What ADH and ALDH Are
Alcohol dehydrogenase (ADH) is a family of zinc-containing enzymes that catalyze the oxidation of primary alcohols (including ethanol) to their corresponding aldehydes. In the human liver, ADH1A, ADH1B, and ADH1C are the three isoforms that handle most ethanol metabolism, with each isoform having slightly different kinetic properties1. Aldehyde dehydrogenase (ALDH) is a separate enzyme family that catalyzes the oxidation of aldehydes (including acetaldehyde, the product of ADH activity on ethanol) to their corresponding carboxylic acids. ALDH2 in the mitochondrial matrix is the dominant isoform for acetaldehyde clearance in the liver.
The two enzymes work in sequence. Ethanol enters the hepatocyte, ADH converts it to acetaldehyde, ALDH converts acetaldehyde to acetate, and the acetate enters general metabolism for breakdown into water and carbon dioxide. The pathway is short, the chemistry is well-mapped, and the rate-limiting step is usually ALDH at higher alcohol loads1.
Why the Genetic Variants Matter
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.
The clearest evidence that ADH and ALDH activity matters comes from the genetic variant literature. The ALDH2 variant common in some East Asian populations produces an enzyme with substantially reduced acetaldehyde-clearance activity. Carriers of the variant convert ethanol to acetaldehyde at normal speed but cannot clear the acetaldehyde efficiently, and the symptom severity (the so-called Asian flush response, but also longer-term elevated cancer risk) scales almost exactly with how much acetaldehyde accumulates2. The natural-experiment evidence that ALDH activity drives outcomes is unusually strong for this part of the cascade.
(this is the part of the biochemistry that finally made the formula click for me, because the upstream enzyme leverage point is more powerful than the downstream antioxidant buffering.)
What DHM Does to ADH and ALDH
Triggers the liver to produce more of the aldehyde- and alcohol-metabolizing enzymes (ADH and ALDH) and boosts their efficiency in breaking down aldehydes and alcohols in foods as well as their by-products.†
† 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 2012 UCLA paper from Shen and colleagues showed that DHM administration in rats induces expression of both ADH1 and ALDH2 in liver tissue, and reduces serum ethanol and acetaldehyde concentrations after alcohol challenge3. A 2020 follow-up confirmed the induction effect and added detail on the lipid-metabolism downstream effects of accelerated ethanol clearance4. The enzyme-induction effect is reproducible across multiple labs, in the published rodent data at least.
The "boosts their efficiency" language in the H180 claim ties to two distinct things in the underlying literature: more enzyme molecules per cell (induction at the protein-expression level) and better substrate-handling per enzyme molecule (often through cofactor restoration -- DHM also helps restore the NAD+ that ADH and ALDH both require to function).
The AST/ALT Connection
Lowers liver enzyme (AST and ALT) levels that are already in the normal range.†
† 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.
AST and ALT are different enzymes from ADH and ALDH (different metabolic functions, different cellular locations) but they serve as serum markers of hepatocellular stress. When DHM is administered to animals during ethanol exposure, AST and ALT levels move toward normal compared to ethanol-only controls4. The mechanism is indirect -- faster acetaldehyde clearance via ADH/ALDH induction means less collateral cellular damage means lower AST/ALT release into serum. The two pieces of the claim are connected through the same upstream enzyme-induction story.
What This Page Is Not Claiming
The enzyme-induction claim is bounded ot what the published animal mechanism literature supports, in DSHEA-compliant terms. We are not claiming DHM cures genetic ALDH2 deficiency, treats alcohol use disorder, or replaces the liver's natural enzyme function. The claim is that DHM upregulates the two enzymes that perform aldehyde and alcohol metabolism, and the result is faster substrate clearance.
For the full mechanism in detail, see How DHM Works -- The ADH/ALDH Pathway. For the headline aldehyde-metabolism claim this maps to, see Aldehyde Metabolism Explained.