Short-term effects of alcohol consumption
The 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; e.g., 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. 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 be caused by asphyxiation when vomit, a frequent result of over-consumption, blocks the trachea and the individual is too inebriated to respond. An appropriate first aid response to an unconscious, drunken person is to place them in the recovery position.
Intoxication frequently leads to a lowering of one's inhibitions, and intoxicated people will do things they would not do while sober, often ignoring social, moral, and legal considerations.
This article primarily covers the short-term effects of alcohol on the adult human body. For the potential long-term cumulative effects of alcohol on the adult human body, please refer to alcohol consumption and health, alcohol and cardiovascular disease, alcohol and cancer, alcohol and weight and alcoholic liver disease. The potential impact of alcohol consumption by pregnant women on their fetuses is explored in the article fetal alcohol syndrome.
Metabolism of alcohol and action on the liver
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. The fats are mostly deposited locally which, according to some,[who?] leads to the characteristic "beer belly".[citation needed] 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.
The alcohol dehydrogenase of women is less effective than that of men[citation needed]. The percentage of water in women's bodies is less than that of men[citation needed]. Therefore, the alcohol has less volume to dissolve in, leading to a higher blood alcohol concentration when the same amount of alcohol is ingested. This contributes to the fact that women become intoxicated more quickly than men. Also contributing is the fact that men have a more active first-pass metabolism of alcohol in the stomach and small intestine.[citation needed]
Some people's DNA code for a different acetaldehyde dehydrogenase, resulting in 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.[1][2] 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.
Dehydration
Overconsumption can therefore lead to dehydration (the loss of water).
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 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. The severity of hangover depends on the effects of the byproducts of the fermentation process that brings out the taste and aroma of the beverage, also known as congeners. With more congeners, the chance of a severe hangover increases. Brandy has the largest amount of congeners, followed by red wine, rum, whiskey, white wine, gin and vodka.
Beneficial effects of alcohol
The World Health Organization (WHO) reports that there is convincing evidence that "low to moderate alcohol intake" results in a decreased risk of coronary heart disease.[3] However, the WHO cautions that "other cardiovascular and health risks associated with alcohol do not favour a general recommendation for its use."[4]
Also it has been suggested that moderate consumption of alcohol can reduce the risk of dementia, facilitate memory and learning,[5] and even improve IQ scores.[6] Moderate drinkers tend to have better health and live longer than those who abstain from alcohol or are heavy drinkers, but this average difference is largely explained by the fact that a large fraction of abstainers are ex-alcoholics or those who have health problems or take drugs that preclude the use of alcohol, and has far less relevance to those who abstain for other reasons.[7] See Alcohol and health.
Effects by dose
Different concentrations of alcohol in the human body have different effects on the subject. The following lists the effects of alcohol on the body, depending on the blood alcohol concentration or BAC.[8][9][10] 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 judgement 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 often occur.
- 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.
- Death (BAC more than 0.50 %)
- Alcohol causes central nervous system to fail, resulting in death.
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 heightened alpha brain waves surging across the brain. 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.
A well-known side effect of alcohol is lowering inhibitions. 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.
Behavioural 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 behaviour 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 behaviour on a par with their alcohol-drinking companions even though their own drinks contained no alcohol whatsoever. [citation needed]
Excessive doses
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 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.
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 (vestibular system), present in the ears. Balance in the body is monitored principally by two systems: the semicircular canals, and the utricle and saccule pair. Inside both of these is a flexible blob called a cupula, which moves when the body moves. This brushes against hair cells in the ear, creating nerve impulses that travel through the vestibulocochlear nerve (Cranial nerve VIII) in to the brain. However, when alcohol gets in to the bloodstream it distorts the shape of the cupola, causing it to keep pressing on to the hairs. The abnormal nerve impulses tell the brain that the body is rotating, causing disorientation and making the eyes spin round to compensate. When this wears off (usually taking until the following morning) the brain has adjusted to the spinning, and interprets not spinning as spinning in the opposite direction causing further disorientation. This is often a common symptom of the hangover.[citation needed]
Anterograde amnesia, colloquially referred to as "blacking out", is another symptom of heavy drinking.
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.
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.
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. A moderate dose for females are 1000 oz. and the moderate dose for males are 2000 oz. a day.
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.[11]
Birds may have even been killed by excessive consumption of alcohol.[12]
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.[13] 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.[14][15][16] The value of antabuse (disulfiram) as a treatment for alcoholism has been tested using a bee model.[17]
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[18][19][20][21]
University of Minnesota Biology Professor PZ Myers is using zebrafish to study ethanol teratogenesis and ethanol gametogenesis.[22] A wide range of other animal models have been used,[23][24] including primate,[25] mouse,[26] and rat models.[27]
References
- ^ http://endeavor.med.nyu.edu/~strone01/doctor.html
- ^ http://www.webremedies.com/quit_alcohol/know.php#5
- ^ http://www.who.int/nutrition/topics/5_population_nutrient/en/index12.html
- ^ http://www.who.int/nutrition/topics/5_population_nutrient/en/index13.html
- ^ http://news.bbc.co.uk/2/hi/health/1780130.stm
- ^ http://news.bbc.co.uk/2/hi/health/1058526.stm
- ^ http://www.benbest.com/health/alcohol.html
- ^ http://www.radford.edu/~kcastleb/bac.html
- ^ http://apps.carleton.edu/campus/wellness/info/alcohol/bac/
- ^ http://www.drugrehab.co.uk/alcohol.htm
- ^ 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
- ^ 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.
- ^ http://icb.oxfordjournals.org/cgi/content/abstract/44/4/269
- ^ 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.
- ^ 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.
- ^ Intoxicated Honey Bees May Clue Scientists Into Drunken Human Behavior, Science Daily, October 25, 2004
- ^ 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.
- ^ 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
- ^ Tecott, L. H. and Heberlein, U. (1998) Y do we drink? Cell 95: 733-735
- ^ Bar Flies: What our insect relatives can teach us about alcohol tolerance., Ruth Williams, Naked Scientist
- ^ ‘Hangover gene’ is key to alcohol tolerance, Gaia Vince, NewScientist.com news service, 22 August 2005
- ^ Pharyngula blog
- ^ Grant, K.A. Behavioral animal models in alcohol abuse research. Alcohol Health & Research World 14(3):187-192, 1990.
- ^ 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.
- ^ 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.
- ^ Lister, R.G. The use of a plus-maze to measure anxiety in the mouse. Psychopharmacology 92:180-185, 1987.
- ^ 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.
External links
- Alcohol and the Human Body
- Global Status Report on Alcohol 2004 by the World Health Organization.
- Impacts of alcohol consumption on human health - a summary of the above WHO report by GreenFacts.
- Molecular Genetic Analysis of Ethanol Intoxication in Drosophila melanogaster, Ulrike Heberlein, Fred W. Wolf, Adrian Rothenfluh and Douglas J. Guarnieri, Integrative and Comparative Biology 2004 44(4):269-274; doi:10.1093/icb/44.4.269