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Short-term effects of alcohol consumption

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The short-term effects of alcohol on the human body can take several forms.

Alcohol, specifically ethanol, is a potent central nervous system depressant, with a range of side effects. The amount and circumstances of consumption play a large part in determining the extent of intoxication; for example, consuming alcohol after a heavy meal causes alcohol to absorb more slowly.[1] Hydration also plays a role, especially in determining the extent of hangovers.[2] The concentration of alcohol in blood is usually measured in terms of the blood alcohol content.

Initially, alcohol generally produces feelings of relaxation and cheerfulness, but further consumption can lead to blurred vision and coordination problems. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream it can diffuse into nearly every biological tissue of the body. After excessive drinking, unconsciousness can occur and extreme levels of consumption can lead to alcohol poisoning and death (a concentration in the blood stream of 0.40% will kill half of those affected[3][4]). Death can also occur through asphyxiation by vomit. An appropriate first aid response to an unconscious, drunken person is to place them in the recovery position.

Effect by dosage

Different concentrations of alcohol in the human body have different effects on the subject.

Moderate doses

French wines.

Ethanol inhibits the ability of glutamate to open the cation channel associated with the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. Although alcohol is typically thought of purely as a depressant, at low concentrations it can actually stimulate certain areas of the brain [citation needed]. Alcohol sensitizes the N-methyl-D-aspartate (NMDA) system of the brain, making it more receptive to the neurotransmitter glutamate [citation needed]. Stimulated areas include the cortex, hippocampus and nucleus accumbens, which are responsible for thinking and pleasure seeking. Another one of alcohol's agreeable effects is body relaxation, possibly caused by neurons transmitting electrical signals in an alpha waves-pattern; Alpha waves are observed (with the aid of EEGs) when the body is relaxed. Heightened pulses are thought to correspond to higher levels of enjoyment.

Alcohol has also been linked with lowered inhibitions, though it is unclear to what degree this is chemical versus psychological as studies with placebos can often duplicate the social effects of alcohol at low to moderate doses. Some studies have suggested that intoxicated people have much greater control over their behavior than is generally recognized, though they have a reduced ability to evaluate the consequences of their behavior.[5] Behavioral changes associated with drunkenness are, to some degree, contextual [citation needed]. A scientific study found that people drinking in a social setting significantly and dramatically altered their behavior immediately after the first sip of alcohol [citation needed], well before the chemical itself could have filtered through to the nervous system.

Areas of the brain responsible for planning and motor learning are dulled. A related effect, caused by even low levels of alcohol, is the tendency for people to become more animated in speech and movement. This is due to increased metabolism in areas of the brain associated with movement, such as the nigrostriatal pathway. This causes reward systems in the brain to become more active, and combined with reduced understanding of the consequences of their behavior, can induce people to behave in an uncharacteristically loud and cheerful manner.

Alcohol has been known to mitigate the production of ADH (antidiuretic hormone), which is a hormone that acts on the kidney, favoring water reabsorption in the kidneys during filtration. This occurs because alcohol confuses osmoreceptors in the hypothalamus, which relay osmotic pressure information to the posterior pituitary, the site of ADH release. Alcohol makes the osmoreceptors signal as if there was a too low osmotic pressure in the blood, which triggers an inhibition of ADH. Consequently, one's kidneys are no longer able to reabsorb as much water as they should be absorbing, leading to creation of excessive volumes of urine and subsequently overall dehydration.

Excessive doses

Excessive doses are generally volumes that cause short- or long-term health effects.

Slowing

NMDA receptors start to become unresponsive, slowing areas of the brain they are responsible for. Contributing to this effect is the activity which alcohol induces in the gamma-aminobutyric acid system (GABA). The GABA system is known to inhibit activity in the brain. GABA could also be responsible for the memory impairment that many people experience. It has been asserted that GABA signals interfere with the registration and consolidation stages of memory formation. As the GABA system is found in the hippocampus, (among other areas in the CNS), which is thought to play a large role in memory formation, this is thought to be possible.

Anterograde amnesia

Anterograde amnesia, colloquially referred to as "blacking out", is another symptom of heavy drinking.

Ataxia

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 though 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 is responsible for the observation that drunk people are clumsy, sway back and forth, and often fall down. It is probably due to alcohol's effect on the cerebellum.

