DHM (Dihydromyricetin)
Also known as: DHM, Ampelopsin, Hovenia dulcis extract.
Rodent ADH/ALDH2 activation (Shen 2012) and GABA-A modulation are well characterized, but two human RCTs (Mackus 2020, n=83; Scholey 2021, n=20) failed to replicate symptom reduction. Possibly a bioavailability or formulation issue — liposomal forms haven't been tested in human trial. Tier 2 because the mechanism is plausible but the human evidence base does not yet support a Tier 1 core claim.
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
Trial evidence is mixed
Rodent data (Shen 2012) is strong for ALDH2/ADH activation. Human RCTs (Mackus et al., Hum Psychopharmacol 2020, n=83; Scholey et al. 2021, n=20) have not replicated the symptom-reduction effect, possibly due to bioavailability or formulation. Liposomal forms may perform better than the standard formulations tested but this is not yet shown in human trial. The protocol retains DHM at Tier 2 because the upstream enzymatic mechanism is well-characterized and the GABA-A rebound effect is independently useful, but the supplement-by-supplement evidence base does not justify a Tier 1 core claim.
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. Whether the liposomal form closes the gap to the rodent data has not been formally tested.
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, when the activation does occur.