What Causes a Hangover? The Biology Behind the Morning After

Everyone has a theory. You didn’t drink enough water. You mixed beer and wine. You’re getting old. Some of these contain a grain of truth; most are incomplete. The actual answer is more specific than “you drank too much” — and it also explains a second question people rarely connect to the first: why do some people get so much worse hangovers than others?

This is a neutral explainer of the biology. It is not medical advice, and nothing here is a promise that any product will change how you feel.

These statements have not been evaluated by the Food and Drug Administration or Health Canada. This product is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before use.


The short answer: a hangover is several processes at once

Researchers generally describe a hangover not as one thing but as several overlapping physiological processes that peak around the same time the morning after:

  1. Acetaldehyde — a toxic intermediate your body produces while metabolising alcohol
  2. GABA rebound — a neurochemical “withdrawal” associated with next-day anxiety and cognitive symptoms
  3. Dehydration and electrolyte loss — driven by alcohol’s diuretic effect
  4. Inflammation — an immune response to alcohol and its byproducts
  5. Disrupted sleep — alcohol degrades the quality of your sleep architecture

A hangover feels like fatigue plus anxiety plus headache plus nausea plus brain fog because, biologically, those tend to come from different processes converging at once. That also sets up the second half of this article: because there are several independent levers, individual differences in any one of them — genetics, age, sleep, what you drank — can make one person’s morning much worse than another’s after the same number of drinks.


1. Acetaldehyde: the toxic intermediate

Your liver processes ethanol in two steps:

Step 1 — Alcohol dehydrogenase (ADH) converts ethanol into acetaldehyde. Step 2 — Aldehyde dehydrogenase (ALDH) converts acetaldehyde into acetate (acetic acid), which is comparatively harmless.

The intermediate, acetaldehyde, is the part researchers most often point to. It is considerably more reactive and toxic than ethanol itself, and while it’s present it has been associated with flushing, nausea, headache, and a raised heart rate. This is your body’s own metabolic chemistry — the two-step pathway is biology, not something a supplement performs for you.

How much acetaldehyde builds up depends on two things: how much alcohol you drank (more ethanol means more acetaldehyde produced upstream) and how quickly your body clears it (largely set by ALDH activity, which varies genetically — more on that below).

The “Asian flush” some people experience makes this visible. It’s linked to a genetic variant of the ALDH2 enzyme that clears acetaldehyde more slowly, so it accumulates and the flushing, nausea, and rapid heartbeat appear quickly. In people without that variant the same process still happens — the acetaldehyde just clears faster, so the effects are milder and spread out.

Where does DHM fit in? Dihydromyricetin (DHM) is the flavonoid studied in this context, and some studies have proposed it may influence the activity of the alcohol-metabolising enzymes ADH and ALDH. That research is mostly preliminary and much of it is in animal models, so it’s best read as “what researchers are investigating,” not an established effect in people.

→ Read more on acetaldehyde and why it matters the morning after, or the deeper dive on how DHM relates to alcohol metabolism.


2. GABA rebound: the anxiety and cognitive symptoms

Alcohol’s main action in the brain is potentiating GABA-A receptors — turning up the brain’s primary inhibitory (“calming”) system. That’s the relaxation and disinhibition people feel while drinking.

The brain adapts to that sustained over-activation by turning its own inhibition down. When the alcohol clears, that adaptation doesn’t reverse instantly, so for a while the nervous system sits more excitable than baseline. Researchers associate this rebound with:

  • Next-day anxiety and unease (“hangxiety”)
  • Restlessness and trouble concentrating
  • Heightened sensitivity to light and sound
  • Racing thoughts

It’s often compared to a mild version of withdrawal from sedatives that act on the same receptor system, which makes mechanistic sense. How strongly you feel it varies with how much and how long you drank, and with individual neurobiology.

DHM has been studied as a GABA-A modulator — most notably a 2012 UCLA study published in the Journal of Neuroscience that examined DHM’s effects on GABA-A signalling in rats. It’s a frequently cited anchor in this area, but it’s a rodent study, and the human evidence is thin. Treat it as interesting preliminary science rather than proof of a next-day benefit.

