Home Supplements That Start With D DHM (Dihydromyricetin): Top Liver Detox Benefits, Hangover Prevention, Proper Dosage, and Safety

DHM (Dihydromyricetin): Top Liver Detox Benefits, Hangover Prevention, Proper Dosage, and Safety

August 28, 2025 Modified date: August 28, 2025

Dihydromyricetin (DHM), also known as ampelopsin, is a flavonoid found in plants like Hovenia dulcis (Japanese raisin tree) and Ampelopsis grossedentata (vine tea). Interest in DHM has grown because early human and animal research suggests it may support liver health, help normalize glucose and lipid markers in metabolic conditions, and influence the brain’s response to alcohol. While it’s widely marketed for “hangover support,” the most rigorous human evidence so far centers on non-alcoholic fatty liver disease (NAFLD), with mixed but promising signals for alcohol-related outcomes from combination formulas. This guide distills what DHM is, how it appears to work, what benefits are supported by studies, practical dosing considerations, and safety—so you can decide, together with your clinician, whether it fits your goals.

Essential Insights for DHM Users

Human RCT in NAFLD used 600 mg/day for 3 months and improved several metabolic and liver markers.
Potential benefit for hangover symptoms is seen with Hovenia dulcis combinations, not DHM alone.
Practical supplemental range: 300–600 mg/day with food; clinical data at 600 mg/day.
Short-term use appears well tolerated; avoid in pregnancy and while breastfeeding due to limited data.

What is DHM and does it work?
What benefits are supported?
How much DHM per day?
How to improve absorption
Is DHM safe and who should avoid it?
Evidence at a glance: strengths and gaps

What is DHM and does it work?

Dihydromyricetin (DHM) is a flavanonol—a subclass of flavonoids—isolated chiefly from Hovenia dulcis fruit and Ampelopsis grossedentata leaves. Beyond its antioxidant profile, DHM has been studied for effects on the central nervous system and the liver. Mechanistically, DHM interacts with γ-aminobutyric acid A (GABA_A) receptors, the primary inhibitory receptors in the brain. In preclinical work, DHM countered ethanol’s potentiation of GABA_A signaling and reduced signs of alcohol intoxication in rodents, likely by modulating receptor subunits and binding at sites influenced by benzodiazepines. That mechanistic signal is one reason DHM shows up in “hangover” products; however, translating this into reliable human outcomes requires more direct clinical trials.

DHM’s hepatic actions appear broader than alcohol-related mechanisms. Animal and cellular studies suggest DHM helps restore oxidative balance and lipid handling in the liver by activating AMP-activated protein kinase (AMPK), sirtuin-1 (SIRT1), and downstream pathways involved in mitochondrial biogenesis, lipophagy, and anti-inflammatory signaling. These pathways matter in conditions like non-alcoholic fatty liver disease (NAFLD) and alcohol-associated liver disease (ALD), where lipid accumulation, oxidative stress, and inflammation drive progression. In mice exposed to ethanol, DHM supplementation improved aminotransferases and blunted inflammatory cytokines while normalizing lipid metabolism markers.

In humans, the most informative trial so far is a randomized, double-blind study in adults with NAFLD that used 600 mg/day DHM for three months and found improvements in liver enzymes, LDL cholesterol, glucose, and insulin resistance indices versus placebo. This suggests DHM can favorably influence metabolic-liver signaling. What we don’t yet have is a large set of trials across diverse populations, long durations, or hard clinical outcomes (e.g., biopsy-verified NASH resolution). For hangover, evidence includes a recent double-blind trial of Hovenia dulcis extract combinations that reduced symptom scores; that formula contained multiple ingredients, so the findings can’t be attributed to DHM alone.

Bottom line: DHM plausibly “works” for specific targets—especially metabolic-liver biomarkers—based on one human RCT and converging mechanistic data, while alcohol-related benefits in humans remain preliminary or confounded by multi-ingredient products. It’s a candidate for consideration when your priorities include metabolic-liver support, with measured expectations and clinician oversight.

What benefits are supported?

Metabolic and liver markers (NAFLD): The best human evidence to date is a randomized controlled trial in NAFLD using 600 mg/day DHM for 12 weeks. Participants experienced significantly greater reductions in alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyl transferase (GGT), fasting glucose, LDL-cholesterol, apolipoprotein B, and HOMA-IR compared with placebo. Several inflammation-related biomarkers also improved (e.g., TNF-α decreased, adiponectin increased). While a single RCT cannot define standard of care, those changes align with preclinical signals and suggest DHM’s potential as an adjunct to diet and exercise for metabolic-liver support.

Alcohol-related outcomes: In rodents, DHM reduced ethanol-induced intoxication and withdrawal features, consistent with GABA_A receptor modulation. In humans, randomized data exist for Hovenia dulcis extract combinations—formulas that include raisin tree extract alongside other botanicals and amino acids. Those trials report improvements in hangover symptom scores and some laboratory measures, but because the products contain multiple active components, the effect cannot be attributed to DHM alone. If your goal is hangover mitigation, product composition, timing, and dose vary widely, and evidence for DHM as a single agent in humans remains limited.

