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Alcohol and your DNA: ADH1B and ALDH2

Genetics explainer · Updated June 2026

How your body handles a drink is shaped by two genes working in sequence. ADH1B sets how fast alcohol is broken down into acetaldehyde — a toxic byproduct — and ALDH2 sets how fast that acetaldehyde is cleared away. This post leads on the ADH1B "speed" step; for the dramatic flush reaction specifically, see our ALDH2 flush guide.

Quick reference: for genotype-by-genotype breakdowns of the markers in this post, browse the Quanome gene library.

The two-step pathway

Alcohol leaves your body through a short relay of two enzymes:

  1. Alcohol → acetaldehyde, handled mainly by alcohol dehydrogenase (the ADH enzymes, including ADH1B).
  2. Acetaldehyde → acetate (harmless), handled by aldehyde dehydrogenase 2 (ALDH2).

Acetaldehyde is the troublemaker in the middle. It's toxic and classified as a carcinogen, and it's what causes facial flushing, a racing heart, and nausea when it builds up. Whether it accumulates depends on the balance between how fast step one makes it and how fast step two clears it.

ADH1B: how fast you make acetaldehyde

The ADH1B gene comes in variants that differ dramatically in speed. The well-studied variant rs1229984 (His48Arg) produces a "fast" form of the enzyme:

On its own, a fast ADH1B tends to make drinking less comfortable: the unpleasant acetaldehyde phase arrives faster. The fast allele is most common in people of East Asian descent but also appears at meaningful frequencies in some Middle Eastern, European, and other populations.

ALDH2: how fast you clear it

If ADH1B is the accelerator on the first step, ALDH2 is the brakes on the second. The rs671 variant (Glu504Lys) largely inactivates the ALDH2 enzyme:

This is the variant behind the so-called "Asian glow." Because it's the more familiar and dramatic of the two, we cover it in depth — including the genotype table and how to find rs671 in your raw data — in the dedicated ALDH2 flush guide.

Why the two genes interact

The reason these markers are usually discussed together is that the effect depends on both steps at once:

This is why two people who both flush can have quite different underlying genetics — and why the flush isn't a single on/off switch.

What it's associated with

A few associations are well established in the research literature:

Heavy drinking also tends to show up on routine bloodwork — it's a common reason for elevated liver enzymes, where an AST higher than ALT is the classic alcohol-related pattern.

What it does and doesn't tell you

Your ADH1B and ALDH2 genotypes explain a real, mechanistic part of how you respond to alcohol — the speed of each step in the pathway. They don't dictate your behavior, and they aren't a diagnosis.

Medical disclaimer: This page is educational and not medical advice. If you carry these variants and drink, that's worth raising with a clinician — especially around long-term cancer risk.

For genotype-by-genotype detail, browse the Quanome gene library. For the flush reaction specifically and how to find rs671 in your raw data, see the ALDH2 flush guide. Or explore the rest of the Quanome blog.

See your alcohol-metabolism markers privately

Quanome reads your raw DNA on your device and surfaces well-studied markers like ADH1B and ALDH2 — without uploading your genome. Learn more about Quanome →

Frequently asked questions

What's the difference between ADH1B and ALDH2?

They work on different steps. ADH1B controls how fast alcohol is converted into acetaldehyde — a fast variant makes that first step happen quickly. ALDH2 controls how fast acetaldehyde is then cleared away into harmless acetate. A problem at either step lets acetaldehyde build up, which causes flushing and nausea.

Does ADH1B cause the alcohol flush?

Indirectly. A fast ADH1B variant produces acetaldehyde more quickly, so it can accumulate faster — contributing to flushing and feeling unwell. The classic, dramatic flush reaction is most strongly driven by the ALDH2 rs671 variant, which slows acetaldehyde clearance.

Why are these variants linked to lower alcohol dependence?

Both the fast ADH1B and the inactive ALDH2 variants make drinking less pleasant — alcohol produces acetaldehyde-related discomfort sooner. People who feel sick faster tend to drink less, and population studies consistently associate these variants with lower rates of alcohol dependence.

Where do these variants come from?

The fast ADH1B (rs1229984) and inactive ALDH2 (rs671) variants are both most common in people of East Asian descent, though the fast ADH1B allele also appears at notable frequencies in some other populations. This is educational, not medical advice.

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