ALDH2 saturation
Alcohol metabolism has a bottleneck. ADH can generate acetaldehyde faster than ALDH2 can clear it. Once ALDH2 saturates, the whole system backs up.
What is happening
Why the bottleneck matters
The ethanol-to-acetaldehyde step is relatively fast. The acetaldehyde-to-acetate step is slower and easier to overwhelm. Hangover biology starts when production outruns clearance.
Ingredients that address this, ranked
- L-Cysteine Tier 1 · Core Impact: high — Chemical trap for acetaldehyde at the source.
- DHM (Dihydromyricetin) Tier 1 · Core Impact: high — Accelerates alcohol clearance; blunts GABA rebound.
- Sulforaphane Tier 1 · Core Impact: high — Nrf2 activator; upregulates ALDH2 before drinking.
How tiers compare for this mechanism
| Goal | Best (Tier 1) | Strong support (Tier 2) | Situational (Tier 3+) |
|---|---|---|---|
| Acetaldehyde clearance | L-Cysteine, DHM (Dihydromyricetin), Sulforaphane | Ubiquinol (CoQ10) | |
| Glutathione support | L-Cysteine, Sulforaphane | ||
| Liver protection | L-Cysteine, DHM (Dihydromyricetin), Sulforaphane | Ubiquinol (CoQ10) | |
| Neurotransmitter modulation | DHM (Dihydromyricetin) | ||
| Ros mitigation | Ubiquinol (CoQ10) |
Deeper science · In more detail
What saturation looks like
Once ALDH2 is operating at full capacity, additional ethanol no longer increases clearance proportionally. It only increases upstream acetaldehyde exposure. That is why "just speed up the enzyme" is not a complete recovery strategy.
Why the protocol layers matter
The protocol compensates for ALDH2 saturation by spreading the burden across multiple routes:
- L-cysteine adds a direct chemical trap.
- DHM and sulforaphane
support the enzymatic side.
- Ubiquinol protects mitochondrial ALDH2 from
oxidative damage over a long night.
Rate-limiting means the queue grows upstream
A saturated downstream enzyme does not merely "work harder." It forces the substrate pool behind it to grow. In this case the substrate is acetaldehyde, which is exactly the molecule the protocol is trying to minimize.
Genetics amplifies the bottleneck
Some people inherit lower-function ALDH2 variants. They start with a tighter bottleneck, which means the same ethanol load produces higher acetaldehyde exposure faster.