<P> Another classic finding of alcohol intoxication is ataxia, in its appendicular, gait, and truncal forms . Appendicular ataxia results in jerky, uncoordinated movements of the limbs, as if each muscle were working independently from the others . Truncal ataxia results in postural instability; gait instability is manifested as a disorderly, wide - based gait with inconsistent foot positioning . Ataxia causes the observation that drunk people are clumsy, sway back and forth, and often fall down . It is presumed to be due to alcohol's effect on the cerebellum . </P> <P> The Mellanby effect is the phenomenon that the behavioral impairment due to alcohol is less, at the same BAC, when the BAC is decreasing than when it is increasing . In other words, at a given point on the upward slope of BAC (while drinking), impairment is greater than at a given point on the downward slope (after drinking), even though the BAC is the same at the two points . This effect was confirmed in a 2017 meta - analysis of 26 studies . </P> <P> Humans metabolize ethanol primarily through NAD - dependent alcohol dehydrogenase (ADH) class I enzymes (i.e. ADH1A, ADH1B, and ADH1C) to acetaldehyde and then metabolize acetaldehyde primarily by NAD - dependent aldehyde dehydrogenase 2 (ALDH2) to acetic acid . Eastern Asians reportedly have a deficiency in acetaldehyde metabolism in a surprisingly high percentage (approaching 50%) of their populations . The issue has been most thoroughly investigated in native Japanese where persons with a single - nucleotide polymorphism (SNP) variant allele of the ALDH2 gene were found; the variant allele, encodes lysine (lys) instead of glutamic acid (glu) at amino acid 487; this renders the enzyme essentially inactive in metabolizing acetaldehyde to acetic acid . The variant allele is variously termed glu487lys, ALDH2 * 2, and ALDH2 * 504lys . In the overall Japanese population, about 57% of individuals are homozygous for the normal allele (sometimes termed ALDH2 * 1), 40% are heterozygous for glu487lys, and 3% are homozygous for glu487lys . Since ALDH2 assembles and functions as a tetramer and since ALDH2 tetramers containing one or more glu487lys proteins are also essentially inactive (i.e. the variant allele behaves as a dominant negative), homozygote individuals for glu487lys have undetectable while heterozygote individuals for glu487lys have little ALDH2 activity . 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 . 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 . </P> <P> The percentages of glu487lys heterozygous 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 . </P>

Immediate effects of alcohol on a human body