This post is long. If you don't read it, here's a summary:
I feel bad for people who don’t drink. When they wake up in the morning, that’s as good as they’re going to feel all day.
Hangovers are an inevitable consequence of alcohol use (and misuse).
If you know what it means to be truly hungover, you've also made empty promises to never drink again. Hangover amnesia is swearing off alcohol on Monday and drinking per usual on Wednesday. And it's a familiar phenomenon.
Hangovers are easy on the young. Aging seems to diminish our ability bounce back from hangovers. In college, I remember being hangover-free until my junior year. Now I experience 2-day hangovers that give me gray hairs and make me seriously re-evaluate my priorities.
There are a handful of theories about the cause of hangovers. Unexpectedly, the science of hangovers is not as well understood as you might imagine. Apparently, Newton could invent (or discover?) calculus by armchair philosophizing but centuries later we can't figure out why a bender makes you hate yourself the next day.
Caption: Hemingway's commitment to ethanol intoxication was unparalleled.
I don't stop drinking until I hate myself.
The main theories about the cause of hangovers can be distilled (no pun intended) down to:
Armchair theories are interesting. But they're hardly helpful when you have a pounding headache and the mere thought of tequila makes you feel deeply unwell.
In this post, I'll be imparting some actionable steps you can take to avoid hangovers altogether and bounce back more quickly when they strike.
Fair enough. Here's the take-home message in under 100 words.
Socrates would like to say that you should probably define a term before discussing it at length.
You'd surprised how many academic papers attempt to come up with a rigorous definition of a hangover and fail to reach a consensus.
I'll skirt the controversy and provide the following pedestrian definition:
Distress that appears several hours after alcohol intoxication.
That was easy. Researchers also seem to agree on these (fairly obvious) facts:
Originally, researchers attributed hangovers to either alcohol itself, alcohol metabolites, alcohol withdrawal or alcohol drinks congener effects (Swift and Davidson, 1998; Wiese et al., 2000).
What are "congener effects"? They're "...minor compounds other than ethanol that occur naturally in alcohol beverages as a result of distilling and fermenting processes" http://www.ncbi.nlm.nih.gov/pubmed/20712591. So not ethanol itself, but natural impurities.
Several factors affect hangover severity:
Hangovers begin 6-8 h after your last drink when your blood alcohol concentration (BAC) is decreasing. Hangover symptoms peak when your BAC hits 0 and can last up to 24 hours.
Wiese et al. (2000) proposed evaluating hangover when there are two or more symptoms, after all alcohol is metabolized, and when BAC reaches 0.
There are some finicky researchers who think that hangover symptoms occur before the BAC reaches 0 (Kim et al., 2003a,b).
More studies are needed to tease apart the relationship between hangover timeline, BAC, and time of eating. Eating seems to reduce the intensity of hangovers - which makes scientific sense as we'll see later.
Many scientists have attempted to explain the hangover phenomenon. We'll discuss the most well-known hypotheses. Most of them are half-truths; they're partially correct but only part of the story.
This is the theory that a hangover is actually the first phase of acute alcohol withdrawal (Swift and Davidson, 1998; Wiese et al., 2000).
Many hangover symptoms seem awfully similar to alcohol withdrawal symptoms. Let me give an example. Here are some overlapping symptoms between alcohol withdrawal and hangover:
McMicken (1990) describes three stages of alcohol withdrawal (minor, major, and delirium tremens). Delirium tremens is confusion brought on by alcohol withdrawal, and sometimes involves hallucinations.
According to these stages, hangovers can only be explained by the minor alcohol withdrawal symptoms which appear within 24h after your last drink. Remember that a hangover manifests a few hours after alcohol consumption and lasts for about 24h (sometimes longer).
Major withdrawal and delirium tremens occur 1–5 days after abstaining from alcohol. Both stages exhibit symptoms that are not typical of hangovers like hallucinations and seizures (Wiese et al., 2000).
While there is a resemblance between alcohol withdrawal and hangover, they are clearly not identical:
It's clear that hangovers are a different phenomenon from withdrawal. Even so, it is possible to be both hungover and in a state of alcohol withdrawal at the same time!
Alcohol is metabolized by two chemical reactions. First, alcohol (ethanol) is oxidized to acetaldehyde, which is further oxidized to acetic acid (that's the acid in vinegar).
When you're drinking acetaldehyde can begin to accumulate. Acetaldehyde causes unmistakable symptoms - the most famous of which is the "Asian flush". Other symptoms include:
If you take a look at the list of flush symptoms above there are similarities between hangover symptoms (e.g., tachycardia) and acetaldehyde poisoning. So maybe a buildup of acetaldehyde causes hangovers?
Several authors suggest that the acetaldehyde metabolite contributes to hangovers (Swift and Davidson, 1998; Wiese et al., 2000).
Protip: there's some evidence that the supplement N-acetylcysteine helps the body eliminate acetaldehyde more quickly.
Even though researchers have pursued this hypothesis, the role of acetaldehyde in hangovers should be considered cautiously. Here's why:
Genetic polymorphisms are linked to the enzyme that metabolizes acetaldehyde.
Some Asians convert alcohol to acetaldehyde too quickly, convert acetaldehyde to acetic acid too slowly, or both. This causes acetaldehyde to accumulate in their body after drinking (Quertemont et al., 2005; Simonetta et al., 2006).
Some researchers wondered whether there might be an evolutionary advantage to being alcohol intolerant. It might have a protective effect against alcoholism, for example. This idea remains speculative, but studies have found that abstainers and infrequent drinkers are more likely to be slow acetaldehyde metabolizers (Higuchi et al., 1994).
