DHM (Dihydromyricetin)
Also known as: DHM, Ampelopsin, Hovenia dulcis extract.
DHM is the rare compound with both an enzymatic-acceleration mechanism (ADH/ALDH2 upregulation) and a neuropharmacological one (GABA-A modulation to blunt rebound anxiety). Human evidence from Hovenia dulcis trials plus animal mechanism work. Tier 1 because it covers two distinct layers with one dose.
Where this fits in the system
What it does
DHM (dihydromyricetin, extracted from Hovenia dulcis) speeds up both stages of ethanol metabolism — ADH and ALDH2 — reducing the peak acetaldehyde concentration that accumulates while drinking. It also acts at GABA-A receptors to reduce the withdrawal-like rebound anxiety that follows alcohol's acute effect.
How it works
Dual mechanism
Most compounds in the protocol operate on one layer. DHM operates on two:
- Metabolic. DHM increases the activity of alcohol dehydrogenase and
aldehyde dehydrogenase in hepatocytes. Net effect: ethanol and acetaldehyde are cleared faster, so less acetaldehyde accumulates at any given drinking rate.
- Neural. DHM modulates GABA-A receptors, the same receptor family
alcohol targets. Animal work suggests it blunts the rebound excitation that follows alcohol clearance — the mechanism behind 3am wakeups and next-day anxiety.
Buying guidance
Liposomal DHM is materially better than powder capsules for this use case. Check the label for actual DHM content per serving — some products report "Hovenia dulcis extract" without specifying DHM concentration, which makes dosing guesswork.
Deep science · DHM (Dihydromyricetin) — deep dive
Why liposomal
Raw DHM has poor oral bioavailability. Liposomal preparations wrap the molecule in phospholipid vesicles that survive gut transit and release DHM into systemic circulation. The Afterburners protocol uses liposomal DHM for the peak-exposure stages (Afterburner, Nightcap, Mayday) and a smaller Debrief dose because the main metabolic rush is over by morning.
GABA-A rebound
Acute alcohol enhances GABA-A activity, producing sedation. The brain adapts by downregulating GABA-A sensitivity. When alcohol clears, the balance shifts toward glutamate excitation — the mechanism behind middle-of-the-night wakefulness, anxiety, and tremor. DHM's partial GABA-A modulation appears to blunt this swing without producing its own sedation during the drinking window.
Enzyme kinetics
DHM upregulates both ADH and ALDH2 rather than inhibiting either. Upregulating only ADH would be dangerous — it would flood the system with more acetaldehyde while ALDH2 remained the bottleneck. Coordinated upregulation is the reason DHM is safe at protocol doses.