Short-term effects of alcohol

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Overview

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 is less likely to produce visible signs of intoxication than consumption on an empty stomach. Hydration also plays a role, especially in determining the extent of hangovers. The concentration of alcohol in blood is usually measured in terms of the blood alcohol content.

Alcohol has a biphasic effect on the body, which is to say that its effects change over time.[1] 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 0.55% will kill half of those affected). 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.

Metabolism of alcohol and action on the liver

Main article: Alcohol metabolism

The liver breaks down alcohols into acetaldehyde by the enzyme alcohol dehydrogenase, and then into acetic acid by the enzyme acetaldehyde dehydrogenase. Next, the acetate is converted into fats or carbon dioxide and water. Chronic drinkers, however, so tax this metabolic pathway that things go awry: fatty acids build up as plaques in the capillaries around liver cells and those cells begin to die, which leads to the liver disease cirrhosis. The liver is part of the body's filtration system which, if damaged, allows certain toxins to build up, leading to symptoms of jaundice.

Some people's DNA code calls for a different acetaldehyde dehydrogenase, resulting in a more potent alcohol dehydrogenase. This leads to a buildup of acetaldehyde after alcohol consumption, causing the alcohol flush reaction with hangover-like symptoms such as flushing, nausea, and dizziness. These people are unable to drink much alcohol before feeling sick, and are therefore less susceptible to alcoholism.[2][3] This adverse reaction can be artificially reproduced by drugs such as disulfiram, which are used to treat chronic alcoholism by inducing an acute sensitivity to alcohol.

Effect by dosage

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

Overview

The following lists the effects of alcohol on the body, depending on the blood alcohol concentration or BAC.[4][5][6] Also, tolerance varies considerably between individuals.

Please note: the BAC percentages provided below are just estimates and used for illustrative purposes only. They are not meant to be an exhaustive reference; please refer to a healthcare professional if more information is needed.
  • Euphoria (BAC = 0.03 to 0.12%).
    • Subject may experience an overall improvement in mood and possible euphoria.
    • They may become more self-confident or daring.
    • Their attention span shortens. They may look flushed.
    • Their judgment is not as good — they may express the first thought that comes to mind, rather than an appropriate comment for the given situation.
    • They have trouble with fine movements, such as writing or signing their name.
  • Lethargy (BAC = 0.09 to 0.25%)
    • Subject may become sleepy.
    • They have trouble understanding or remembering things, even recent events. They do not react to situations as quickly.
    • Their body movements are uncoordinated; they begin to lose their balance easily, stumbling; walking is not stable.
    • Their vision becomes blurry. They may have trouble sensing things (hearing, tasting, feeling, etc.).
  • Confusion (BAC = 0.18 to 0.30%)
    • Profound confusion — uncertain where they are or what they are doing. Dizziness and staggering occur.
    • Heightened emotional state — aggressive, withdrawn, or overly affectionate. Vision, speech, and awareness are impaired.
    • Poor coordination and pain response. Nausea and vomiting sometimes occurs.
  • Stupor (BAC = 0.25 to 0.40%)
    • Movement severely impaired; lapses in and out of consciousness.
    • Subjects can slip into a coma; will become completely unaware of surroundings, time passage, and actions.
    • Risk of death is very high due to alcohol poisoning and/or pulmonary aspiration of vomit while unconscious.
  • Coma (BAC = 0.35 to 0.50%)
    • Unconsciousness sets in.
    • Reflexes are depressed (i.e., pupils do not respond appropriately to changes in light).
    • Breathing is slower and more shallow. Heart rate drops. Death usually occurs at levels in this range.

Moderate doses

Although alcohol is typically thought of purely as a depressant, at low concentrations it can actually stimulate certain areas of the brain. Alcohol sensitises the N-methyl-D-aspartate (NMDA) system of the brain, making it more receptive to the neurotransmitter glutamate. 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 correctly evaluate the consequences of their behavior.[7] Behavioral changes associated with drunkenness are, to some degree, contextual. A scientific study found that people drinking in a social setting significantly and dramatically altered their behavior immediately after the first sip of alcohol, well before the chemical itself could have filtered through to the nervous system. Likewise, people consuming non-alcoholic drinks often exhibit drunk-like behavior on a par with their alcohol-drinking companions even though their own drinks contained no alcohol whatsoever. [citation needed]

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.

Dehydration

Alcohol has been known to mitigate the production of the 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.

Mallenby effect

The Mallenby effect is the phenomenon whereby self-perceptions of the effects of alcohol on the person change between the absorption and the elimination phases of alcohol consumption.

During the absorption phase, individuals compare their perceived state with their condition before consuming alcohol. They tend to over estimate the effects of alcohol.

