The medical term for the hangover is Veisalgia. Kveis is Norwegian
and is defined as uneasiness following debauchery. And, algia
is Greek meaning pain. The hangover defined is having, at least,
two of the following listed symptoms with sufficient severity
to disrupt the performance of daily task and responsibilities
(percentage of population experiencing each symptom): headache
(66%), poor sense of overall well being (60%), diarrhea (36%),
anorexia (21%), tremulousness (20%), fatigue (20%), and nausea
(9%). Experimentally an alcohol dose of 1.5 - 1.75 gms/kg body
weight (5 to 7 standard cocktails) will almost always produce
hangover symptoms in those susceptible individuals .
Wouldn’t it be wonderful if the hangover were a result
of dehydration as many of us thought when we first started drinking?
Unfortunately preventing a hangover is much more complicated
than just drinking lots of fluids along with our alcoholic beverages.
Aside from dehydration, hangovers are a result of alterations
in endocrine function, dysregulation of cytokine pathways, and
proper elimination of toxins produced during alcohol preparation
and normal liver metabolism.
Anti-diuretic hormone (ADH) is produced by the pituitary gland
and causes the body to retain water. While drinking and during
acute intoxication, ADH production is decreased and so we see
an increase in urination resulting in dehydration. However, during
the hangover phase, ADH production is increased causing a retention
of body fluids resulting in puffiness in tissues for example
in the face and around the eyes .
Other hormonal alterations include the adrenal cortex hormones,
aldosterone and cortisol. Aldosterone helps regulate blood levels
of sodium, chloride, and potassium. During drinking aldosterone
levels decrease causing a decrease in sodium and an increase
in potassium levels resulting in decreased blood volumes and
a temporary decrease in blood pressure. However, during the hangover
period aldosterone increases causing an increase in serum sodium
levels and an increase in blood volumes and blood pressure. These
electrolyte imbalances can be responsible for muscle weakness,
fatigue, vomiting, and loss of appetite experienced during the
Cortisol is a regulator of fat, carbohydrate, and protein metabolism.
It also works with aldosterone to balance electrolytes, and functions
as an important anti-inflammatory. During times of hangover,
cortisol causes an increase in blood sugar levels by converting
amino acids into glucose in the liver known as gluconeogenesis.
Increased blood sugar levels would cause in increase in insulin
production and abnormal stress on pancreatic and liver function.
Cortisol also decreases protein in skeletal muscles and causes
a redistribution of body fat from the legs and arms to the trunk
and shoulder blade regions of the body.
Next, rennin production, an enzyme produced by the kidneys and
responsible for regulating blood pressure, is increased. Rennin
acts on angiotensin to form a vasopressor substance known as
angiotensin I. This causes an increase in blood pressure and
an increase in heart rate and left ventricular ejection . This
may be responsible for increases noted in mortality rates due
to myocardial infarction during hangover periods.
Other important factors involved in the intensity and production
of hangover symptoms include the production and elimination of
toxins (conversion of ethanol into acetaldehyde and acetate in
the liver) and the increased production of thromboxanes. Thromboxanes
are products of fatty acid metabolism and are responsible for
blood vessel constriction (raising blood pressure), blood platelets
sticking together (increase in clot formation), and decreases
of natural killer cells (decreased immunity). An increase in
thromboxane-B2 during the hangover has also been found to cause
symptoms similar to those in a viral infection, including nausea,
headache, and diarrhea .
Lastly, the level of congeners found in alcoholic beverages
can be a major causative factor in the production of hangover
symptoms . Congeners are the by-products of alcohol preparations.
Higher concentrations are found in dark liquors such as brandy,
wine, dark tequila, and whiskey. Lower concentrations are found
in clear liquors, such as rum, vodka, clear tequila, and gin.
Experimental studies revealed that 33% of test subjects who consumed
1.5 gms/kg of bourbon experienced hangover symptoms while only
3% of those who consume the same volume of vodka experienced
Report of a Subcommittee of the National Advisory Council on
Alcohol Abuse and Alcoholism on the Review of the Extramural
Research Portfolio for Prevention, National Institute on Alcohol
Abuse and Alcoholism, U.S. Department of Health and Human Services,
Doernberg D, Stinson F. U.S. Alcohol Epidemiologic Data Reference Manual. Vol
1, U.S. Apparent Consumption of Alcoholic Beverages Based on State Sales, Taxation,
or Receipt Data. Rockville, MD: U.S. Department of Health and Human Services,
Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration,
Stockwell T. Towards Guidelines for Low-risk Drinking: Quantifying the Short
and Long-term Costs of Hazardous Alcohol Consumption. Alcohol Clin Exp Res.
Wiese JG, Shlipak MG, and Browner WS, The Alcohol Hangover, Ann Intern Med.
Sainio K, et al. Electroencephalographic Changes During Experimental Hangover.
Electroencephalogr Clin Neuro-physiol. 1976:40:535-8.
Linkola J, et al. Plasma Vasopressin in Ethanol Intoxication and Hangover.
Acta Physiol Scand. 1978;104:180-7.
Linkola J, et al. Renin-aldosterone Axis in Ethanol Intoxication and Hangover.
Eur J Clin Invest. 1976;6:191-4.
Kangasaho M, et al. Effects of Ethanol Intoxication and Hangover on Plasma
Levels of Thromboxane B2 Formation By Platelets in Man. Thromb Haemost. 982;48:232-4.
Damrau F, Goldberg AH. Adsorption of Whisky Congeners by Activated Charcoal.
Chemical and Clinical Studies Related to Hangover. Southwest Med. 1971;52:179-82.
Chapman LF. Experimental Induction of Hangover. Q J Stud Alcohol, 1970;5(Suppl
Diaz A, et al. Comparative Study Between A Complex of Flavonoids and Polyphenols
and Placebo in Hepatic Disease Due To Alcohol. General Hospital of Mexico.
International Meeting of Hepatology. Military School of Medicine.