Description and symptoms of alcohol consumption
The hangover is a general malaise that can manifest through a constellation of symptoms (physical, mental, physiological and psychological effects) and appears hours after an excessive consumption of alcohol.
The physical symptoms include fatigue, headache, high sensitivity to light and sound, red eyes, muscle pain and dry mouth. It can also be seen an increase in sympathetic activity (increase of the systolic pressure, tachycardia, tremor, and sweating). At the gastrointestinal level, there may be stomach pain, nausea and vomiting.
The intake of alcohol affects neurotramiters as histamine, serotonin and glutamate that control the waking cycle-dream. In general terms, the intake of alcohol produces a decrease in sleep latency and in REM sleep, and an increase of slow-wave sleep. The complex interactions between alcohol intake and sleep can have direct implications for cognitive and psychomotor performance. The mental symptoms include dizziness, vertigo, cognitive alterations (decrease in attention and concentration), and alterations of mood (depression, anxiety, irritability).
The cause of the hangover resides in some residual substances that are generated simultaneously to the process of obtaining alcohol, so are called congeners, above all the methanol, acetaldehyde, various polyphenols and especially the histamine. In addition to the broken down produce various substances harmful also responsible for the physical and mental symptoms of the hangover.
Alcohol and human functioning
It has been described a relationship between the harmful effects in the next day at the level of psychomotor performance, cognitive and psychological effects on the physiology of sleep caused by alcohol. Sleep fragmentation (which translates into a bad quality of sleep) due to the nocturnal intake of high doses of alcohol and the subsequent hangover is associated with a high daytime sleepiness the next day, with negative effects on attention, memory, concentration ability and psychomotor performance.
The excessive daytime sleepiness, the decrease in psychomotor performance and cognitive capacity may result, among others, an increase in the number of accidents and/or traffic accidents, an increase of absenteeism as well as interpersonal conflicts. This involves a great economic and social cost that should not be underestimated.
These consequences are much more dramatic if one takes into account that a very important part of the population that suffers from these symptoms repeatedly found in academic age. Needless to say, the cognitive function and memory are essential for the development of the daily activities of learning.
Histamine and DAO deficiency in the etiology of the effects of acute intake of alcohol
It is known that the acute intake of alcohol gives rise to a raise in the levels of circulating histamine, due to the fact that alcohol causes:
- Decrease in the amount of enzyme diamine oxidase (DAO) in the intestinal mucosa even in healthy individuals without genetic enzyme deficiency.
- DAO activity inhibition, because the metabolite acetaldehyde (alcohol) competes with the metabolites of histamine by aldehyde dehydrogenase (which also participates in the degradation of histamine). The consequence of this competition is that the metabolites of histamine accumulate and eventually inhibit the DAO.
- Increase of histamine release by mast cells of the intestine, which would contribute to the generation of damage to the intestinal mucosa.
The endogenous histamine is a biogenic amine that acts as a neurotransmitter and participates in local immune reactions. Is synthesized primarily in neurons of the central nervous system, in mast cells and endothelial cells. It is degraded by DiAmine Oxidase (DAO), which is synthesized in kidney, intestine and placenta.
Enzyme diamine oxidase (DAO) and histamine: new biomarker for the prevention of the effects of alcohol consumption
The exogenous histamine, contained in the foods we eat, can go through the intestinal epithelium and reach the blood. The intestinal epithelium also presents DAO that degrades much of this exogenous histamine, preventing its assimilation. In addition, some foods stimulate endogenous synthesis of histamine, thus modifying the circulating levels of histamine.
High levels of circulating histamine due to a reduction in the ability to degrade the histamine (by having a low DAO activity by genetic disorders or by a functional reduction of DAO activity by alcohol intake) can cause a syndrome characterized by abdominal pain, headache and/or migraine, hives, tachycardia, hypotension, muscle pain and respiratory obstruction.
Prevention of the effects of alcohol with enzyme supplementation diamine oxidase (DAO)
DR Healthcare studies show that, at least in great part, the harmful effects of the hangover are a result of the increased blood levels of histamine induced by alcohol intake by inhibiting the enzymatic DAO activity (DAO). Based on this, the minimization of this increase of circulating-histamine through the empowerment of the action of the enzyme DAO avoid, or at least diminishes, the symptomatology of hangover.
Supplementation of DAO acts complementing the enzyme when the functional activity of this is reduced by an inhibition induced by the ingestion of alcohol, allowing for the correct metabolism of exogenous histamine.
Therefore, the administration of DAO with DAOfood before a meal accompanied by alcoholic beverage, increases the amount of active DAO in the small intestine and the ability to degrade the histamine swallowed, although part of the enzyme has been blocked by the excessive alcohol intake “along with” and “after” the lunch or dinner.
The decline in levels of circulating histamine results in a decrease of the symptomatology of the hangover, a harmful effects on sleep architecture and a decrease in behavioral, cognitive and psychological associated with acute intake of alcohol.