Short-term effects of alcohol consumption

Extreme levels of consumption can cause alcohol poisoning and death; a concentration in the blood stream of 0.36% will kill half of those affected.

BAC can be different for each person depending on their age, sex, pre-existing health condition, even if they drink the same amount of alcohol.

Stimulated areas include the cortex, hippocampus, and nucleus accumbens, which are all responsible for both thinking and pleasure seeking.

[15][16] A related effect, which is caused by even low levels of alcohol, is the tendency for people to become more animated in speech and movement.

This causes reward systems in the brain to become more active, which may induce certain individuals to behave in an uncharacteristically loud and cheerful manner.

This occurs because alcohol confuses osmoreceptors in the hypothalamus, which relay osmotic pressure information to the posterior pituitary, the site of antidiuretic hormone release.

Alcohol causes the osmoreceptors to signal that there is low osmotic pressure in the blood, which triggers an inhibition of the antidiuretic hormone.

As a consequence, one's kidneys are no longer able to reabsorb as much water as they should be absorbing, therefore creating excessive volumes of urine and the subsequent overall dehydration.

[citation needed] Symptoms of ethanol overdose may include nausea, vomiting, CNS depression, coma, acute respiratory failure, or death.

Directly translated to human beings, this would mean that if a person who weighs 70 kg (150 lb) drank a 500 mL (17 US fl oz) glass of pure ethanol, they would theoretically have a 50% risk of dying.

Acute alcohol intoxication through excessive doses in general causes short- or long-term health effects.

The excess amount of blood aldehyde produce facial flushing, nausea, rapid heartbeat, and other adverse effects.

[27][28] Presence of these alleles causes rapid conversion of alcohol to acetaldehyde which can be toxic in large amount.

[30] Individuals will have unique experiences of the effects of alcohol, including measurable differences in the extent of stimulating experiences during the beginning of a drinking episode as breath alcohol content (BAC) rises and sedative effects later in a drinking episode as BAC wanes.

[32] There is also mounting evidence for consideration of SR as an endophenotype with some studies suggesting that it accounts for a significant proportion of genetic risk for the development of alcohol use disorder.

[38] In consequence, Japanese individuals homozygous or, to only a slightly lesser extent, heterozygous for glu487lys metabolize ethanol to acetaldehyde normally but metabolize acetaldehyde poorly and are susceptible to a set of adverse responses to the ingestion of, and sometimes even the fumes from, ethanol and ethanol-containing beverages; these responses include the transient accumulation of acetaldehyde in blood and tissues; facial flushing (i.e. the "oriental flushing syndrome" or Alcohol flush reaction), urticaria, systemic dermatitis, and alcohol-induced respiratory reactions (i.e. rhinitis and, primarily in patients with a history of asthma, mild to moderately bronchoconstriction exacerbations of their asthmatic disease.

[39] These allergic reaction-like symptoms, which typically occur within 30–60 minutes of ingesting alcoholic beverages, do not appear to reflect the operation of classical IgE- or T cell-related allergen-induced reactions but rather are due, at least in large part, to the action of acetaldehyde in stimulating tissues to release histamine, the probable evoker of these symptoms.

For example, the surveyed incidence of self-reported ethanol-induced flushing reactions in Scandinavians living in Copenhagen as well as Australians of European descent is about 16% in individuals homozygous for the "normal" ADH1B gene but runs to ~23% in individuals with the ADH1-Arg48His SNP variant; in vitro, this variant metabolizes ethanol rapidly and in humans, it is proposed, may form acetaldehyde at levels that exceed the capacity of ALDH2 to metabolize.

[40][42] Notwithstanding such considerations, experts suggest that the large proportion of alcoholic beverage-induced allergic-like symptoms in populations with a low incidence of the glu487lys genotype reflect true allergic reactions to the natural and/or contaminating allergens particularly those in wines and to a lesser extent beers.

Alcohol also acts as a stimulant in low doses, as it triggers the release of dopamine in the striatum, with this mechanism also being responsible for the compound's interaction with the brain's reward system.

People with a family history of alcoholism may exhibit genetic differences in the response of their NMDA glutamate receptors as well as the ratios of GABAA subtypes in their brain.

[60] Alcohol causes generalized CNS depression, is a positive allosteric GABAA modulator and is associated and related with cognitive, memory, motor, and sensory impairment.

[61] Complications of this disease could include a burning pain in the abdomen, bloating and in severe cases, the presence of dark black stools indicate internal bleeding.

[62] A person who drinks alcohol regularly is strongly advised to reduce their intake to prevent PUD aggravation.

Consequently, LPS levels increase in the portal vein, liver and systemic circulation after alcohol intake.

Immune cells in the liver respond to LPS with the production of reactive oxygen species, leukotrienes, chemokines and cytokines.

Rebound effects occur once the alcohol has been largely metabolized, causing late night disruptions in sleep maintenance.

Enhancements in REM sleep and SWS following moderate alcohol consumption are mediated by reductions in glutamatergic activity by adenosine in the central nervous system.

By changing the viscosity of the endolymph to become less dense when alcohol enters the system, the hair cells can move more easily within the ear, which sends the signal to the brain and results in exaggerated and overcompensated movements of body.

[69] A Cochrane systematic review based on only randomized controlled trials which investigates the acute effect of alcohol consumption in healthy and hypertensive adults is in progress.