-A receptors — competes with ethanol at the benzodiazepine site (Shen 2012 J Neurosci); upregulates hepatic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH2) expression to accelerate acetaldehyde clearance — particularly relevant for the ~36% of East Asians with ALDH2 deficiency ("Asian flush"); also reduces hepatic steatosis in preclinical models
Studied, labeled, or reported dose & route
300-500 mg PO with first drink and/or before bed; typical biohacker protocols 300-1000 mg total/day; lower-bound products use ~100 mg
This records doses and routes described in studies, approved labeling, clinical practice, or documented use. It is not individualized guidance and does not establish safety; context changes with indication, formulation, health history, monitoring, and other medicines.
Citations
- pmc.ncbi.nlm.nih.gov
- jneurosci.org
- ncbi.nlm.nih.gov
- PubMed · PMID 34225031
- today.usc.edu
- DOI · 10.3390/nu18142221
A link means the source informed this entry; it does not mean every claim on the page comes from that source. If a citation looks wrong or you want a claim re-checked, send a correction.
Common questions
- What does the evidence show about DHM (dihydromyricetin / ampelopsin)'s effects?
- Read Off Label rates the evidence for DHM (dihydromyricetin / ampelopsin) as Preclinical and the benefit magnitude as unclear, producing an overall grade of C+ (5.3/10). Dihydromyricetin (DHM) is a flavonoid most concentrated in Hovenia dulcis (Japanese raisin tree) and Ampelopsis grossedentata (vine tea) — both used in traditional East Asian medicine for alcohol-related complaints.
- What safety findings are reported for DHM (dihydromyricetin / ampelopsin)?
- DHM (dihydromyricetin / ampelopsin) has a low risk profile in the database. Low (no serious AEs reported; benzodiazepine-site GABA-A modulation theoretical tolerance/dependence concerns at chronic high doses — not documented; very rare hepatotoxicity case reports for Hovenia dulcis-containing supplements per NIH LiverTox) Legal status: OTC dietary supplement (US/EU/Asia); not FDA-approved for any indication; sold as the active ingredient in branded "anti-hangover" products including Cheers, Flyby, NeverLate.
- What doses or routes are reported for DHM (dihydromyricetin / ampelopsin)?
- 300-500 mg PO with first drink and/or before bed; typical biohacker protocols 300-1000 mg total/day; lower-bound products use ~100 mg This is context from studies, approved labeling, clinical practice, or documented use; it is not individualized guidance and does not establish safety.
- How does DHM (dihydromyricetin / ampelopsin) work?
- Flavonoid (ampelopsin) from Hovenia dulcis (Japanese raisin tree) and Ampelopsis grossedentata (Chinese vine tea); positive allosteric modulator at α1-containing GABA-A receptors — competes with ethanol at the benzodiazepine site (Shen 2012 J Neurosci); upregulates hepatic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH2) expression to accelerate acetaldehyde clearance — particularly relevant for the ~36% of East Asians with ALDH2 deficiency ("Asian flush"); also reduces hepatic steatosis in preclinical models
This is an independent synthesis of published research by a non-clinician. Scores are opinions supported by citations, not prescriptions. See the full disclaimer and methodology for how this score was produced and what it does and doesn't mean.