Getting noticeably drunk after one drink when that wasn't always the case is a real physiological phenomenon, not imagined sensitivity. Several distinct mechanisms can cause increased alcohol sensitivity, and identifying which one applies to your situation is more useful than just accepting "I'm a lightweight now."
Tolerance reversal after abstinence. The most common cause. If you were previously a heavy or regular drinker and have recently reduced or stopped, your tolerance has dropped. Alcohol tolerance is not a permanent trait — it is a metabolic and neural adaptation to chronic exposure. When exposure stops, the adaptation reverses, often within weeks. Someone who previously drank six drinks to feel significant impairment may now feel that same impairment from two drinks after a month of abstinence. This is actually a physiological success story — the brain and liver have recovered their normal sensitivity. The risk is underestimating this change and drinking your previous volume with your new tolerance.
Low body weight or recent weight loss. Alcohol distributes through body water. Lower body mass means less water volume to dilute alcohol, producing higher BAC per drink. Significant weight loss (intentional or not) can produce a noticeable increase in alcohol sensitivity without any change in drinking habits.
Food intake. Drinking on an empty stomach versus with food makes an enormous difference to absorption rate and peak BAC. Food — particularly fat and protein — slows gastric emptying and dramatically delays alcohol absorption. One drink on an empty stomach can produce effects comparable to two drinks after a meal.
Medication interactions. A significant number of medications increase alcohol sensitivity, either by impairing liver metabolism (reducing the rate alcohol is processed) or by having additive sedative or CNS depressant effects. Antihistamines, benzodiazepines, sleep aids, certain antidepressants (particularly SSRIs and tricyclics), opioid pain medications, and antiepileptics all interact with alcohol. If you've started a new medication and noticed increased alcohol sensitivity, the interaction is almost certainly real.
Liver function changes. A compromised liver metabolises alcohol more slowly, producing higher BAC from the same intake. Fatty liver disease (common in regular drinkers), hepatitis, or other liver conditions reduce alcohol-processing capacity. If increased sensitivity is accompanied by abdominal discomfort, jaundice, or unusual fatigue, a liver function test is warranted.
ALDH2 deficiency. A genetic variant common in East Asian populations that reduces the ability to metabolise acetaldehyde (the toxic intermediate in alcohol metabolism), producing flushing, rapid heart rate, and pronounced intoxication from small amounts. If you've always had this reaction, it's genetic. If it's new, something else is operating.
The practical implication in recovery: if you've been sober and are considering drinking again, your previous tolerance is gone. The amount that felt manageable before will hit much harder now. This is useful information — not a reason to reset your sobriety, but an important fact if you're navigating social situations where alcohol is present.