Introduction
Despite the fact that alcohol hangover is omnipresent in throughout the world wherever alcohol is consumed, surprisingly little scientific research has been published on the topic. In their 2009 review of the topic of hangover, Dr. Gemma Prat and her colleagues sum up the state of the knowledge about alcohol hangover in scientific circles today. They note that there is not even a generally agreed upon operational definition of hangover. Only in very recent years have scales been introduced to measure hangover and most research available on the topic of hangover has not used any form of standardized scale. We will follow Dr. Prat in defining hangover as a state of distress which occurs after Blood Alcohol Content (BAC) has reached zero.
Not only do we lack an agreed upon definition of what a hangover is, we are also uncertain of mechanism by which heavy alcohol consumption causes hangovers, although there are several hypotheses about what might be happening. If you ever visit a web site which claims to explain to you exactly how a hangover works, then you may assume that the site is less than trustworthy--because we are still far, far from having all the answers to this question.
Hangover Symptoms
Physical symptoms of a hangover include fatigue, headache, increased sensitivity to light and sound, redness of the eyes, muscle aches, and thirst. Signs of increased sympathetic nervous system activity can accompany a hangover, including increased systolic blood pressure, rapid heartbeat (i.e., tachycardia), tremor, and sweating. Mental symptoms include dizziness; a sense of the room spinning (i.e., vertigo); and possible cognitive and mood disturbances, especially depression, anxiety, and irritability.
The Withdrawal Hypothesis
Some researchers have speculated that hangover is a form of minor alcohol withdrawal. There is overlap between some of the symptoms of minor withdrawal and hangover such as nausea, headache, and hypersensitivity to light and sound. However there are also some distinct differences. In particular, during a hangover the brain waves measured on an EEG slow down, whereas during alcohol withdrawal the brain waves speed up.
The Acetaldehyde Hypothesis
When alcohol is metabolized in the body it is first converted into acetaldehyde and then this acetaldehyde is converted into acetic acid which is further broken down into carbon dioxide and water. Acetaldehyde is rather poisonous and can cause vomiting, headache, rapid heartbeat and flushing. Antabuse--the drug which makes people sick if they drink alcohol--works by causing acetaldehyde to build up in the body. It is this acetaldehyde which makes people sick when they drink on antabuse. In severe cases mixing antabuse and alcohol can lead to death.
Acetaldehyde is not present during hangovers; by the time one begins to get hangover symptoms the acetaldehyde has already been metabolized by the body and is gone. Some researchers hypothesize that hangover symptoms are caused by the aftereffects of acetaldehyde on the central nervous system. This hypothesis has yet to be confirmed, although Dr. Yokoyama and his colleagues (2005) have found some evidence that individuals who have difficulty metabolizing acetaldehyde have more severe hangovers than do other people.
The Direct Alcohol Effect Hypothesis
Alcohol causes the following effects both during and after intoxication
- Dehydration and electrolyte imbalance: Alcohol inhibits the production of anti-diuretic hormone. This leads to increased urination and dehydration
- Irritated stomach lining: Alcohol directly irritates the stomach lining and this can lead to nausea, vomiting and diarrhea.
- Low blood sugar: Alcohol causes some lowering of blood sugar in all drinkers because alcohol interferes with the generation of glucose by the liver. In most cases this does not lead to severe low blood sugar, however this can lead to severe low blood sugar in individuals who drink on an empty stomach or those with a tendency towards low blood sugar. Low blood sugar can be associated with tiredness, crankiness, and dizziness.
- Sleep disturbances: Alcohol disturbs the quality of sleep, leads to less REM sleep, and can lead to early waking. These sleep disturbance might contribute to the tiredness and cognitive dysfunction associated with hangover.
- Dilation of blood vessels: This is a possible cause of hangover headache.
- Increased production of cytokines: Cytokines are like hormones that function at the cellular level. Examples of cytokines are interleukins and interferons. Cytokines are responsible for the inflammation and fever which the body uses to fight infections. Alcohol increases the production of cytokines and cytokines might be a cause of muscle aches, headache or poor memory performance while hungover.
The Congener Hypothesis
Congeners are chemical compounds other than alcohol and water which are found in alcoholic beverages and which contribute to giving them a pleasing color and flavor and smell. Examples of typical congeners are amines, amides, acetones, polyphenols, methanol, and histamine.
In 1970 Dr. LF Chapman did an experiment to see whether congeners increase the likelihood of people having hangovers. Dr. Chapman gave one group of subjects bourbon whiskey, a beverage which is very high in congeners. Another group of subjects were given vodka which is very low in congeners. Both groups were given the same dosage of alcohol (1.5g/kg). 33% of the subjects who received the bourbon reported hangover, whereas only 3% of subjects who received vodka reported hangover.
There are a couple of studies (Woo et al, 2005, Bendtsen et al 1998) which suggest that the congener methanol may be involved in hangover. Methanol is also known as methyl alcohol or wood alcohol and is a highly poisonous compound which can cause blindness or death. The human body breaks methanol down into the toxic components formaldehyde and formic acid. Trace amounts of methanol are found in alcoholic beverages, but they are also found in orange or apple juices.
