Abstract
BackgroundThe mechanism of veisalgia cephalgia or hangover headache is unknown. Despite a lack of mechanistic studies, there are a number of theories positing congeners, dehydration, or the ethanol metabolite acetaldehyde as causes of hangover headache.MethodsWe used a chronic headache model to examine how pure ethanol produces increased sensitivity for nociceptive behaviors in normally hydrated rats.ResultsEthanol initially decreased sensitivity to mechanical stimuli on the face (analgesia), followed 4 to 6 hours later by inflammatory pain. Inhibiting alcohol dehydrogenase extended the analgesia whereas inhibiting aldehyde dehydrogenase decreased analgesia. Neither treatment had nociceptive effects. Direct administration of acetate increased nociceptive behaviors suggesting that acetate, not acetaldehyde, accumulation results in hangover-like hypersensitivity in our model. Since adenosine accumulation is a result of acetate formation, we administered an adenosine antagonist that blocked hypersensitivity.DiscussionOur study shows that acetate contributes to hangover headache. These findings provide insight into the mechanism of hangover headache and the mechanism of headache induction.
Highlights
Alcohol hangover headache is one of the most common types of headache, yet the mechanism of how ethanol causes headache pain is unknown [1,2]
This suggests that the headache experienced after the combination of ethanol and disulfiram and in individuals who lack functional aldehyde dehydrogenase-2 (ALDH-2) is not due to the same mechanism as the hangover headache experienced in the absence of disulfiram
We show the effects of ethanol and its two major metabolites, acetaldehyde and acetate, in an animal model of trigeminal pain
Summary
Alcohol hangover headache is one of the most common types of headache, yet the mechanism of how ethanol causes headache pain is unknown [1,2]. Disulfiram, an aldehyde dehydrogenase inhibitor, given with ethanol, causes symptoms similar to those seen in individuals expressing functionally inactive ALDH-2. This indirect evidence suggests that increased acetaldehyde concentrations may induce headaches. Serum acetaldehyde concentrations with ethanol alone are very low in normal individuals because acetaldehyde is rapidly metabolized into acetate [17,18,19] This suggests that the headache experienced after the combination of ethanol and disulfiram and in individuals who lack functional ALDH-2 is not due to the same mechanism as the hangover headache experienced in the absence of disulfiram. Despite a lack of mechanistic studies, there are a number of theories positing congeners, dehydration, or the ethanol metabolite acetaldehyde as causes of hangover headache
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