Alcohol-associated liver disease (ALD) signals (preclinical): Animal studies demonstrate hepatoprotective effects under chronic ethanol exposure, with better aminotransferases, less steatosis, and lower inflammatory cytokines after DHM. Molecular pathways involve AMPK/SIRT1 activation, improved lipophagy, and suppression of NF-κB–linked inflammation. These findings are promising but cannot be assumed to apply in human ALD without clinical trials.

Broader antioxidant and anti-inflammatory activity: Across models, DHM scavenges reactive oxygen species, supports mitochondrial function, and modulates inflammatory mediators. These features likely contribute to its liver and metabolic effects and may extend to other tissues; however, clinical confirmation outside NAFLD is sparse. A few early human exploratory studies in other conditions exist but are not yet robust enough to guide practice.

What to expect in practice: If you and your clinician decide to trial DHM for NAFLD-related goals, the most evidence-aligned expectation is modest improvement in routine labs (ALT/AST, LDL, fasting glucose) over ~12 weeks when combined with foundational measures like weight management, diet quality, and activity. For alcohol-related goals, expectations should be conservative; multi-ingredient products may provide symptomatic relief for some people, but DHM’s independent contribution is unclear.

As always, individual responses vary. Track baseline labs, symptoms, and any side effects, and reassess at 8–12 weeks to decide whether to continue.

How much DHM per day?

Studied doses: The clearest human dosing signal comes from the NAFLD RCT: 600 mg/day (two 150 mg capsules, taken twice daily) for 12 weeks. That regimen produced favorable changes in multiple metabolic and liver markers relative to placebo. Outside of that trial, supplement labels typically provide 100–300 mg per capsule, with suggested intakes ranging from 300–600 mg/day for general use. Because product quality and bioavailability can vary, mirroring the 600 mg/day schedule used in the RCT is a reasonable evidence-anchored option when you’re targeting liver-metabolic outcomes and have clinician oversight.

Timing: Take DHM with food to minimize gastrointestinal upset and potentially improve absorption. For those trying DHM around social drinking, products are often taken 30–60 minutes before alcohol and/or again after; however, this timing strategy is based more on tradition and multi-ingredient product protocols than on DHM-only human trials.

Practical starting approach:

General metabolic-liver support: 300 mg/day with food for 1–2 weeks to assess tolerance, then consider increasing to 600 mg/day if needed.
Short-term “event” use (subjective hangover support): If you choose to experiment, many users take 300–600 mg split before and after drinking. Because DHM-only human data are limited here, manage expectations and prioritize harm-reduction basics (hydration, pacing, meals, and safe transport).

Upper limits: There is no established tolerable upper intake level for DHM. Some formulations provide higher daily amounts, but safety data beyond 12–16 weeks are limited. In the absence of medical supervision, it’s prudent not to exceed 600–900 mg/day for extended periods. People with chronic conditions, on multiple medications, or preparing for surgery should discuss DHM with their clinician first.

When to stop: Discontinue if you experience persistent gastrointestinal upset, dizziness, unusual bruising/bleeding, jaundice, dark urine, severe fatigue, or any concerning new symptoms, and seek medical evaluation. Re-check labs (ALT/AST, fasting glucose/lipids) after ~12 weeks if you’re using DHM for metabolic-liver goals; continue only if benefits outweigh risks.

Form and label quality: Choose standardized extracts from reputable manufacturers with third-party testing (e.g., USP, NSF, Informed Choice). Because plant sources and extraction methods vary, actual DHM content and purity can differ between brands.

How to improve absorption

Like many polyphenols, DHM has poor oral bioavailability, influenced by low solubility, rapid metabolism (glucuronidation and sulfation), and a relatively short half-life in animal models. That means a portion of what you swallow may be transformed before reaching systemic circulation, potentially limiting clinical effect. While the NAFLD RCT shows benefit despite these hurdles, you can take practical steps to help:

Take with food. Co-ingestion with a mixed meal—especially containing some fat—can support absorption of lipophilic compounds and reduce stomach upset.
Split doses. Dividing total daily intake (e.g., 300 mg twice daily) may help maintain steadier exposure than a single bolus, aligning with the RCT schedule.
Consider delivery innovations. Some products use liposomes, solid dispersions, or “floating” gastro-retentive tablets designed to increase residence time and bioavailability. Early studies in animals and in vitro suggest improved pharmacokinetics with such technologies, but human comparative data are scarce. If you choose these forms, prioritize brands that disclose technology, excipients, and independent testing.
Pair wisely. Because DHM is metabolized via phase II pathways, theoretical interactions with other polyphenols or supplements that compete for the same enzymes could alter exposure, though robust human evidence is lacking. Avoid stacking multiple high-dose polyphenol blends without medical guidance.
Lifestyle synergy. In NAFLD and metabolic contexts, DHM is an adjunct—not a replacement—for nutrition patterns (e.g., Mediterranean-style), resistance and aerobic training, sleep, and alcohol moderation. These foundational steps often provide larger effect sizes than any supplement and may enhance the likelihood that DHM’s modest pharmacologic signal translates into meaningful outcomes.