→ More on this: hangxiety and next-day anxiety after drinking, GABA rebound explained, and the neuroscience-focused DHM and GABA receptors.


3. Dehydration and electrolyte loss

Alcohol suppresses antidiuretic hormone (vasopressin), the signal that tells your kidneys to hold on to water. With it suppressed, you excrete more fluid than usual — which is why you make more trips to the bathroom on a night out.

That produces dehydration, but the more easily missed piece is electrolyte loss. The extra urine carries out sodium, potassium, and magnesium, which matter for nerve conduction, muscle function, and fluid balance. Dehydration is associated with headache (vascular changes from reduced volume); electrolyte depletion is associated with cramps, weakness, and worse brain fog.

This is the kernel of truth in “drink water” — but plain water replaces volume, not minerals. It’s why people often pair fluids with electrolytes. (Hovenia is single-ingredient DHM and contains no electrolytes; this is general background, not a product feature.)


4. Inflammation: the “I feel mildly sick” part

Your immune system treats alcohol and acetaldehyde as something to respond to. That response involves inflammatory signalling molecules (cytokines) that don’t stay put in the liver — they circulate, which is part of why a hangover can feel flu-like: fatigue, body aches, nausea, sensitivity to light and sound.

There’s also a gut angle. Alcohol can increase intestinal permeability, letting bacterial byproducts (such as LPS, lipopolysaccharide) cross into the bloodstream, where they can amplify that inflammatory picture. So the heavy, achy feeling isn’t only dehydration — low-grade systemic inflammation is part of it.


5. Disrupted sleep

Alcohol is a sedative, not a sleep aid. It can help you fall asleep, but it suppresses REM sleep early in the night, then — as it clears — the brain tends to “rebound” with extra REM later, producing vivid dreams and fragmented, less restorative sleep.

The result is the familiar “I was in bed eight hours and feel like I slept three.” Because sleep is your main overnight recovery mechanism, poor sleep quality tends to amplify every other symptom on this list — the cognitive fog, the emotional edge, the fatigue.


Why some people get much worse hangovers

Same drinks, same night — and one person bounces back while another is wrecked. That variation is real and well documented. It comes down to differences in the same five processes above, plus a few individual factors layered on top.

ALDH2 genetics (the single biggest factor)

The best-characterised genetic driver is a variant often written ALDH2*2, which substantially reduces the activity of the ALDH2 enzyme that clears acetaldehyde in step 2 of metabolism. With slower clearance, acetaldehyde builds up higher and lingers longer — and acetaldehyde is tied to some of the roughest symptoms (nausea, headache, flushing, racing heart).

This variant is common in people of East Asian descent and is the basis of the visible Asian flush. If you’re of East Asian descent and your hangovers are noticeably worse than peers who drink the same, this enzyme variation is a likely contributor.

ADH variants (how fast you make acetaldehyde)

On the other side of the pathway, ADH variants affect how quickly ethanol becomes acetaldehyde. Some variants are faster. A “fast production, slow clearance” combination — a fast ADH variant alongside the slow ALDH2*2 variant — can push acetaldehyde exposure especially high, which is part of why discomfort and flushing are more common in some populations.

Age

A common observation: the drinks that produced a manageable hangover at 22 produce a two-day ordeal at 38. Several age-related changes are associated with this:

  • Slower enzyme activity. Alcohol-metabolising enzyme activity tends to decline with age, so processing is slower.
  • Less total body water. Body composition shifts with age (more fat, less lean mass), so the same dose is more concentrated in the bloodstream.
  • Reduced antioxidant reserve. The body’s capacity to make glutathione, used to handle reactive byproducts, tends to fall with age.
  • More fragile sleep. Older adults often have less resilient sleep, so alcohol’s disruption hits proportionally harder.

This is biology, not a weakness of willpower or “tolerance.”

Sex differences

On average, women experience more severe effects than men at the same dose, for documented physiological reasons — typically lower total body water (so a higher effective blood-alcohol concentration), differences in first-pass metabolism, and hormonal interactions that can vary across the menstrual cycle. Public-health drinking guidelines that differ by sex reflect this physiology.