Pharmacology

At low or moderate doses, alcohol primarily acts 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 which can cause a tendency towards violence in some people.[6][7][8][9][10][11][12]

At higher dose ranges, other targets also become important. Alcohol at high doses acts as an antagonist of the NMDA receptor, and since the NMDA receptor is involved in learning and memory, this action is thought to be responsible for the "memory blanks" that can occur at extremely high doses of alcohol. 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 GABA-A subtypes in their brain. 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 the convulsions that can occur in acute alcohol withdrawal, as well as other effects such as cardiac arrhythmia. Also chronic NMDA receptor blockade may produce apoptosis in neurons which is likely to be one of the factors involved in producing the brain damage seen in long-term alcoholic patients. 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.[13][14][15][16][17][18][19][20]

Animal and insect models

Animal models using mammals and invertebrates have been informative in studying the effects of ethanol on not only pharmacokinetics of alcohol, but also in pharmacodynamic, particularly in the nervous system. Ethanol-induced intoxication is not uncommon in the animal kingdom, as noted here:

Many of us have noticed that bees or yellow jackets cannot fly well after having drunk the juice of overripe fruits or berries; bears have been seen to stagger and fall down after eating fermented honey; and birds often crash or fly haphazardly while intoxicated on ethanol that occurs naturally as free-floating microorganisms convert vegetable carbohydrates to alcohol.[21]

Birds may have even been killed by excessive consumption of alcohol.[22]

Studies using animal models have elucidated biochemical pathways, on which ethanol acts, in the nervous system. Traditionally, many biological studies are done in mammals, such as mice, rats, and non-human primates. However, non-mammalian animal models have also been employed; in particular, Ulrike Heberlein group at UC San Francisco has used the fruit fly, Drosophila melanogaster, taking advantage of its facile genetics to dissect the neural circuits and molecular pathways, upon which ethanol acts. The series of studies carried in the Heberlein lab has identified insulin and its related signaling pathways as well as biogenic amines in the invertebrate nervous system as being important in alcohol tolerance. [23][24][25] The value of antabuse (disulfiram) as a treatment for alcoholism has been tested using a bee model.[26] Importantly, analogous biochemical pathways and neural systems have already been known to be important in humans and other mammals, and the area remains a hot topic of research, as scientists inch toward understanding the problem of alcohol addiction.

In addition to the studies carried out in invertebrates, researchers have also used vertebrate animal models to study various effects of ethanol on behaviors. Of note are studies carried out by the Myers group in University of Minnesota, who used the zebrafish model to study ethanol-induced teratogenesis and gametogenesis.[27]