During the elimination phase, they tend to underestimate their state of alcohol impairment. [8]

Excessive doses

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

Slowing

The effect alcohol has on the NMDA receptors, earlier responsible for pleasurable stimulation, turns from a blessing to a curse if too much alcohol is consumed. NMDA receptors start to become unresponsive, slowing thought in the 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.

Blurred vision

Blurred vision is another common symptom of drunkenness. Alcohol seems to suppress the metabolism of glucose in the brain. The occipital lobe, the part of the brain responsible for receiving visual inputs, has been found to become especially impaired, consuming 29% less glucose than it should. With less glucose metabolism, it is thought that the cells aren't able to process images properly.

Vertigo

Often, after much alcohol has been consumed, it is possible to experience vertigo, the sense that the room is spinning (sometimes referred to as 'The Spins'). This is associated with abnormal eye movements called nystagmus, specifically positional alcohol nystagmus.

In this case, alcohol has affected the organs responsible for balance, i.e. the vestibular system in the ears. Balance in the body is monitored principally by two systems: the semicircular canals, and the utricle and saccule pair. Inside the semicircular canals there are flexible blobs called cupulas, which moves when the body moves. Upon bendin of the cupula, hair cells inside them create nerve impulses that travel through the vestibulocochlear nerve (Cranial nerve VIII) to the brain. The cupula is surrounded by endolymph, which has the same density.

However, when alcohol gets in to the bloodstream it dilutes it, reducing its density. When this blood reaches the cupula, the cupula becomes less dense. The endolymph surrounding it, on the other hand, is not connected directly to the circulatory system, and keeps the same density. Thus, the cupula becomes less dense than the surrounding fluid and is forced upwards, creating a false impulse just as if the head was rotating in the opposite direction. [9] The abnormal nerve impulses tell the brain that the body is rotating, causing disorientation and making the eyes spin round to compensate.

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.

Hangovers

Main article: Hangover

A common after-effect of ethanol intoxication is the unpleasant sensation known as hangover, which is partly due to the dehydrating effect of ethanol. Hangover symptoms include dry mouth, headache, nausea, and sensitivity to movement, light and noise. These symptoms are partly due to the toxic acetaldehyde produced from alcohol by alcohol dehydrogenase, and partly due to general dehydration. The dehydration portion of the hangover effect can be mitigated by drinking plenty of water between and after alcoholic drinks. Other components of the hangover are thought to come from the various other chemicals in an alcoholic drink, such as the tannins in red wine, and the results of various metabolic processes of alcohol in the body, but few scientific studies have attempted to verify this. Consuming water between drinks and before bed is the best way to prevent or lessen the effects of a hangover.

Rare effects

Extreme overdoses can lead to alcohol poisoning and death due to respiratory depression.

A rare complication of acute alcohol ingestion is Wernicke encephalopathy, a disorder of thiamine metabolism. If not treated with thiamine, Wernicke encephalopathy can progress to Korsakoff psychosis, which is irreversible.

Chronic alcohol ingestion over many years can produce atrophy of the vermis, which is the part of the cerebellum responsible for coordinating gait; vermian atrophy produces the classic gait findings of alcohol intoxication even when its victim is not inebriated.

Other causes

Severe drunkenness and hypoglycemia can be mistaken for each other on casual inspection, with potentially serious medical consequences for diabetics. Measurement of the serum glucose and ethanol concentrations in comatose individuals is routinely performed in the emergency department or by properly-equipped prehospital providers and easily distinguishes the two conditions.

Pharmacology

At low or moderate doses, alcohol primarily acts as an unselective GABAA agonist. 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.[10][11][12][13][14][15][16]

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 delerium tremens during severe alcohol withdrawal, such as delerium 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 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.[17][18][19][20][21][22][23][24]

Animal and insect models

There have been some attempts to use animal and insect models to study the effects of ethanol on humans. Other creatures are not immune to the effects of alcohol:

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.[25]

Birds may have even been killed by excessive consumption of alcohol.[26]

In Sweden, drunken moose have been observed. The theory is that they had eaten large amounts of overly ripe berries.