What you drank (congeners)

Darker drinks (bourbon, whiskey, brandy, red wine) contain more congeners — fermentation byproducts like methanol, tannins, and fusel alcohols — than clearer ones (vodka, gin, white wine). Controlled research supports a real effect: a 2010 study by Rohsenow and colleagues in Alcoholism: Clinical and Experimental Research found bourbon produced worse next-day symptoms than vodka at matched alcohol content. Congeners aren’t the primary cause of a hangover, but they appear to make a bad one worse.

Sleep and gut microbiome

Two more sources of individual variation. Poor sleep both worsens and is worsened by drinking, so going in already sleep-deprived stacks the deck. And because alcohol can increase gut permeability, differences in individual gut microbiome and baseline gut barrier function may influence how strong the inflammatory response is — a newer, still-developing research area.


Putting it together

SymptomOften associated withAlso linked to
HeadacheDehydration; acetaldehydeInflammation
NauseaAcetaldehyde; gut inflammationElectrolyte imbalance
FatigueDisrupted sleepInflammation; dehydration
Anxiety / dreadGABA reboundSleep loss
Brain fogGABA rebound; sleep lossInflammation
Body achesInflammationDehydration
Light / sound sensitivityInflammation; GABA excitabilityDehydration

Because a hangover is multi-causal, no single thing — water, a painkiller, greasy food — addresses all of it. It also explains the individual variation: change one input (your ALDH2 genetics, your age, what you drank, how you slept) and the whole morning shifts. You can’t change your genetics, age, or sex; you can choose lower-congener drinks, prioritise sleep, and pace your drinking.

Where does a DHM supplement sit in that picture? DHM is the most-studied single compound in this category — one analysis published in a Sage journal in 2025 found DHM in roughly 47.6% of US recovery products — but the human evidence is still preliminary and much of the mechanistic work is in animal models. Hovenia’s approach is deliberately narrow: one studied compound at a full dose, and nothing else. That’s a position on simplicity, not a claim that it treats or prevents a hangover.

→ If you want the dosing and timing detail: what is DHM? and when to take DHM.


Frequently Asked Questions

What is the main cause of a hangover? There isn’t a single one. Researchers describe a hangover as several overlapping processes — acetaldehyde from alcohol metabolism, GABA rebound, dehydration and electrolyte loss, inflammation, and disrupted sleep — peaking together. That’s why it feels like several different symptoms at once.

Is a hangover just dehydration? No. Dehydration is one contributor, but it doesn’t explain the anxiety, the flu-like aches, the brain fog, or the poor sleep. Plain water helps the dehydration piece and not much else — which is why “just drink water” is incomplete advice.

Why do I get worse hangovers than my friends on the same drinks? Individual variation is real. The biggest single factor is genetics around the acetaldehyde-clearing enzyme ALDH2 (the basis of the “Asian flush”), but age, sex, how much you slept, your gut, and whether you drank high-congener dark spirits all stack on top.

Why do hangovers get worse with age? Several age-related shifts line up: slower alcohol-metabolising enzyme activity, less total body water (so alcohol is more concentrated), lower antioxidant reserve, and more fragile sleep. The same drinks simply land harder than they did a decade earlier.

Do dark drinks really cause worse hangovers? The evidence points that way. Controlled research (Rohsenow et al., 2010) found bourbon produced worse next-day symptoms than vodka at matched alcohol content, attributed to congeners. They’re a severity multiplier, not the root cause.

Does DHM cure or prevent hangovers? No, and we won’t say it does. DHM is the most-studied compound in the recovery category and there’s preliminary research — much of it in animal models — into how it interacts with alcohol-metabolising enzymes and GABA-A receptors. That’s an area of active study, not a settled treatment.


→ Keep reading: acetaldehyde, the morning-after intermediate · the hangover symptom timeline · supplements people take before drinking · a sensible pre-drinking routine · DHM vs. acetaminophen, and why one is risky after drinking


Reviewed for accuracy against the cited primary literature. Hovenia is a liver-health supplement company; our product supports healthy liver function and is not intended to diagnose, treat, cure, or prevent any disease. This statement has not been evaluated by the FDA or Health Canada.

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