See also

References

  1. ^ M. Horowitz, A. Maddox, M. Bochner, J. Wishart, R. Bratasiuk, P. Collins and D. Shearman. Relationships between gastric emptying of solid and caloric liquid meals and alcohol absorptionAm J Physiol Gastrointest Liver Physiol 257: G291-G298, 1989
  2. ^ http://ask.yahoo.com/20020805.html
  3. ^ Alcohol Awareness Page
  4. ^ Carleton College: Wellness Center: Blood Alcohol Concentration (BAC)
  5. ^ Grattan KE, Vogel-Sprott M. Maintaining intentional control of behavior under alcohol. Alcoholism, clinical and experimental research 2001 Feb;25(2):192-7
  6. ^ Huang Q, He X, Ma C, Liu R, Yu S, Dayer CA, Wenger GR, McKernan R, Cook JM. Pharmacophore/Receptor Models for GABAA/BzR Subtypes (α1β3γ2, α5β3γ2, and α6β3γ2) via a Comprehensive Ligand-Mapping Approach. Journal of Medicinal Chemistry 2000, (43):71-95.
  7. ^ Platt DM, Duggan A, Spealman RD, Cook JM, Li X, Yin W, Rowlett JK. Contribution of α1GABAA and α5GABAA Receptor Subtypes to the Discriminative Stimulus Effects of Ethanol in Squirrel Monkeys. Journal of Pharmacology and Experimental Therapeutics 2005, 313(2):658-667
  8. ^ Duke AN, Platt DM, Cook JM, Huang S, Yin W, Mattingly BA, Rowlett JK. Enhanced sucrose pellet consumption induced by benzodiazepine-type drugs in squirrel monkeys: role of GABAA receptor subtypes. Psychopharmacology (Berlin). 2006 Aug;187(3):321-30.
  9. ^ Wallner M, Hanchar HJ, Olsen RW. Low-dose alcohol actions on α4β3δ GABAA receptors are reversed by the behavioral alcohol antagonist Ro15-4513. Proceedings of the National Academy of Sciences U S A. 2006 30 May;103(22):8540-5.
  10. ^ Mehta AK, Ticku MK. Ethanol potentiation of GABAergic transmission in cultured spinal cord neurons involves gamma-aminobutyric acidA-gated chloride channels. Journal of Pharmacology and Experimental Therapeutics 1988, (246):558-564. PMID 2457076
  11. ^ Becker HC, Anton RF. The benzodiazepine receptor inverse agonist Ro15-4513 exacerbates, but does not precipitate, ethanol withdrawal in mice. Pharmacology, Biochemistry and Behaviour. 1989 Jan;32(1):163-7. PMID 2543989
  12. ^ Hanchar HJ, Chutsrinopkun P, Meera P, Supavilai P, Sieghart W, Wallner M, Olsen RW. Ethanol potently and competitively inhibits binding of the alcohol antagonist Ro15-4513 to alpha4/6beta3delta GABA-A receptors. Proceedings of the National Academy of Sciences U S A. 2006 30 May;103(22):8546-51.
  13. ^ Petrakis IL, Limoncelli D, Gueorguieva R, Jatlow P, Boutros NN, Trevisan L, Gelernter J, Krystal JH. Altered NMDA Glutamate Receptor Antagonist Response in Individuals With a Family Vulnerability to Alcoholism. American Journal of Psychiatry. 2004, (161):1776–1782.
  14. ^ Nutt DJ. Alcohol alternatives – a goal for psychopharmacology? Journal of Psychopharmacology. 2006, 20(3):318-320.
  15. ^ Qiang M, Denny AD, Ticku MK. Chronic intermittent ethanol treatment selectively alters N-methyl-D-aspartate receptor subunit surface expression in cultured cortical neurons. Molecular Pharmacology. 2007 Jul;72(1):95-102.
  16. ^ Hendricson AW, Maldve RE, Salinas AG, Theile JW, Zhang TA, Diaz LM, Morrisett RA. Aberrant synaptic activation of N-methyl-D-aspartate receptors underlies ethanol withdrawal hyperexcitability. Journal of Pharmacology and Experimental Therapeutics. 2007 Apr;321(1):60-72.
  17. ^ Dodd PR, Buckley ST, Eckert AL, Foley PF, Innes DJ. Genes and gene expression in the brains of human alcoholics. Annals of the New York Academy of Sciences. 2006 Aug;1074:104-15.
  18. ^ Sircar R, Sircar D. Repeated ethanol treatment in adolescent rats alters cortical NMDA receptor. Alcohol. 2006 May;39(1):51-8.
  19. ^ Klein G, Gardiwal A, Schaefer A, Panning B, Breitmeier D. Effect of ethanol on cardiac single sodium channel gating. Forensic Science International. 2007 13 September;171(2-3):131-5.
  20. ^ Shiraishi M, Harris RA. Effects of alcohols and anesthetics on recombinant voltage-gated Na+ channels. Journal of Pharmacology and Experimental Therapeutics. 2004 Jun;309(3):987-94.
  21. ^ Drug Policy and Human Nature: Psychological Perspectives On The Prevention, Management, and Treatment of Illicit Drug Abuse, Warren K. Bickel, Richard J. DeGrandpre, Springer 1996 ISBN 0306452413
  22. ^ Suspected Ethanol Toxicosis in Two Wild Cedar Waxwings, SD Fitzgerald. JM Sullivan. RJ Everson. Avian Diseases, Vol. 34, No. 2, 488-490. April - Jun., 1990.
  23. ^ Latest Buzz in Research: Intoxicated Honey bees may clue Scientists into Drunken Human Behavior, The Ohio State Research News, Research Communications, Columbus OH, 23 October 2004.
  24. ^ The Development of an Ethanol Model Using Social Insects I: Behavior Studies of the Honey Bee (Apis mellifera L.): Neurobiological, Psychosocial, and Developmental Correlates of Drinking, Charles I. Abramson, Sherril M. Stone, Richard A. Ortez, Alessandra Luccardi, Kyla L. Vann, Kate D. Hanig, Justin Rice, Alcoholism: Clinical & Experimental Research. 24(8):1153-1166, August 2000.
  25. ^ Intoxicated Honey Bees May Clue Scientists Into Drunken Human Behavior, Science Daily, 25 October 2004
  26. ^ Development of an ethanol model using social insects: II. Effect of Antabuse on consumatory responses and learned behavior of the honey bee (Apis mellifera L.)., Abramson CI, Fellows GW, Browne BL, Lawson A, Ortiz RA., Psychol Rep. 2003 Apr;92(2):365-78.
  27. ^ Pharyngula blog
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