Be cautious of exaggerated claims that “megadose” DHM or proprietary blends overcome bioavailability; transparent labeling and realistic expectations serve you better than marketing.

Is DHM safe and who should avoid it?

Overall tolerability: Short-term use of DHM in clinical research has been well tolerated, with no signal for clinically apparent liver injury reported in surveillance resources. In the NAFLD trial, DHM was administered for 12 weeks without major safety concerns. Preclinical toxicology generally indicates a wide margin of safety, though extrapolating animal doses to humans has limits.

Common side effects: When they occur, they’re typically mild—gastrointestinal discomfort (nausea, loose stools), headache, or transient dizziness. Taking DHM with meals and avoiding large first doses can reduce these effects.

Potential interactions and cautions:

CNS-active drugs: Because DHM modulates GABA_A signaling in preclinical models, be cautious if you use benzodiazepines, barbiturates, sedative antihistamines, or other CNS depressants. While DHM’s net effect in animals often counters ethanol’s GABA_A potentiation, we lack definitive human interaction data; discuss with your prescriber.
Diabetes medications: DHM improved insulin resistance markers in a NAFLD RCT. If you’re on glucose-lowering therapy, monitor for additive effects on glycemia when starting DHM.
Hepatic conditions: If you have significant liver disease, consult your hepatologist. Although DHM shows hepatoprotective signals, polyphenol supplements can complicate management or interact with medications.
Surgery/anesthesia: Stop supplements, including DHM, at least 1–2 weeks before planned procedures unless your surgeon says otherwise.

Who should avoid DHM (or use only with specialist guidance):

Pregnant or breastfeeding individuals. There’s insufficient safety data.
Children and adolescents. No established dosing or safety.
People with severe chronic illnesses (advanced liver/kidney disease, bleeding disorders) unless a clinician advises and monitors.
Anyone with prior reactions to Hovenia dulcis, vine tea, or DHM-containing products.

Quality and contamination risks: Choose products with third-party testing to reduce the chance of adulterants or mislabeled doses. Report any suspected adverse reactions to your health authority’s supplement safety portal; this contributes to better post-market surveillance.

Alcohol harm-reduction reminder: No supplement “prevents” intoxication or eliminates risks of impaired driving, injury, or alcohol-related disease. If you drink, apply basic safety practices: pace drinks, hydrate, eat beforehand, plan transportation, and know your personal limits.

Evidence at a glance: strengths and gaps

What’s strongest:

NAFLD: One randomized, double-blind, placebo-controlled human trial using 600 mg/day for 12 weeks improved multiple liver and metabolic biomarkers. This aligns with mechanistic data on AMPK/SIRT1 activation, improved lipophagy, and reduced inflammatory signaling.
Mechanistic plausibility: In animals, DHM normalizes ethanol-perturbed GABA_A signaling and counters intoxication-like behaviors. In hepatic models (ethanol and non-ethanol), DHM reduces oxidative stress and steatosis while improving mitochondrial function and lipid metabolism.

Where evidence is preliminary:

Hangover relief in humans: Positive findings exist for Hovenia dulcis combinations containing multiple actives; DHM’s independent effect in randomized human studies remains to be proven. This matters for setting realistic expectations if you purchase DHM alone.
Alcohol-associated liver disease (ALD): Robust human trials are lacking. Animal data are encouraging but not definitive for clinical practice.

Key limitations:

Bioavailability: DHM’s absorption is modest and metabolism rapid, raising questions about dose-response and formulation differences. Innovative delivery systems may help, but human head-to-head data are sparse.
Duration and diversity: Most data are short-term (≤12–16 weeks) and from limited populations. We need longer studies with diverse participants and clinically meaningful endpoints (e.g., imaging or histology for NASH).
Standardization: Plant source, extraction method, and product quality vary, affecting actual DHM content and pharmacokinetics.

Practical takeaway: If your primary goal is metabolic-liver support, a clinician-supervised trial of 600 mg/day DHM for ~12 weeks is the most evidence-aligned strategy, alongside lifestyle therapy. For alcohol-related symptoms, be cautious with expectations; benefits seen in multi-ingredient formulas don’t isolate DHM’s role, and harm-reduction fundamentals remain essential.

References

Medical Disclaimer

This information is educational and is not a substitute for personalized medical advice, diagnosis, or treatment. Supplements can interact with medicines and underlying conditions. Always speak with your qualified healthcare professional before starting, stopping, or changing any supplement, including DHM. If you are pregnant, breastfeeding, under 18, preparing for surgery, or managing a chronic illness, seek individualized guidance first.

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