Alcohol is broken down primarily in the liver. The enzyme that breaks down alcohol is alcohol dehydrogenase (ADH), which converts ethanol into acetaldehyde. A second enzyme, aldehyde dehydrogenase (ALDH2), then converts acetaldehyde into acetate, which is harmless and enters normal energy metabolism. The liver processes approximately 90 to 95 percent of consumed alcohol at a rate of roughly one standard drink per hour. The remaining 5 to 10 percent is eliminated unchanged through breath, urine, and sweat. Genetic variations in ADH and ALDH2 enzymes significantly affect how fast individuals process alcohol and what health risks they face.
Dr. Ponlawat Pitsuwan, physician and addiction medicine specialist at Phuket Island Rehab: Individual differences in alcohol metabolism are not merely academic curiosities. They have real clinical implications. Understanding a patient’s genetic background, sex, age, and overall liver health allows more accurate risk assessment and more personalised treatment. When I assess a patient with alcohol use disorder, knowing whether they carry ALDH2*2 changes how I counsel them about cancer risk. Knowing their CYP2E1 induction status changes how I think about their medication interactions. The biochemistry of alcohol metabolism is the foundation of personalised addiction medicine.
What Organ Processes Alcohol?
The liver is the primary organ responsible for processing alcohol, handling approximately 90 to 95 percent of all consumed ethanol. The liver contains the highest concentrations of alcohol-metabolising enzymes in the body and is uniquely positioned to intercept alcohol absorbed from the gastrointestinal tract before it reaches systemic circulation.
A small amount of alcohol metabolism also occurs in the stomach through gastric alcohol dehydrogenase, representing first-pass metabolism. This gastric contribution is more significant in men than women: men have higher levels of gastric ADH, meaning more alcohol is metabolised before reaching the bloodstream. This is one reason women achieve higher blood alcohol concentrations than men for equivalent consumption amounts per body weight.
Other organs including the brain, pancreas, and colon also metabolise small amounts of alcohol, but their contribution to overall elimination is negligible. For clinical and practical purposes, alcohol processing is a liver function.
What Is the Enzyme That Breaks Down Alcohol?
Two enzymes perform the primary work of breaking down alcohol in the body, operating in sequence.
| Enzyme | Location | Reaction | What it produces |
| Alcohol dehydrogenase (ADH) | Liver cytosol; also in stomach lining | Converts ethanol to acetaldehyde | Acetaldehyde (toxic intermediate) + NADH |
| Aldehyde dehydrogenase (ALDH2) | Liver mitochondria (primarily) | Converts acetaldehyde to acetate | Acetate (harmless) + NADH |
| CYP2E1 (microsomal pathway) | Liver endoplasmic reticulum | Alternative ethanol oxidation, induced by chronic use | Acetaldehyde + reactive oxygen species |
| Catalase (minor pathway) | Liver peroxisomes | Minor ethanol oxidation | Acetaldehyde (minor contribution) |
Alcohol dehydrogenase (ADH) is the primary enzyme that breaks down alcohol. It operates in the liver cytosol, converting ethanol into acetaldehyde. This reaction simultaneously converts NAD+ to NADH, shifting the cellular redox balance and affecting multiple other metabolic pathways. ADH operates at a relatively fixed rate once it becomes saturated, which is why the liver processes approximately one standard drink per hour regardless of how much has been consumed.
The second enzyme, aldehyde dehydrogenase (ALDH2), is the rate-limiting step for overall alcohol clearance in most people. It rapidly converts the toxic intermediate acetaldehyde into harmless acetate. If ALDH2 activity is impaired by genetic variation or liver disease, acetaldehyde accumulates and causes the flush reaction, nausea, and rapid heartbeat associated with Asian alcohol sensitivity.
Source: Zakhari S. Overview: how is alcohol metabolized by the body? Alcohol Res Health. 2006;29(4):245-254. pubmed.ncbi.nlm.nih.gov/17718403
What Does Alcohol Turn Into in the Body?
Alcohol is converted in sequence through a two-step enzymatic process before being fully eliminated.
Step 1: Ethanol to acetaldehyde
ADH converts ethanol (the alcohol in drinks) into acetaldehyde. Acetaldehyde is a highly toxic and reactive compound. It forms protein adducts, damages DNA, and is classified as a Group 1 carcinogen by the International Agency for Research on Cancer. Acetaldehyde is the compound responsible for many of the harmful effects of chronic alcohol use, including liver damage, cancer risk, and the symptoms of the alcohol flush reaction. It is also the primary cause of hangover symptoms.
