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Alcohol and your liver

Liver disease - image of a medical model

Facts and figures
Chronic Liver Disease
Acute Liver Disease
Advice and Getting Help

Introduction

Drink enough alcohol, and you are likely to damage your liver. This can happen quickly or over a longer period. Increasing numbers of people in the UK are being hospitalised and dying, as a result of liver disease associated with alcohol.

Up to one in three adults drinks enough alcohol to create a risk of developing alcohol-related liver disease.

Facts and Figures

A major risk factor for liver disease is alcohol consumption, but the evidence is unclear as to the precise relationship between the amount of alcohol you drink and the incidence of liver disease.

For example, an Italian study found that liver disease risk increased after consuming 30g (about 3.8 units) of alcohol per day and that after this risk increased with the amount of alcohol consumed (1). Whereas a Chinese study found that 20g of alcohol (about 2.5 units) per day doubled the risk of liver disease, but thereafter found the risk did not increase with each additional dose. (2).

A number of studies suggest that consuming enough alcohol might trigger the disease process, but that higher levels of alcohol consumption do not have any additional impact (a relationship known as a threshold effect).

Other risk factors include:

Alcohol dependence: However, around 8 in 10 people with alcohol dependence will not have liver damage.(3)
Gender: Women are more susceptible to alcohol-related liver damage than men, with one study suggesting the risk is almost 50% higher (4).
Body mass index: Being overweight or obese increases the risk of alcohol-related liver disease.
Race: Some data suggests people of African origin are more susceptible than Caucasians (5).
Genetic predisposition: There’s no clear data on this, but the fact that only a minority of heavy drinkers develop liver disease suggests a genetic predisposing factor (6).
Pattern of drinking: Drinking alcohol only at meal times appears to carry a lower risk of alcohol-related liver disease than other patterns of alcohol consumption (1).

Progression

There are two patterns of liver disease, acute (known as acute alcoholic hepatitis) and chronic, which reflect whether it develops over a matter of months or years respectively.

Chronic Liver Disease

There are four stages of chronic liver disease.

1. The commonest and mildest form of liver damage is a ‘fatty’ liver. This can be identified by blood tests, and is reversible with abstinence from alcohol.

2. The next step cannot be identified by blood tests, but a liver biopsy will show inflammation in addition to the excess fat. This is called steatohepatitis. In severe cases, jaundice may develop. A diagnosis of acute alcoholic hepatitis can then be made (see below).

3. At the next stage, fibrosis (scar tissue) is present. Again, this cannot be detected by blood tests or routine scans.

4. Cirrhosis occurs when the fibrosis reaches the stage when the normally soft liver is divided into thousands of pea-sized pockets of liver tissue, wrapped in fibrosis. Once cirrhosis develops, the prognosis partly depends on whether or not you continue drinking. People with compensated cirrhosis – meaning they have no symptoms – and who then stop drinking, have an 80% chance of being alive after 10 years.

The majority of those with decompensated cirrhosis – displaying symptoms – will die within three years.

Acute Liver Disease- known as Acute Alcoholic Hepatitis

This type of liver disease is caused by heavy drinking over a period of months. This is the pattern that is likely to occur when young people get liver disease, although older people who drink excessively later in life are also susceptible. It is potentially reversible with no long-term effects if you recover and stop drinking alcohol completely.

However, 70-90% of patients with acute alcoholic hepatitis – likely to be those who have been drinking for longer, and therefore unlikely to be young people - will have cirrhosis (see above). Jaundice is the usual first symptom. In hospitalised cases, there’s a mortality rate of around 50% associated with acute alcoholic hepatitis. Liver transplants are usually not an option, partly because of the history of recent alcohol abuse.

Advice and Getting Help

The majority of patients who develop cirrhosis will have been unaware of the earlier stages of the disease, unless tests have been carried out. Early symptoms of liver disease can be non-specific, including fatigue, nausea, vomiting, diarrhoea or abdominal pains. For heavy drinkers, early monitoring could help detect liver damage before it reaches an advanced stage.

Eventually, when liver damage does reach a more advanced stage, specific liver-related symptoms can develop because of:

Liver failure: seen as jaundice, or encephalopathy – mental effects caused by the liver’s inability to clear toxins from the blood.
Portal hypertension: an increase in pressure in the vein draining blood in to the liver, which can lead to bleeding in the gut.
Cancer, with the development of the liver cancer known as hepatocellular carcinoma.

It is therefore important, if you are concerned in any way about your drinking to discuss it with your GP.

Links

British Liver Trust – the national charity for adults with liver disease. The Trust campaigns to highlight the problem of liver disease in the UK and runs a helpline (0800 652 7330) and website.

For help in Scotland, you can contact Alcohol Focus Scotland, on 0141 572 6700.

