Topic 6A
Alcohol
NG W EN J IE
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Introduction
The alcohol present in alcoholic drinks is ethanol (ethyl alcohol),
C2H5OH.
Ethanol is produced by the fermentation of glucose in plants.
- Sugars in grapes and apples are fermented to produce wine and cider.
- Barley starch is hydrolysed to glucose in the production of beer.
- Rice for sake and rye for whisky.
By law, drink labels must show the strength of alcohol present; this is
expressed as the percentage alcohol by volume (abv). 10% abv is
equivalent to 7.9 g of alcohol per 100 ml.
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Types
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Nutritional values
Alcohol is an energy source providing
29 kJ (7 kcal) per gram.
Alcoholic drinks may also contain
sugars, small amounts of other alcohols,
e.g. propyl alcohol, potassium, and small
amounts of riboflavin and niacin.
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Intakes
In the UK the Department of Health recommends
that men consume no more than 3–4 units of
alcohol /d and women no more than 2–3 units.
It is also recommended that 2 d/wk should be
alcohol free.
The National Diet and Nutrition Survey found that on
average men consumed approximately 20–21 units
per week and women consumed 8–9 units per week;
this figure was calculated including non-drinkers.
Nearly 40% of men and 25% of women exceeded
the recommended intakes, with younger people
consuming more alcohol than older people.
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Pregnant women are advised not to
drink and to consume no more than
2–4 units per week.
Excessive alcohol consumption during
pregnancy may lead to foetal alcohol
syndrome which may cause facial
deformities and growth problems.
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Metabolism
Ethanol is quickly absorbed in the stomach and jejunum and distributed throughout total body water
including blood.
Alcohol is distributed via the blood to the brain and the liver where it is metabolized by alcohol
dehydrogenase (ADH) to acetaldehyde which is converted to acetate by the enzyme aldehyde
dehydrogenase (ALDH).
Alcoholics have an induced system of alcohol metabolism known as the microsomal ethanol-oxidizing
system (MEOS).
On average approximately 5–10 g of alcohol (1/2–1 unit of alcoholic drink) is metabolized per hour.
Some alcohol (2-10%) is excreted in breath, which provides an easy monitor of alcohol intoxication.
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Alcohol absorption can be slowed by the presence
of food in the stomach.
Smaller people have smaller livers and metabolize
alcohol more slowly; women have smaller livers
than men and become intoxicated more quickly.
The build up of acetaldehyde leads to headache,
nausea and vomiting.
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Toxicity
The most common effects are increase in heart
rate and peripheral vasodilatation → facial
flushing.
Alcohol is a central nervous system depressant
and acts as an anaesthetic.
Diuresis results from the action of alcohol on
the pituitary gland and leads to dehydration.
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Acetaldehyde (reactive metabolite)
- Acute toxicity: CNS suppression
sedative and hypnotic effects, cognitive impairment, motor incoordination
hallucinogenic, euphoriant effects, learning and memory deficits
- Chronic toxicity: liver damage
accumulation of fat
oxidative stress, inflammation & necrosis in liver, even liver failure and cancer
- Teratogenicity: birth defects
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Thiamine deficiency can result
from chronic and excessive
alcohol intake as thiamine is
required for ethanol
metabolism and dietary intake
may be poor.
This can lead to Wernicke’s
encephalopathy and
Korsakoff’s psychosis.
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Genetic polymorphisms in alcohol metabolism
◦ East Asians + American Indians: higher
efficiency of ADH
◦ The one which normally breaks down
acetaldehyde is called ALDH2
◦ East Asians: ALDH2*2 – less efficient
than ALDH2 → Asian flush syndrome/
Asian glow
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Benefits
Light to moderate consumption of alcohol has been shown
to have beneficial health effects in reducing the risk of
coronary heart disease in men and post-menopausal
women.
The most established mechanism is that this level of
alcohol consumption increase plasma high-density
lipoprotein (HDL).
An additional proposed mechanism is that alcohol lower
platelet aggregation and lower the risk of thrombosis.
It has been proposed that polyphenolic compounds
(resveratrol) in wines have antioxidant properties that
reduce the plasma levels of low-density lipoproteins (LDL).
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Chronic administration of
ethanol causes microsomal
enzyme (CYP2E1) induction
with increased toxic metabolic
activation of paracetamol and
enhanced hepatotoxicity.
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