Step 2: Acetaldehyde to acetate
ALDH2 converts acetaldehyde into acetate. Acetate is harmless and is released into the bloodstream, where it travels to other tissues. Most tissues convert acetate to acetyl-CoA using the enzyme acetyl-CoA synthetase. Acetyl-CoA enters the citric acid cycle for energy production or is used as a building block for fatty acid and cholesterol synthesis. The body essentially treats acetate as a fuel source.
What does alcohol break down into: the complete sequence
| Stage | Compound | Enzyme involved | Status |
| Starting compound | Ethanol (alcohol) | None | Psychoactive, intoxicating |
| After ADH reaction | Acetaldehyde | Alcohol dehydrogenase (ADH) | Toxic, carcinogenic, causes flush reaction |
| After ALDH2 reaction | Acetate | Aldehyde dehydrogenase (ALDH2) | Harmless; enters energy metabolism |
| Final stage | Acetyl-CoA then CO2 and water | Acetyl-CoA synthetase; citric acid cycle | Completely non-toxic; excreted |
How Fast Does the Body Process Alcohol?
The standard alcohol elimination rate is approximately 100 to 120 milligrams of ethanol per kilogram of body weight per hour. For a 70kg adult, this is approximately 7 to 8.4 grams of ethanol per hour. One standard drink in most countries contains approximately 10 to 14 grams of ethanol, meaning the average adult processes roughly one standard drink per hour.
This rate is governed primarily by ADH enzyme activity, which follows zero-order kinetics at typical blood alcohol concentrations: the rate remains constant regardless of how much alcohol is present once the enzyme is saturated. This is why drinking faster than one standard drink per hour leads to progressive accumulation of alcohol in the blood, producing increasing intoxication.
| Factor | Effect on processing speed |
| ADH genetic variant (ADH1B*2, high activity) | Faster: ethanol cleared more quickly; more acetaldehyde produced |
| ALDH2*2 variant (reduced activity) | Bottleneck at step 2: acetaldehyde accumulates; flush reaction; cancer risk elevated |
| Sex (female vs male) | Slower in women: lower gastric ADH, different body composition, 10 to 20% slower hepatic clearance |
| Age (older adults) | Slower: decreased liver blood flow, reduced hepatocyte mass, lower enzyme activity |
| Liver disease | Much slower: reduced functional hepatocyte mass; cirrhosis can reduce clearance by 50% |
| Chronic heavy drinking (CYP2E1 induction) | Faster metabolic tolerance: CYP2E1 upregulated; more oxidative stress generated |
| Food consumption | Does not change clearance rate; slows absorption reducing peak BAC |
| Body weight | Higher weight = larger distribution volume = lower peak BAC per drink; clearance rate per kg stays constant |
The one standard drink per hour rule: This is an average. Individuals with fast ADH variants, men, younger adults, and those with induced CYP2E1 from chronic drinking may clear slightly faster. Women, older adults, those with liver disease, or those with ALDH2*2 variants clear more slowly. No technique speeds up clearance: coffee, food, exercise, and water do not accelerate liver enzyme activity.
Genetic Variations That Affect Alcohol Processing
Two enzyme variants have the most significant clinical impact on how individuals process alcohol.
ALDH2*2: the flush variant
Approximately 40 percent of East Asian populations carry at least one copy of the ALDH2*2 variant, which produces an enzyme with dramatically reduced activity. When these individuals drink, acetaldehyde accumulates rapidly because the second step of the metabolic sequence cannot keep pace with the first. The result is facial flushing, rapid heartbeat, nausea, and headache from acetaldehyde toxicity. This is the alcohol flush reaction.
The ALDH2*2 variant provides some protection against alcohol use disorder because drinking is unpleasant. However, individuals who continue drinking despite the flush reaction face dramatically elevated cancer risk: some studies show 10-fold or higher increases in oesophageal cancer. Continued acetaldehyde exposure causes DNA adduct formation and mutagenic damage. The flush reaction is not merely an inconvenience. It is a warning signal.
