what is the only effective way to remove alcohol from the body

  • Journal Listing
  • BMJ
  • v.330(7482); 2005 January viii
  • PMC543875

BMJ. 2005 Jan viii; 330(7482): 85–87.

ABC of alcohol

Alcohol in the body

Alcohol (ethanol) is a drug, and health professionals should know something of its physiological and pathological effects and its handling past the body. It is a small, water soluble molecule that is relatively slowly absorbed from the breadbasket, more rapidly absorbed from the pocket-size intestine, and freely distributed throughout the body. Alcoholic drinks are a major source of free energy—for instance, half dozen pints of beer contain about 500 kcal and half a litre of whisky contains 1650 kcal. The daily energy requirement for a moderately active man is 3000 kcal and for a adult female 2200 kcal.

Absorption

Charge per unit of absorption of booze depends on several factors. Information technology is quickest, for example, when alcohol is drunk on an empty tum and the concentration of alcohol is 20-xxx%. Thus, sherry, with an alcohol concentration of about twenty% increases the levels of booze in claret more rapidly than beer (three-eight%), while spirits (40%) delay gastric emptying and inhibit absorption. Drinks aerated with carbon dioxide—for example, whisky and soda, and champagne—get into the organization quicker. Food, and particularly carbohydrate, retards absorption: blood concentrations may non achieve a quarter of those accomplished on an empty stomach. The pleasurable furnishings of alcohol are all-time accomplished with a meal or when alcohol is drunk diluted, in the case of spirits.

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Rate of absorption of booze (arrows) is affected by concentration of alcohol

Alcohol is distributed throughout the h2o in the body, so that most tissues—such as the heart, brain, and muscles—are exposed to the aforementioned concentration of alcohol every bit the blood. The exception is the liver, where exposure is greater because blood is received direct from the breadbasket and small bowel via the portal vein. Alcohol diffuses rather slowly, except into organs with a rich blood supply such as the brain and lungs.

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Most tissues are exposed to the aforementioned alcohol concentration as in the blood

Other factors

Very little alcohol enters fat because of fat's poor solubility. Claret and tissue concentrations are therefore higher in women, who take more subcutaneous fat and a smaller blood volume, than in men, even when the amount of alcohol consumed is adjusted for body weight. Women also may have lower levels of alcohol dehydrogenases in the stomach than men, then that less alcohol is metabolised before absorption. Alcohol enters the fetus readily through the placenta and is eliminated by maternal metabolism.

Blood alcohol concentration varies according to sex, size and trunk build, phase of the menstrual bike (information technology is highest premenstrually and at ovulation), previous exposure to alcohol, type of drink, whether booze is taken with food or drugs, such as cimetidine (which inhibits gastric alcohol dehydrogenase) and antihistamines, phenothiazines, and metoclopramide (which enhance gastric emptying, thus increasing assimilation).

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Metabolism of alcohol

More than 90% of booze is eliminated by the liver; 2-5% is excreted unchanged in urine, sweat, or jiff. The first step in metabolism is oxidation by alcohol dehydrogenases, of which at least four isoenzymes be, to acetaldehyde in the presence of cofactors. Acetaldehyde is a highly reactive and toxic substance, and in healthy people it is oxidised rapidly by aldehyde dehydrogenases to harmless acetate.

This article is adapted from the quaternary edition of the ABC of Booze, which will exist available in February

Several isoenzymes of aldehyde dehyrdrogenase be, ane of which is missing in about 50% of Japanese people and maybe other south Asian people (but rarely in white people). Unpleasant symptoms of headache, nausea, flushing, and tachycardia are experienced by people who lack aldehyde dehydrogenases and who drink; this is believed to be because of accumulation of acetaldehyde. Under normal circumstances, acetate is oxidised in the liver and peripheral tissues to carbon dioxide and water.

On an empty tummy, claret alcohol concentration peaks nigh one hour after consumption, depending on the amount drunk; information technology and then declines in a more or less linear manner for the next iv hours. Alcohol is removed from the blood at a rate of about 3.3 mmol/hour (fifteen mg/100 ml/hour), but this varies in different people, on different drinking occasions, and with the amount of alcohol drunkard.

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Concentrations of booze in the claret after 6 units of alcohol (equivalent to 48 g alcohol)

At a blood alcohol concentration of four.4 mmol (20 mg/100 ml), the curve flattens out, but detectable concentrations are present for several hours after three pints of beer or three double whiskies in healthy people; enough alcohol to impair normal operation could exist present the morning after an evening session of drinking. Alcohol consumption by heavy drinkers represents a considerable metabolic load—for example, half a bottle of whisky is equivalent in molar terms to 500 g aspirin or 1.two kg tetracycline.