In order to test the hypothesis that methanol is responsible for hangover it would be necessary to conduct the following experiment: a mixture of pure ethanol and water would need to be compared to a mixture of ethanol and water which contained a trace of methanol and both of these should be compared to water containing a trace of methanol. If such an experiment were conducted it would work to confirm or disconfirm the methanol hypothesis of hangover.
There are several other congeners which are also hypothesized to contribute to hangover, including isopentanol, ethylic acetate, and ethyl formate, etc. The hypothesis that these congeners contribute to hangover could be tested the same as the methanol hypothesis above. Such experiments have yet to be carried out.
The Lactic Acid Hypothesis
Alcohol metabolism produces an excess of NADH which leads to excessive production of lactic acid which in turn leads to lactic acidosis. Lactic acidosis could be responsible for the muscle cramps associated with hangover.
Other Factors Contributing to Hangover
Several researchers have proposed that people with a tendency towards alcohol addiction have a tendency to have more severe hangovers and withdrawal symptoms. This is interesting since it is also proposed that people in active alcohol addiction rarely have hangovers compared to normal drinkers.
In a 1993 study, Dr. E Harbourg and his colleagues found that people were likely to have more severe hangovers if they felt guilty about drinking; if they were neurotic; if they were angry or depressed when they drank or if they were drinking in response to negative life events
It is rather surprising that no studies have been carried out at all on the importance of eating well, being well hydrated, and drinking slowly on the severity of hangover. Based on our personal experiences here at HAMS we believe that avoiding blood alcohol spikes is of paramount importance in both preventing blackout and in reducing severity of hangover. We can only hope that these factors are researched in a scientific manner in the future. In the meantime we shall merely say that good nutrition can't hurt.
. Conclusions
- Withdrawal: It is still a matter of debate as to whether alcohol hangover should be considered a form of minor alcohol withdrawal or an independent entity in its own right.
- Acetaldehyde: We need further experimental evidence to determine the extent to which acetaldehyde contributes to hangover.
- Ethanol itself: Some direct effects of alcohol itself quite clearly contribute to hangover. These direct effects of alcohol include dehydration; dilation of blood vessels which can lead to headache; irritation of the stomach lining which can lead to nausea and vomiting; sleep disturbances which can lead to cognitive dysfunction; cytokine effects which can lead to headaches and memory dysfunction, sleep disturbances which can lead to feelings of tiredness and memory dysfunction and low blood sugar which can lead to mood changes or fatigue and dizziness.
- Congeners: We have good evidence that congeners can contribute to the intensity of a hangover but are not yet precisely certain of which congeners do so or the exact mechanism by which this happens.
- Lactic Acid: Lactic acidosis may contribute to hangover in the form of muscle aches,
- Mood: You are more likely to get a hangover if you drink when you are in a bad mood than of you drink when you are in a good mood.
More Info
For more information about hangovers please visit our web pages:
Can You Prevent a Hangover?
And
Hangover Cures
REFERENCES:
Bendtsen P, JonesW, Helander A. 1998. Urinary excretion of methanol and 5-hydroxytryptophol as biochemical markers of recent drinking in the hangover state. Alcohol Alcohol 33: 431-438.
Chapman LF. (1970). Experimental induction of hangover. Q J Stud Alcohol 5: 67-85.
Harbourg E, Gunn R, Gleiberman L, DiFranceisco W, Schork A. 1993. Psychosocial factors, alcohol use, and hangover sings among social drinkers: a reappraisal. J Clin Epidemiol 46: 413-422.
Ophardt, C. (2003). Alcohol Metabolism Effects - Elmhurst College
http://chemistry.elmhurst.edu/vchembook/642alcoholmet.html
Prat G, Adan A, Sánchez-Turet M. (2009). Alcohol hangover: a critical review of explanatory factors. Hum Psychopharmacol. Jun;24(4):259-67.
Rohsenow DJ, Howland J, Minsky SJ, Greece J, Almeida A, Roehrs TA. (2007). The acute hangover scale: a new measure of immediate hangover symptoms. Addict Behav 32: 1314-1320.
Slutske WS, Piasecki TM, Hunt-Carter E. (2003). Development and initial validation of the hangover symptoms scale: prevalence and correlates of hangover symptoms in college students. Alcohol Clinical and Experimental Research 27: 1442-1450.
Swift R, Davidson D. (1998). Alcohol hangover: mechanisms and mediators. Alcohol Health and Research World. 22(1):54-60.
http://pubs.niaaa.nih.gov/publications/arh22-1/54-60.pdf
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT. (2005). Concentration changes of methanol in blood samples during an experimentally induced alcohol hangover state. Addict Biol 10: 351-355.
Yokoyama M, Yokoyama A, Yokoyama T, et al. (2005). Hangover susceptibility in relation to aldehyde dehydrogenase-2 genotype, alcohol flushing and mean corpuscular volume in Japanese workers. Alcohol Clinical and Experimental Research 29: 1165-1171.