ADH1B*2: fast ethanol metabolism
The ADH1B*2 allele produces an ADH enzyme approximately 40 times more active than the common variant. Individuals with this variant convert ethanol to acetaldehyde much faster than average. If ALDH2 function is normal, this typically accelerates overall alcohol clearance and provides some protection against alcohol use disorder through reduced intoxication duration. Combined with ALDH2*2 impairment, it creates the most pronounced flush reaction.
Source: Edenberg HJ. The genetics of alcohol metabolism: role of alcohol dehydrogenase and aldehyde dehydrogenase variants. Alcohol Res Health. 2007;30(1):5-13. pubmed.ncbi.nlm.nih.gov/17718399
The Microsomal Pathway: What Happens with Chronic Drinking
The ADH and ALDH2 pathway is the primary route for alcohol metabolism. A secondary pathway, the microsomal ethanol-oxidising system (MEOS) centred on the enzyme CYP2E1, becomes increasingly important with chronic heavy alcohol use.
Unlike ADH, which operates at a fixed rate, CYP2E1 can be induced by chronic alcohol exposure: the liver produces more of it in response to regular heavy drinking. This is one mechanism by which metabolic tolerance develops. Heavy drinkers clear alcohol more quickly from the bloodstream, which is why they need more alcohol to achieve the same effect.
The cost of this adaptation is significant. CYP2E1 metabolism generates reactive oxygen species as obligate byproducts. These free radicals cause direct cellular damage, lipid peroxidation, and mitochondrial dysfunction. CYP2E1 induction is a primary driver of oxidative stress in the liver of heavy drinkers and contributes directly to the progression of alcoholic liver disease. Metabolic tolerance is not a beneficial adaptation. It is a sign of increasing hepatic stress.
Warning: CYP2E1 induction from chronic drinking also alters the metabolism of many medications. Chronic heavy drinkers may metabolise some drugs faster, reducing their effectiveness, while acutely inhibiting other drugs and increasing their toxicity. Always disclose heavy alcohol use to your prescribing physician.
Acetaldehyde: Why the Intermediate Compound Matters
Acetaldehyde is the most clinically important intermediate in alcohol metabolism. It is produced every time alcohol is consumed and is responsible for much of the long-term harm from drinking.
Acetaldehyde binds to proteins, forming adducts that alter protein structure and trigger immune responses. It binds to DNA, creating mutagenic adducts that can lead to cancer. It is classified as a Group 1 carcinogen by the International Agency for Research on Cancer, with strongest evidence for cancers of the oral cavity, pharynx, oesophagus, larynx, liver, colorectum, and female breast.
The ALDH2 enzyme normally clears acetaldehyde so rapidly that it does not accumulate to dangerous levels. But ALDH2*2 genetic variants, liver disease reducing ALDH2 activity, or simply overwhelming the enzyme with very high alcohol intake can allow acetaldehyde to reach tissue-damaging concentrations. This is why both genetics and drinking quantity affect cancer risk, and why no safe threshold of alcohol consumption for cancer has been established.
What Happens to the 5 to 10 Percent Not Metabolised by the Liver?
Approximately 5 to 10 percent of consumed alcohol is eliminated from the body unchanged through non-metabolic routes. Pulmonary excretion accounts for the largest share: alcohol evaporates from the blood as it passes through the lungs and is exhaled. This is the basis of breathalyser testing. The exhaled alcohol concentration directly proportional to blood alcohol concentration allows blood alcohol level estimation from breath.
Renal excretion eliminates a small percentage through urine. Urine alcohol concentrations typically exceed blood levels because urine is concentrated in the bladder during storage. Sweat contains measurable alcohol and forms the basis for transdermal alcohol monitoring devices used in some treatment and supervision programmes. Tears, saliva, and other secretions also contain trace amounts.
When Alcohol Processing Becomes a Problem
The liver processes alcohol efficiently in most people for moderate consumption. Problems arise when the quantity consumed exceeds the liver’s capacity to keep pace, when genetic variants impair the pathway at any step, or when chronic heavy use induces CYP2E1-mediated oxidative stress and liver damage.
Chronic heavy drinking also disrupts the NAD+/NADH ratio throughout the body. Both ADH and ALDH2 reactions consume NAD+ and produce NADH. High NADH levels inhibit gluconeogenesis (contributing to hypoglycaemia), impair fatty acid oxidation (promoting fatty liver), and alter the metabolism of lactate and pyruvate. These metabolic disruptions are a direct consequence of the biochemistry of alcohol metabolism at high doses.