Dr John O'Grady, MD, FRCPI, is a consultant hepatologist at the Institute of Liver Studies based at King's College Hospital, London, and is president of the British Association for the Study of the Liver.

References

1 Bellantani S, Saccoccio G, Costa G, et al. Drinking habits as co-factors of risk for alcohol induced liver injury: the Dionysos Study Group. GUT 1997;41:845-50.

2 Shen Z, Li YM, Yu CH, et al. Risk factors for alcohol-related liver injury in the island population of China: a population-based case-control study. World J Gastroenterol 2008;14:2255-61.

3 Stokkeland K, Hilm G, Spak F, et al. Different drinking patterns for women and men with alcohol dependence with and without cirrhosis. Alcohol Alcohol 2008;43:39-45.

4 Corroa G, Arico S, Zambon A, et al. Female sex and the risks of liver cirrhosis: Collaborative for the Study of Liver Disease in Italy. Scand J Gastroenterol 1997;32:1174-80.

5 Stranges S, Freudenheim JL, Muti P, et al. Greater hepatic vulnerability after alcohol intake in African Americans compared with Causasians: a population-based study. J Natl Med Association; 2004:1185-92.

6 Zintzaras E, Stefanidis I, Santos M, Vidal F. Do alcohol-metabolising enzyme gene polymorphisms increase the risk of alcoholism and alcoholic liver disease. Hepatology 2006;43:352-61.

Background reading

Becker PU, Deis A, Sorensen TI, et al. Prediction of risk of liver disease by alcohol intake, sex and age: a prospective population study. Hepatology 1996;23:1025-9.

Teli MR, Day CP, Burt AD, Bennett MK, James OJ. Determinants of progression to cirrhosis or fibrosis in pure alcoholic fatty liver. Lancet 1995;346:987-90.

Sorensen TI, Orholm M, Bentsen KD, et al. Prospective evaluation of alcohol abuse and alcoholic liver injury in men as predictors of development of cirrhosis. Lancet 1984;ii:241-4.

Savolainen VT, Liesto K, Mannikko P, et al. Alcohol consumption and alcoholic liver disease : evidence of a threshold level of effects of ethanol. Alcohol Clin Exp Res 1993;17:1112-7.

Corroa G, Arico S, Lepore R, et al. Amount and duration of alcohol intake as risk factors of symptomatic cirrhosis: a case-control study. J Clin Epidemiol 1993;46:601-7.

Kamper-Jorgensen M, Gronbaek M, Tolstrup J, Becker U. alcohol and cirrhosis: dose-response or threshold effect? J Hepatol 2004;41:25-30.

Ruhl CE, Everhart JE. Joint effects of body weight and alcohol on elevated serum alanine aminotransferase in the United States population. Clin Gastroenterol Hepatol 2005;3:1195-7.

Puukka K, Hietala J, Koivisto H, et al. Additive effects of moderate drinking and obesity on serum gamma-glutamyl transferase activity. Am J Clin Nutr 2006;83:1351-4.

Poikolainen K, Vartianen E. Determinants of gamma-glutamyltransferase : positive interaction with alcohol and body mass index, negative association with coffee. Am J Epidemiology 1997;146:1019-24.

Stewart SH. Racial and ethnic differences in alcohol-associated aspartase aminotransferase and gamma-glutamyltransferase elevation. Arch Int Med 2002;162:2236-9.

Stranges S, Freudenheim M, Muti P, et al. Differential effects of alcohol drinking pattern on liver enzymes in men and women. Alcohol Clin Exp Res 2004;28:949-56.

Corroa TG, Lepore AR, Torchio P, et al. The effect of drinking coffee and smoking cigarettes on the risk of cirrhosis associated with alcohol consumption . a case control study. Provincial Group for the Study of Chronic Liver Disease. Eur J Epidemiology 1994;10:657-64.

Tanaka K, Tokunaga S, Kono S, et al. Coffee consumption and decreased serum gamma-glutamyltransferase and aminotransferase activities among male alcohol drinkers. Int J Epidemiol 1998;27:438-43.

Page last updated by: Matthew Bateman, 31 Oct 2011.

Page checked on: 17 Sep 2008

Understanding unit guidelines

You should not regularly exceed…

Women: 2–3 units daily
Men: 3–4 units daily

The government advises that women should not regularly drink more than the daily unit guidelines of 2–3 units, or…

3 × 25ml shots of whiskey
1.3 × 175ml glasses of white wine
1.3 pints of 4% lager

The government advises that men should not regularly drink more than the daily unit guidelines of 3–4 units, or…

4 × 25ml shots of whiskey
1.7 × 175ml glasses of white wine
1.7 pints of 4% lager