One study reported a greater susceptibility to hangovers in Asian subjects, suggesting a link between excess acetaldehyde and hangovers (Yokoyama et al., 2005). This study needs replication, but it hints that the inactive aldehyde dehydrogenase may have a protective effect against alcoholism by making hangovers intolerable.
Why can't alcohol itself cause hangovers? Why do we need to invoke some "additional thing" beyond the fact that ethanol is a toxic to explain the phenomena of a hangover?
Scientists indeed suggest that several hangover symptoms could be explained by a direct effect of ethanol on human physiology (Swift and Davidson, 1998; Wiese et al., 2000).
Consider these physiological effects of alcohol which are clearly linked to hangover:
Alcohol has is a diuretic effect; it makes you want to urinate.
As your BAC approaches zero, you're left dehydrated. Plasma levels of antidiuretic hormone [ADH](Vamvakas et al., 1998) become elevated - this is your body's attempt to retain fluids in a hypovolemic state.
Antidiuretic (ADH) levels are correlated with hangover severity. This makes intuitive sense: the more you alcohol you drink the more dehydrated you become and the more ADH your body releases to compensate in order to retain fluids.
GI discomfort tends to occur after a bender rather than moderate indulgence in alcohol. This symptom is heavily influenced by the type of alcohol consumed (Linnoila et al., 1979).
Headaches are arguably among the worst hangover symptoms. So what causes a hangover-induced headache?
There are a few factors at play:
Alcohol can also elicit cytokine release, which contributes to headaches. For example, alcohol increases thromboxane B2 levels which may explain other hangover symptoms in addition to headaches like nausea, diarrhea, and tiredness (Kangasaho et al., 1982).
What the hell is a cytokine?
Cytokine refers to an inflammatory molecule or protein like interferon or interleukin that are secreted by certain cells of the immune system.
During a hangover, cytokines line IL- 10, IL-12 and IFN-gamma increase (Kim et al., 2003b).
Reichenberg et al. (2001) note a correlation between cytokines and memory impairments in humans. Reversible cognitive impairment is another negative consequence of a hangover (Prat et al., 2008).
Elevated cytokine levels are related positively with the scores in a subjective hangover scale (Kim et al., 2003a). These data agree with the preventive effect on the hangover of tolfenamic acid, a prostaglandin inhibitor (Pittler et al., 2006).
In brief, cytokines and inflammation play a role in hangovers.
Hangovers go hand-in-hand with hypoglycemia (a drop in blood sugar).
If you're otherwise perfectly healthy, the hypoglycemic effect of a hangover is modest or negligible.
But when glycogen stores are depleted (chronic alcoholics, subjects on a low-carbohydrate diet or in fasting people missing a meal while drinking), alcohol consumption leads to a hypoglycemic state (Siler et al., 1998). Glycogen is how sugar is stored in your liver. Glycogen is the reason you can fast for days without dying.
Alcohol is also able to induce reactive hypoglycemia (O’Keeffe and Marks, 1977). After a carbohydrate-rich meal combined with alcohol, the insulin response to rising blood glucose levels can be increased and leads to hypoglycemia 2–3 hours after a meal (O’Keeffe and Marks, 1977).
The drop in blood sugar could affect brain function since the brain requires a constant influx of energy. So alcohol-induced hypoglycemia can lead to a state of weakness, tiredness, and changes in mood observed during a hangover. But alcohol is usually mixed with low caloric soft drinks or meals and that which would offset this effect.
** Protip: if you're hungover, have something simple to eat even if you don't feel like. Something that won't exacerbate nausea like a slice of plain bread. **
Alcohol is not good for sleep. Yet paradoxically, some people say they drink in the evening to help them fall asleep. How is this possible?
It's true that alcohol reduces sleep latency (the time it takes to fall asleep). But as blood levels of alcohol fall, your sleep architecture becomes disrupted. Sleep architecture is just a neuroscience buzzword for the amount of time you spend in REM vs slow wave sleep, which are different sleep stages.
Drinkers spend less time in REM sleep, don't synthesize as much melatonin in the evening, and their total time asleep is reduced.
These negative effects on sleep quality may explain some hangover symptoms, particularly cognitive impairment (Prat et al., 2008; Verster and Rohers, 2007).
All this goes to show that some hangover symptoms are because of the direct physiological effects of alcohol intake. Such effects include increased cytokines, electrolyte imbalances, sleep deprivation, hypoglycemia, and others.
This hypothesis says that hangover symptoms are due to the deleterious effects of compounds that are present in alcohol beverages. These compounds are called congeners (Calder, 1997).
Congeners tend to be amines, amides, acetones, polyphenols, methanol, and histamines. They're created during the alcoholic fermentation or are added during production and are part of what makes the experience of drinking a pinot noir so different from a mojito.
Chapman (1970) discovered that one-third of the subjects that consumed 1.5 grams/kg of bourbon (which is rife with congeners) experienced a hangover. By contrast, only 3% of subjects that had the same dose of vodka got a hangover.
More recent surveys seem to confirm that hangover severity is greater in beverages including larger numbers of congeners (Vester, 2006).
Protip: drinking a low-congener alcohol like vodka reliably reduces next-day hangover symptoms.
Among the best-studied congeners is methanol.
Jones (1987) argues that hangovers are caused by metabolites of methanol, formaldehyde, and formic acid. These chemicals are more hazardous than acetaldehyde.
Here's the evidence:
The short and sweet version.
Surprisingly, there's no "unified theory of hangovers" and no consensus on how to measure hangover severity
Another facet that is unrecognized is the potential differences of gender in a hangover.
Slutske et al. (2005) have noted that women are more vulnerable to both hangovers and the intoxicating effects of alcohol itself. Future research should look carefully into this since the data to be obtained would have prophylactic consequences of tremendous worth.
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