As a result, animal and insect models are fairly attractive. Heberlein et al. conducted studies of fruit fly intoxication at the University of California, San Francisco in 2004.[27] The brains and nervous systems of bees bear similarities to those of humans, so honey bees are used in studies of the effect of alcohol.[28][29][30] The value of antabuse (disulfiram) as a treatment for alcoholism has been tested using a bee model.[31]

Ulrike Heberlein's group at University of California, San Francisco has used fruit flies as models of human inebriation and even identified genes that seem to be responsible for alcohol tolerance accumulation (believed to be associated with veisalgia, or hangover), and produced genetically engineered strains that do not develop alcohol tolerance[32][33][34][35]

University of Minnesota Biology Professor PZ Myers is using zebrafish to study ethanol teratogenesis and ethanol gametogenesis.[36] A wide range of other animal models have been used,[37][38] including primate,[39] mouse,[40] and rat models.[41]

References

  1. Hanson, David J. How Alcohol Effects Us: The Biphasic Curve (html). Alcohol: Problems and Solutions. State University of New York. Retrieved on 2007-12-12.
  2. http://endeavor.med.nyu.edu/~strone01/doctor.html
  3. http://www.webremedies.com/quit_alcohol/know.php#5
  4. http://www.radford.edu/~kcastleb/bac.html
  5. http://apps.carleton.edu/campus/wellness/info/alcohol/bac/
  6. http://www.drugrehab.co.uk/alcohol.htm
  7. http://www2.potsdam.edu/hansondj/Controversies/1048596839.html
  8. Haggin, Daniel J. Advanced DUI Investigation, Springfield, IL: Charles C. Thomas Publisher, 2005, pp. 77-78.
  9. Sportkat.com - Why can alcohol cause vertigo?
  10. 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.
  11. 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
  12. 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.
  13. 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 May 30;103(22):8540-5.
  14. 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
  15. 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
  16. 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 May 30;103(22):8546-51.
  17. 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.
  18. Nutt DJ. Alcohol alternatives – a goal for psychopharmacology? Journal of Psychopharmacology. 2006, 20(3):318-320.
  19. 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.
  20. 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.
  21. 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.
  22. Sircar R, Sircar D. Repeated ethanol treatment in adolescent rats alters cortical NMDA receptor. Alcohol. 2006 May;39(1):51-8.
  23. Klein G, Gardiwal A, Schaefer A, Panning B, Breitmeier D. Effect of ethanol on cardiac single sodium channel gating. Forensic Science International. 2007 Sep 13;171(2-3):131-5.
  24. 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.
  25. 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
  26. Suspected Ethanol Toxicosis in Two Wild Cedar Waxwings, SD Fitzgerald. JM Sullivan. RJ Everson. Avian Diseases, Vol. 34, No. 2, 488-490. Apr. - Jun., 1990.
  27. http://icb.oxfordjournals.org/cgi/content/abstract/44/4/269
  28. Latest Buzz in Research: Intoxicated Honey bees may clue Scientists into Drunken Human Behavior, The Ohio State Research News, Research Communications, Columbus OH, October 23, 2004.
  29. 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.
  30. Intoxicated Honey Bees May Clue Scientists Into Drunken Human Behavior, Science Daily, October 25, 2004
  31. 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.
  32. Moore, M. S., Dezazzo, J., Luk, A. Y., Tully, T., Singh, C. M., and Heberlein, U. (1998) Ethanol intoxication in Drosophila: Genetic and pharmacological evidence for regulation by the cAMP pathway. Cell 93, 997-1007
  33. Tecott, L. H. and Heberlein, U. (1998) Y do we drink? Cell 95: 733-735
  34. Bar Flies: What our insect relatives can teach us about alcohol tolerance., Ruth Williams, Naked Scientist
  35. ‘Hangover gene’ is key to alcohol tolerance, Gaia Vince, NewScientist.com news service, 22 August 2005
  36. Pharyngula blog
  37. Grant, K.A. Behavioral animal models in alcohol abuse research. Alcohol Health & Research World 14(3):187-192, 1990.
  38. Samson, H.H. Initiation of ethanol-maintained behavior: A comparison of animal models and their implication to human drinking. In: Thompson, T.; Dews, P.B.; and Barrett, J.E., eds. Neurobehavioral Pharmacology: Volume 6. Advances in Behavioral Pharmacology. Hillsdale, NJ: Lawrence Erlbaum Associates, 1987. pp. 221-248.
  39. Higley, J.D.; Hasert, M.F.; Suomi, S.J.; & Linnoila, M. Nonhuman primate model of alcohol abuse: Effects of early experience, personality, and stress on alcohol consumption. Proceedings of the National Academy of Sciences 88(16):7261-7265, 1991.
  40. Lister, R.G. The use of a plus-maze to measure anxiety in the mouse. Psychopharmacology 92:180-185, 1987.
  41. Schwarz-Stevens, K.; Samson, H.H.; Tolliver, G.A.; Lumeng, L.; & Li, T.-K. The effects of ethanol initiation procedures on ethanol reinforced behavior in the alcohol-preferring rat. Alcoholism: Clinical and Experimental Research 15(2):277-285, 1991.

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