Heavy drinkers

Two mechanisms dispose of excess booze in heavy drinkers and business relationship for "tolerance" in established drinkers. Firstly, normal metabolism increases, equally shown past high blood concentrations of acetate. Secondly, the microsomal ethanol oxidising arrangement is brought into play; this is dependent on cytochrome P450, which is ordinarily responsible for drug metabolism, and other cofactors. This procedure is chosen enzyme induction, and the effect is also produced by other drugs that are metabolised by the liver and by smoking.

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Charge per unit of subtract of concentrations of booze in the claret in heavy, social, and naïve drinkers. The two lines represent maximum and minimum rates for each category

The two mechanisms lead to a redox country, in which free hydrogen ions build upwards and take to be disposed of by several different pathways. Some of the resultant metabolic aberrations tin can have clinical consequences: hepatic gluconeogenesis is inhibited, the citric acid bike is reduced, and oxidation of fatty acids is impaired. Glucose product is thus reduced, with the risk of hypoglycaemia; overproduction of lactic acid blocks uric acid excretion by the kidneys; and accumulated fat acids are converted into ketones and lipids.

Behavioural effects

Alcohol is a sedative and mild anaesthetic. It is believed to activate the pleasance or reward centres in the encephalon by triggering release of neurotransmitters such as dopamine and serotonin. Alcohol produces a sense of wellbeing, relaxation, disinhibition, and euphoria. These feelings are accompanied by physiological changes such as flushing, sweating, tachycardia, and increases in blood pressure, probably because of stimulation of the hypothalamus and increased release of sympathomimetic amines and pituitary-adrenal hormones. The kidneys secrete more urine, not only considering of the fluid drunk just also because of the osmotic effect of alcohol and inhibition of secretion of antidiuretic hormone.

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Event of alcohol on behaviour

Increasing consumption leads to a state of intoxication, which depends on the amount drunk and previous feel of drinking. Even at a depression blood alcohol concentration of around 6.v mmol/fifty (30 mg/100 ml), the gamble of unintentional injury is higher than in the absence of alcohol, although individual experience and complexity of task have to be taken into account. In a fake driving test, for case, omnibus drivers with a blood alcohol concentration of ten.ix mmol/fifty (50 mg/100 ml) thought they could drive through obstacles that were likewise narrow for their vehicles. At 17.4 mmol/l (eighty mg/100 ml)—the current legal limit for driving in the United Kingdom—the risk of a road traffic incident more than doubles, and at 34.7 mmol/l (160 mg/100 ml), information technology increases more than x-fold.

People become garrulous, elated, and aggressive at concentrations in a higher place 21.7 mmol/l (100 mg/100 ml) and then may terminate drinking equally drowsiness supervenes. Later on furnishings ("hangover") include insomnia, nocturia, tiredness, nausea, and headache.

If drinking continues, slurred speech and unsteadiness are likely at around 43.4 mmol/fifty (200 mg/100 ml), and loss of consciousness may result. Concentrations to a higher place 86.viii mmol/l (400 mg/100 ml) usually are fatal as a event of ventricular fibrillation, respiratory failure, or inhalation of vomit (this is peculiarly likely when drugs have been taken in addition to alcohol).

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Risks associated with concentrations of booze in the blood

Notes

The figure showing the metabolism of ethanol is adapted from C South Lieber et al. Northward Engl J Med 1978;298: 356 [PubMed] [Google Scholar] . The figure showing the event of booze on behaviour is adapted from Transport and Road Research Laboratory. The facts about drinking and driving. Crowthorne: Berkshire, 1983. The effigy showing concentrations of alcohol in the blood in heavy, social, and naïve drinkers is synthetic from figures supplied past K Lewis BMJ 1987;295: 800-1 [PMC free commodity] [PubMed] [Google Scholar] .

Competing interests: None declared.

The ABC of Alcohol is edited by Alex Paton, retired consultant physician, Oxfordshire (moc.loa@xelAnotaP) and Robin Touquet, consultant in blow and emergency medicine, St London (ku.ca.lairepmi@teuquoT.R)

References

  • Lewis KO. Back calculation of claret alcohol concentration. BMJ 1987;295: 800-1 [PMC costless article] [PubMed] [Google Scholar]
  • Lieber CS, Salaspuro MP. Alcoholic liver disease. In: Millward-Sadler CHM, Wright R, Arthur MJP, eds. Wright's liver and biliary disease, third ed. London: Saunders, 1992: 899-964
  • Paton A. The body and its health. In: Cooper DB, ed. Booze use. Oxford: Radcliffe, 2000: 25-38.

Articles from The BMJ are provided here courtesy of BMJ Publishing Group


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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC543875/

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