Hypoglycemia, dehydration, acetaldehyde intoxication, glutamine rebound, and vitamin B12 deficiency are all theorized causes of hangover symptoms. Hangover symptoms may persist for several days after alcohol was last consumed. Approximately 25-30% of drinkers may be resistant to hangover symptoms. Some aspects of a hangover are viewed as symptoms of acute ethanol withdrawal, similar to the longer-duration effects of withdrawal from alcoholism, as determined by studying the increases in brain reward thresholds in rats (the amount of current required to receive to electrodes implanted in the lateral hypothalamus) following ethanol injection. Dehydration is caused by alcohol's ability to inhibit the release of anti-diuretic hormone.

The term hangover was originally a 19th century expression describing unfinished business—something left over from a meeting—or "survival." In 1904, the meaning "morning after-effect of drinking too much" first surfaced.

In Norwegian, veisalgia derives from kveis (uneasiness following debauchery) and the Greek algia (pain).

An alcohol hangover is associated with a variety of symptoms that may include dehydration, fatigue, headache, body aches, vomiting, diarrhea, flatulence, weakness, elevated body temperature, hypersalivation, difficulty concentrating, sweating, anxiety, dysphoria, irritability, sensitivity to light and noise, erratic motor functions (including tremor), trouble sleeping, severe hunger, halitosis, and lack of depth perception. Many people will also be repulsed by the thought, taste or smell of alcohol during a hangover. The symptoms vary from person to person, and occasion to occasion, usually beginning several hours after drinking. It is not clear whether hangovers directly affect cognitive abilities.

Ethanol has a dehydrating effect by causing increased urine production (diuresis), which causes headaches, dry mouth, and lethargy. Dehydration also causes fluids in the brain to be less plentiful. This can be mitigated by drinking water after consumption of alcohol. Alcohol's effect on the stomach lining can account for nausea.

Another contributing factor is the presence of products from the breakdown of ethanol by liver enzymes. Ethanol is converted to acetaldehyde by the enzyme alcohol dehydrogenase, and then from acetaldehyde to acetic acid by the enzyme acetaldehyde dehydrogenase. Acetaldehyde (ethanal) is between 10 and 30 times more toxic than alcohol itself, as well as being cocarcinogenic (not carcinogenic solely by itself) and mutagenic.

These two reactions also require the conversion of NAD+ to NADH. With an excess of NADH, three enzymes of the Citric Acid Cycle are inhibited (citrate synthase, isocitrate dehydrogenase, and alpha-ketoglutarate dehydrogenase) essentially shutting it down. Pyruvate (the end product of glycolysis) starts to accumulate, and the excess NADH drives lactate dehydrogenase to produce lactate from pyruvate in order to regenerate NAD+ and sustain life. This diverts pyruvate from other pathways such as gluconeogenesis, thereby impairing the ability of the liver to compensate for a drop in blood glucose levels, especially for brain. Because glucose is the primary energy source of the brain, this lack of glucose (hypoglycemia) contributes to symptoms such as fatigue, weakness, mood disturbances, and decreased attention and concentration.

Alcohol consumption can result in depletion of the liver's supply of glutathione and other reductive detoxification agents, reducing its ability to effectively remove acetaldehyde and other toxins from the bloodstream. Additionally, alcohol induces the CYP2E1 enzyme, which itself can produce additional toxins and free radicals.

In addition, it is thought that the presence of other alcohols (such as fusel oils), by-products of the alcoholic fermentation also called congeners, exaggerate many of the symptoms (congeners may also be zinc or other metals added primarily to sweet liqueurs to enhance their flavor); this probably accounts for the mitigation of the effects when distilled alcohol, particularly vodka, is consumed instead. A 2009 study provided evidence that darker-coloured liquors, such as bourbon, cause worse hangovers than lighter-coloured liquors, such as vodka. The higher amount of congeners found in darker liquors compared to lighter ones was indicated as the cause.

Most people of East Asian descent have a mutation in their alcohol dehydrogenase gene that makes this enzyme unusually effective at converting ethanol to acetaldehyde, and about half of such people also have a form of acetaldehyde dehydrogenase that is less effective at converting acetaldehyde to acetic acid. This combination causes them to suffer from alcohol flush reaction, in which acetaldehyde accumulates after drinking, leading to immediate and severe hangover symptoms. These people are therefore less likely to become alcoholics.