What DHM Is

DHM (dihydromyricetin) is a flavonoid compound found in the Japanese raisin tree (Hovenia dulcis) and in Chinese vine tea (Ampelopsis grossedentata). It has been part of traditional Asian medicine for roughly a thousand years, originally as a hangover-and-liver remedy made from the dried fruit and stems of the tree. Modern research caught up to traditional use slowly through the 1980s and 1990s, accelerated in the 2000s, and produced the foundational pharmacological work in the early 2010s1.

DHM is not a "miracle hangover cure." It is a flavonoid with a specific set of effects on liver enzymes, GABA receptors, and oxidative stress pathways. Some of those effects are well-supported in animal studies. Others have weaker human translation. The point of this section of the site is to be honest about which is which.

Older papers often call DHM ampelopsin; it is the same compound. Beyond the enzyme question below, one line of research looks at the liver itself: in a 2023 mouse study from the University of Southern California, DHM given to mice on an alcohol diet improved their liver enzymes (AST and ALT), lowered blood fats and reduced inflammatory markers5. None of this makes DHM a license to drink more. What the animal evidence points to, with mixed results, is help processing what you have already drunk, not a shield while you drink. I started testing DHM at 300mg and worked up.

For the longer version, see What Is DHM.

What Animal Studies Show at the Liver Enzyme Level

The headline mechanism is enzyme induction, and the evidence for it comes from animal studies with mixed results. In a 2020 mouse study, injected DHM raised the two liver enzymes that actually metabolize alcohol -- alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) -- restored the NAD+ cofactor that ethanol metabolism depletes, and lowered blood ethanol and acetaldehyde after alcohol 4. A 2020 rat study that gave DHM by mouth found no change in ADH and no drop in blood ethanol or acetaldehyde 2. No study has measured this in people.

If it holds up, this is the part of DHM's profile that would distinguish it most cleanly from other "liver support" ingredients, most of which work as antioxidant buffers downstream of the metabolic damage rather than on the metabolism itself. (it took me about a month of reading to decide the published animal data was worth betting on, honestly, mixed results and all.)

For the full mechanism breakdown, see How DHM Works: The ADH/ALDH Pathway.

The Dose Question

1,500mg is where my testing settled: my own tests, and what I saw directly in the people I tested with. No study was used to set it.

DHM is not cheap, and 1,500mg per serving is meaningfully more expensive to make than a smaller amount. Going higher did not justify the cost per serving.

For where the number came from and what the published studies can and cannot tell you, see DHM Dose-Response.

DHM and Anxiety: The GABA Side

DHM also acts on the GABA-A receptor system in the brain, which is the receptor system alcohol primarily targets. DHM is a positive modulator at the benzodiazepine binding site but, unlike actual benzodiazepines, it does not sedate at the doses that block alcohol's effects on the receptor. This combination matters because the morning-after anxiety that comes after even moderate drinking is largely a GABA-rebound story.

Animal studies show DHM blunts both the acute alcohol response and the withdrawal-related anxiety that follows it, in the data we have so far at least. The mechanism is reproducible across labs but the human clinical data on DHM specifically for anxiety is still thin.

For the full GABA story, see DHM and GABA Modulation.

DHM and Brain Aging

A separate line of DHM research focuses on neuroprotection and brain aging rather than acute alcohol effects. DHM crosses the blood-brain barrier, suppresses microglial inflammation in mouse models of Alzheimer's disease, and activates the AMPK/SIRT1 signaling pathway that protects against age-related neuronal stress3. The brain-aging research is preclinical only -- there are no human clinical trials of DHM for cognitive outcomes -- but the mechanisms are real and consistent across labs.

This research is part of why we feel comfortable building the formula around DHM long-term. The compound has supporting evidence well outside the acute alcohol use case.

For the full brain-aging story, see DHM and Brain Aging.

How DHM Compares to Other Liver Supplements

The three ingredients DHM most often gets compared against are milk thistle, prickly pear cactus extract, and N-acetylcysteine. Each has its own mechanism story and its own evidence base, and each has a different relationship to alcohol metabolism specifically.

Milk thistle (silymarin) has decent evidence for fatty liver disease but weak evidence for alcohol-related outcomes. Prickly pear has one famous JAMA hangover study but works on inflammation rather than metabolism. NAC works mechanistically as a glutathione precursor but the human hangover-prevention trials are mixed and the effective dose is in the gram range. None of these is reported to act on ADH or ALDH; DHM was, in a 2020 mouse study4, though a 2020 rat study that gave DHM by mouth found no change in ADH2. That is the published-evidence difference, and it is still an animal-only one.

For the head-to-head pages, see DHM vs. Milk Thistle, DHM vs. Prickly Pear, and DHM vs. NAC.

The Bioavailability Problem and the Delivery Solution

DHM is poorly absorbed when swallowed, at least in animals: the usual figure, about 4 percent oral bioavailability, comes from rats. The molecule is poorly water-soluble and chemically unstable in the gut. We pair DHM with fulvic acid, which functions as a cellular delivery agent through chelation chemistry.

The fulvic acid pairing is the part of the formula architecture that people ask about the least but that probably contributes the most to whether a given dose works for a given person. Bioavailability is a quiet variable, and also one of the most important ones.

For the full bioavailability story, see DHM Bioavailability. For the fulvic acid delivery mechanism, see DHM and Fulvic Acid -- The Delivery Mechanism.

Where the Claims Land

Acts by promoting aldehyde and alcohol metabolism of foods.†

† These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Helps you feel fresh.†

† These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Supports overall liver health.†

† These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

The structure-function claims H180 is permitted to make about DHM are narrow and specific. They follow the same metabolic pathway the published animal research describes, they are the claims we are confident defending in front of FDA reviewers, and they are the ones every sub-page in this cluster ties back to.