Alcohol hangovers occur when blood alcohol concentrations (BAC) return to zero. The event is characterized by pounding headache, sensitivity to lights and loud noises, dizziness, drowsiness, nausea, vomiting, dry mouth, sweating, concentration problems, hyper-excitability, and anxiety and/or depression.
The biology of hangovers is complex and surprisingly, has not been well-researched. Dehydration and sleep deprivation may be contributors to the state of being hung over, but biological changes during suggest that, as with a majority of disease, imbalances of immune factors, especially excessive production of inflammatory cytokines, may be the culprit.
Hangovers are reminiscent of “sickness behavior”, the feelings that sick individuals have during the course of fighting an infection. “Feeling poorly” is the effect of increased levels of proinflammatory cytokines, that increase inflammation in the brain.
During inflammation, a great deal of cross-talk, mediated by cytokines, goes on between the immune system, the brain, and the intestines, which stimulates a wide range of physical, hormonal, nervous , gastrointestinal, and emotional responses.
Increased levels of inflammatory cytokines, such as IL-12 and interferon-gamma (IFN-gamma) are found in individuals suffering from hangovers. Additionally IL-10 , which suppresses inflammatory cytokines, is also found at higher levels in hangover subjects.
C-reactive proteins (CRP) are found in the blood and are considered an excellent marker for inflammation in the body. High levels of C-reactive protein are strongly associated with the severity of hangover events. The response may be related to inflammation induced by excessive ingestion of certain alcohol components such as congeners, or alcohol metabolites.
Numerous anecdotal reports suggest that when the body is in immune inflammatory balance, that hangovers will not occur at all, or, will be severely limited in their scope.
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