plus homozygous genotypes are about 35% in native caboclo of brazil, 30% in chinese, 28% in koreans, 11% in thai people, 7% in malaysians, 3% in natives of india, 3% in hungarians, and 1% in filipinos; percentages are essentially 0 in individuals of native african descent, caucasians of western european descent, turks, australian aborigines, australians of western european descent, swedish lapps, and alaskan eskimos. the prevalence of ethanol-induced allergic symptoms in 0 or low levels of glu487lys genotypes commonly ranges above 5%. these "ethanol reactors" may have other gene-based abnormalities that cause the accumulation of acetaldehyde following the ingestion of ethanol or ethanol-containing beverages. 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. 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. pathophysiology epidemiology: disability-adjusted life year for alcohol use disorders per 100,000 inhabitants in 2004. no data less than 50 50–150 150–250 250–350 350–450 450–550 550–650 650–750 750–850 850–950 950–1050 more than 1050 at low or moderate doses, alcohol acts primarily as a positive allosteric modulator of gabaa. alcohol binds to several different subtypes of gabaa, but not to others. the main subtypes responsible for the subjective effects of alcohol are the α1β3γ2, α5β3γ2, α4β3δ and α6β3δ subtypes, although other subtypes such as α2β3γ2 and α3β3γ2 are also affected. activation of these receptors causes most of the effects of alcohol such as relaxation and relief from anxiety, sedation, ataxia and increase in appetite and lowering of inhibitions that can cause a tendency toward violence in some people. alcohol has a powerful effect on glutamate as well. alcohol decreases glutamate's ability to bind with nmda and acts as an antagonist of the nmda receptor, which plays a critical role in ltp by allowing ca2+ to enter the cell. these inhibitory effects are thought to be responsible for the "memory blanks" that can occur at levels as low as 0.03% blood level. in addition, reduced glutamate release in the dorsal hippocampus has been linked to spatial memory loss. chronic alcohol users experience an upregulation of nmda receptors because the brain is attempting to reestablish homeostasis. when a chronic alcohol user stops drinking for more than 10 hours, apoptosis can occur due to excitotoxicity. the seizures experienced during alcohol abstinence are thought to be a result of this nmda upregulation. alteration of nmda receptor numbers in chronic alcoholics is likely to be responsible for some of the symptoms seen in delirium tremens during severe alcohol withdrawal, such as delirium and hallucinations. other targets such as sodium channels can also be affected by high doses of alcohol, and alteration in the numbers of these channels in chronic alcoholics is likely to be responsible for as well as other effects such as cardiac arrhythmia. other targets that are affected by alcohol include cannabinoid, opioid and dopamine receptors, although it is unclear whether alcohol affects these directly or if they are affected by downstream consequences of the gaba/nmda effects. 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. alcohol inhibits sodium-potassium pumps in the cerebellum and this is likely how it corrupts cerebellar computation and body co-ordination. contrary to popular belief, research suggests that acute exposure to alcohol is not neurotoxic in adults and actually prevents nmda antagonist-induced neurotoxicity. alcohol and sleep main article: alcohol use and sleep low doses of alcohol (one 360 ml (13 imp fl oz; 12 us fl oz) beer) appear to increase total sleep time and reduce awakening during the night. the sleep-promoting benefits of alcohol dissipate at moderate and higher doses of alcohol. previous experience with alcohol also influences the extent to which alcohol positively or negatively affects sleep. under free-choice conditions, in which subjects chose between drinking alcohol or water, inexperienced drinkers were sedated while experienced drinkers were stimulated following alcohol consumption. in insomniacs, moderate doses of alcohol improve sleep maintenance. moderate alcohol consumption 30–60 minutes before sleep, although decreasing, disrupts sleep architecture. rebound effects occur once the alcohol has been largely metabolized, causing late night disruptions in sleep maintenance. under conditions of moderate alcohol consumption where blood alcohol levels average 0.06–0.08 percent and decrease 0.01–0.02 percent per hour, an alcohol clearance rate of 4–5 hours would coincide with disruptions in sleep maintenance in the second half of an 8-hour sleep episode. in terms of sleep architecture, moderate doses of alcohol facilitate "rebounds" in rapid eye movement (rem) following suppression in rem and stage 1 sleep in the first half of an 8-hour sleep episode, rem and stage 1 sleep increase well beyond baseline in the second half. moderate doses of alcohol also very quickly increase slow wave sleep (sws) in the first half of an 8-hour sleep episode. enhancements in rem sleep and sws following moderate alcohol consumption are mediated by reductions in glutamatergic activity by adenosine in the central nervous system. in addition, tolerance to changes in sleep maintenance and sleep architecture develops within three days of alcohol consumption before bedtime. alcohol consumption and balance alcohol can affect balance by altering the viscosity of the endolymph within the otolithic membrane, the fluid inside the semicircular canals inside the ear. the endolymph surrounds the ampullary cupula which contains hair cells within the semicircular canals. when the head is tilted, the endolymph flows and moves the cupula. the hair cells then bend and send signals to the brain indicating the direction in which the head is tilted. 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. this can also result in vertigo, or "the spins". alcohol and postprandial triglycerides alcohol taken with a meal increases and prolongs postprandial triglyceridemia. this is true despite the observation that the relationship between alcohol consumption and triglyceridemia is "j-shaped," meaning that fasting triglycerides concentration is lower in people who drink 10–20 g/alcohol a day compared to people who either abstain from alcohol or who drink more per day. alcohol and blood pressure a systematic review reported that alcohol has bi-phasic effect on blood pressure. both systolic and diastolic blood pressure fell when they were measured couple of hours after alcohol consumption. however, the longer term measurement (20 hours average) showed a modest but statistically significant increase in blood pressure: a 2.7 mmhg rise in systolic blood pressure and 1.4 mmhg rise in diastolic blood pressure. 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. alcohol and pain a 2015 literature review found that alcohol administration confers acute pain-inhibitory effects. it also found the relationship between alcohol consumption and pain is curvilinear; moderate alcohol use was associated with positive pain-related outcomes and heavy alcohol use was associated with negative pain-related outcomes.