Understanding these mechanisms helps explain why alcohol use disorder is a medical condition with specific, measurable biochemical consequences rather than simply a behavioural problem. The biochemistry of alcohol processing is directly connected to the physiology of dependence, withdrawal, and recovery.
Summary
Alcohol is broken down primarily in the liver by two enzymes operating in sequence. Alcohol dehydrogenase (ADH) converts ethanol into acetaldehyde, a toxic and carcinogenic intermediate. Aldehyde dehydrogenase (ALDH2) then converts acetaldehyde into harmless acetate, which enters normal energy metabolism as acetyl-CoA. The liver processes approximately 90 to 95 percent of consumed alcohol at roughly one standard drink per hour. The remaining 5 to 10 percent is eliminated unchanged through breath, urine, and sweat.
Genetic variations in ADH and ALDH2 significantly affect individual processing rates and health risks. ALDH2*2 variants impair acetaldehyde clearance, causing flush reaction and dramatically elevating cancer risk in those who continue drinking. ADH1B*2 variants accelerate ethanol conversion. Chronic heavy drinking induces the CYP2E1 microsomal pathway, producing metabolic tolerance alongside increased oxidative stress and liver damage. No technique speeds up alcohol clearance: only time and liver enzyme activity determine how fast alcohol leaves the body.
Frequently Asked Questions
What is the enzyme that breaks down alcohol?
Alcohol dehydrogenase (ADH) is the primary enzyme that breaks down alcohol, converting ethanol into acetaldehyde in the liver cytosol. A second enzyme, aldehyde dehydrogenase (ALDH2), then converts the toxic acetaldehyde intermediate into harmless acetate. Together these two enzymes handle the primary pathway for alcohol elimination. A third pathway using CYP2E1 becomes more active during chronic heavy drinking.
What does alcohol turn into in the body?
Alcohol (ethanol) is converted by ADH into acetaldehyde, a toxic and carcinogenic intermediate. ALDH2 then converts acetaldehyde into acetate, which is harmless. Acetate is released into the bloodstream and converted to acetyl-CoA in most tissues, entering the citric acid cycle for energy production. The complete breakdown products are carbon dioxide and water.
What breaks down alcohol in the body?
The liver breaks down 90 to 95 percent of consumed alcohol using two key enzymes: alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH2). The stomach contributes minor first-pass metabolism via gastric ADH, more significant in men than women. The remaining 5 to 10 percent is eliminated unchanged through exhaled air, urine, and sweat without being metabolised.
What organ processes alcohol?
The liver is the primary organ that processes alcohol, handling 90 to 95 percent of consumed ethanol. It contains the highest concentrations of ADH and ALDH2 enzymes. A small amount of first-pass metabolism occurs in the stomach. Other organs including the brain, pancreas, and colon contain minor amounts of these enzymes but their contribution to overall elimination is negligible.
What does alcohol break down into?
Ethanol is broken down sequentially into: acetaldehyde (toxic, by ADH), then acetate (harmless, by ALDH2), then acetyl-CoA (by acetyl-CoA synthetase in peripheral tissues), and finally carbon dioxide and water through the citric acid cycle. The intermediate acetaldehyde is a Group 1 carcinogen and responsible for much of the long-term harm from alcohol.
How fast does the body process alcohol?
The average adult processes approximately one standard drink per hour, reflecting the fixed rate of ADH enzyme activity at blood alcohol concentrations typical of social drinking. This equates to approximately 100 to 120 milligrams of ethanol per kilogram of body weight per hour. Women, older adults, people with liver disease, and those with ALDH2*2 variants process alcohol more slowly. Chronic heavy drinkers may process it slightly faster due to CYP2E1 induction, but at the cost of increased oxidative liver damage. Nothing speeds up this rate: coffee, food, and exercise do not accelerate liver enzyme activity.
Dr. Ponlawat Pitsuwan is a physician and addiction medicine specialist at Phuket Island Rehab, Thailand. His clinical focus covers alcohol use disorder, drug dependence, and the medical conditions that co-occur with addiction including metabolic disorders and cardiovascular complications. He provides medical oversight for detoxification and patient assessment at Phuket Island Rehab