Alcohol And Liver

Alcohol cannot be stored and must be oxidized, predominantly in the liver. Alcohol metabolism has a limit in the liver, although someone who has been drinking alcohol for some time may induce his liver enzymes thus allowing the liver to metabolise more. Alcohol provides empty calories as energy only with no other contribution to nutrition.

80-85% of ethanol oxidation is by initial conversion to acetaldehyde by ADH, which if it accumulates in cells can cause cell damage.

Acetaldehyde is further metabolized by several pathways, one of which results in carbon dioxide and water, while another leads to other biochemically important compounds such as fatty acids. Triglyceride accumulation can lead to fatty liver.

10-15% of alcohol is metabolized by a microsomal P450 ethanol oxdising system (MEOS). Through this pathway, potentially injurious reactive oxygen radicals (free radicals) are produced. A lack of protection against free radicals may partly explain mitochondrial injury inside cells.

Four pathological types of alcoholic liver disease are recongised:

  • Fatty liver due to accumulation of triglycerides in the liver. This can lead to steatohepatitis and eventual liver cirrhosis.
  • Acute hepatitis. This often follows binge drinking and is due to acute toxic effect of a high quantity of alcohol on the liver. The patient can be very ill and mortality is high.
  • Chronic hepatitis. This is more insidious and progression to cirrhosis is almost certain without abstinence.
  • Cirrhosis. Permanent scarring of the liver with loss of liver function and all the consequences including liver failure and liver cancer.

The more alcohol is consumed the greater the risk of alcoholism (alcohol dependency syndrome) as well the risk of liver disease.

Daily alcohol misuse is more harmful than 'binge drinking' although this is NOT a recommendation for binge drinking. It is thought that acute exposure to alcohol followed by a period of no alcohol usage allows time for liver cells