Acetaldehyde syndrome is a condition characterized by unpleasant physiological reactions following alcohol consumption. These reactions are not an allergy but are the result of the body’s inability to properly process alcohol, leading to the accumulation of a toxic compound called acetaldehyde. When its levels rise in the bloodstream, it triggers a cascade of effects felt throughout the body.
The Biological Cause
The metabolism of alcohol, or ethanol, is a two-step process that occurs in the liver. First, an enzyme called alcohol dehydrogenase (ADH) converts ethanol into acetaldehyde, a toxic substance. Following this, a second enzyme, aldehyde dehydrogenase 2 (ALDH2), breaks down the toxic acetaldehyde into a harmless substance called acetate, which the body can use for energy.
Acetaldehyde syndrome occurs when this second step is disrupted. If the ALDH2 enzyme is not functioning correctly, it cannot process acetaldehyde efficiently, leading to its rapid buildup in the blood. This accumulation of acetaldehyde is what directly causes the array of symptoms associated with the syndrome.
Think of the process like a factory assembly line. The first worker (ADH) takes ethanol and quickly converts it into a component part, acetaldehyde. The second worker (ALDH2) is supposed to take that acetaldehyde and immediately convert it into the final, safe product (acetate). If the second worker is slow or absent, the component parts start to pile up on the conveyor belt, causing problems for the entire system.
Triggers and Genetic Factors
The most common cause of acetaldehyde syndrome is a genetic deficiency in the ALDH2 enzyme. A specific genetic variation, the ALDH22 allele, results in a less effective or nonfunctional version of the enzyme. This genetic trait is prevalent in individuals of East Asian descent; it is estimated that about 36% of people in East Asia (Japan, China, and Korea) carry this mutation. Globally, this deficiency affects approximately 540 million people, or about 8% of the world’s population.
Individuals who inherit one copy of the ALDH22 gene have reduced enzyme activity, while those with two copies have almost no ability to metabolize acetaldehyde. This inherited inability to clear acetaldehyde is why some people experience immediate negative effects after drinking small amounts of alcohol, a reaction often called “Asian Flush” or “Alcohol Flush Reaction.”
Beyond genetics, certain medications can trigger the syndrome by inhibiting the ALDH2 enzyme. The drug disulfiram, prescribed to treat alcohol use disorder, intentionally blocks the enzyme to cause a severe reaction to alcohol and discourage consumption. Another medication that can cause a similar effect is the antibiotic metronidazole. Consuming alcohol while taking these medications prevents the breakdown of acetaldehyde, leading to its accumulation.
Recognizable Symptoms
Symptoms appear quickly after consuming alcohol as a direct result of acetaldehyde buildup. The most common reactions include:
- Facial flushing, where skin on the face, neck, and chest becomes red and warm
- A throbbing headache
- A rapid, pounding heartbeat (tachycardia)
- Intense nausea and vomiting
- Dizziness, weakness, or lightheadedness, which can be caused by a drop in blood pressure
- Nasal congestion
Associated Health Risks
While the immediate symptoms are uncomfortable, the long-term health consequences of repeated exposure to high levels of acetaldehyde are more serious. Acetaldehyde is classified as a Group 1 carcinogen, meaning it is a substance known to cause cancer in humans. When individuals with an ALDH2 deficiency consume alcohol regularly, they repeatedly expose their tissues to this toxic compound.
This chronic exposure increases the risk of developing certain types of cancer, with the strongest link being an elevated risk of esophageal cancer. Studies show that after drinking, the concentration of acetaldehyde in the saliva of those with ALDH2 deficiency can reach toxic levels, directly damaging the esophagus and increasing the risk for head and neck cancers.