Alcohol and human health
Alcohol and human health

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Alcohol and human health

1.3.1 Alcoholic liver disease

Rachael's story illustrates the start of damage to the liver (Vignette 1).

Vignette 1 Rachael's health problems as the result of her drinking

Rachael drank heavily throughout her time as a manager in a travel company. For many years she was able to cope with the heavy demands of her job without apparently developing any harmful effects. Indeed it seemed as though the alcohol had a positive effect on her employment prospects. The other managers enjoyed her company in the pub after a tense day at the office and she enjoyed quite a reputation as a woman who could drink as much as the men.

When Rachael was 45 years old her company asked her to re-locate to their new headquarters in Milton Keynes. As part of her application for insurance to cover her new mortgage Rachael went to see her own doctor for a medical check. On routine questioning Rachael disclosed that she often had abdominal discomfort, occasionally felt nauseous and had frequent diarrhoea.

During the medical examination Rachael disclosed that she was drinking the equivalent of four units of alcohol each day, usually more at the weekends (in fact it was much more). Her doctor calculated that this represented approximately 32 units each week, far in excess of the UK Government's recommended maximum of 14 units per week for both men and women.

On examination her liver was found to be slightly enlarged, but she had no other external signs of liver disease. The doctor took a blood sample that was sent off for analysis.

Because many people tend to underestimate their alcohol consumption when questioned, some health workers use specific sets of questions when screening for excessive alcohol intake (Walsh and Alexander, 2000). A popular version is called the CAGE questionnaire:

CHave you ever felt the need to cut down your drinking?
AHave you ever felt annoyed by criticism of your drinking?
GHave you ever felt guilty about your drinking?
EHave you ever taken a drink (eye opener) first thing in the morning?

A positive answer to two or more of these questions suggests an excessive alcohol intake.

After a week Rachael went back to see her doctor for the results of her blood tests. The doctor informed her that two of the commonest signs of liver damage related to excessive alcohol consumption had been detected in her blood sample.

Making a diagnosis

Rachael's liver disease was picked up almost by chance at a fairly early stage. The doctor was able to make a diagnosis of liver malfunctioning from her medical history and symptoms that were discussed, and the examination which showed an enlarged liver. The blood tests confirmed that Rachael's liver wasn't working very well, but this falls short of establishing a firm diagnosis. An accurate diagnosis can only be made by techniques that differentiate between the different reasons why her liver may be working less than optimally. A liver biopsy (Figure 3) was used to make certain that Rachael's liver disorder was related to her alcohol consumption.

At this stage it was confirmed that her diagnosis is known as alcoholic fatty liver.

Rachael was upset by the diagnosis, but relieved to hear from her doctor that this condition could be reversed if she stopped drinking alcohol. She resolved to stop, or at least severely restrict, her alcohol intake.

Figure 3
Figure 3 Taking a liver biopsy. (a) Indicates the position of the liver and the location through which the biopsy needle is usually inserted. (b) A small slender core of tissue is removed

During a liver biopsy a small hollow needle is inserted through the skin and into the liver (Figure 3). A sample of liver tissue is extracted that can be examined under a miscroscope. Biopsies may be used to diagnose a condition, and also to monitor its progress in future years.

Perhaps the best known long-term harmful side-effect of drinking excessive alcohol is damage to the liver. Alcoholic liver disease is categorised into three progressive stages; fatty liver, hepatitis and cirrhosis. Fatty liver is an early and reversible consequence of excessive alcohol consumption during which fat accumulates within the cells of the liver (Figure 4). The mechanisms by which this occurs are complex and still under investigation, but they include the release of fats from adipose tissue (cells where fat is normally stored), reduced fat breakdown in the liver, and in cases of chronic alcoholism other nutritional deficiencies play a role.

Figure 4
Figure 4 At the microscopic level it is possible to detect the presence of fat in thin slices of liver tissue using a red dye. (a) The cells in a sample of normal liver contain little fat compared with (b) cells in a sample of fatty liver. Magnification × 100 (Photos: Hilary MacQueen)


Why might there be nutritional deficiencies in chronic alcoholism?


Ethanol has a high energy content, so can supply much of the daily energy requirements of a heavy drinker. However, unlike other food sources, it provides none of the other essential nutrients (vitamins, proteins, etc.) so malnutrition is common in alcoholism.

Fatty liver itself does not cause long-term damage to the liver and is reversed by abstaining from drinking alcohol. However, it can be an important early indication that harm is being done and that continued excessive alcohol consumption could lead to the more serious conditions of hepatitis and cirrhosis (Figure 5).

Figure 5
Figure 5 (a) Comparison between samples of liver from three people showing normal liver, fatty liver and cirrhosis (Photo: Arthur Glauberman/Science Photo Library)

Hepatitis means ‘inflammation of the liver’ and can range from being mild (only detectable through blood tests) to severe, causing sickness, jaundice (yellowing of the skin) and pain. Very severe hepatitis can lead to liver failure which is often fatal.

Cirrhosis is a gradual and irreversible change in about 10% of chronic heavy drinkers whereby liver cells are replaced by scar tissue. Not only does this decrease the ability of the liver to perform its many essential biological functions, it also disrupts the blood flow through the liver tissue, which causes serious complications such as damage to the spleen (an organ involved in blood maintenance) and the blood vessels of the gut (as blood pressure increases in the portal vein).

Because the liver is vital for a wide range of functions including digestive processes, regulation of blood glucose levels, storage of vitamins and break-down of noxious substances, the disruption caused by cirrhosis affects many body systems. Death from cirrhosis of the liver tends to be due to liver failure or sudden catastrophic bleeding from the disrupted blood vessels of the gut.

Relatively little is understood about the precise changes that occur within the individual cells of the liver that lead to damage, inflammation and cirrhosis. The observation that relatively few individuals who drink excessively suffer serious liver injury (hepatitis and cirrhosis are rare, whereas most heavy drinkers will have fatty liver) suggests that other factors, such as obesity and genetic makeup, may be important in addition to alcohol (Reuben, 2006). In addition, deficits in vitamins and other essential nutrients can lead to disruption of the chemical reactions in the body which maintain healthy tissues and repair damage, so it is possible that malnutrition could contribute to the cause or the progression of alcoholic liver disease.

Several potential mechanisms have been proposed that attempt to explain how the presence of ethanol (or its metabolites) could cause damage to liver cells; however, research in this area is difficult due to the enormous number of interlinked chemical reactions that simultaneously occur within cells.

Understanding the molecular processes within liver cells that lead to alcoholic liver disease in some individuals and not others could allow the development of therapies to reduce or perhaps even reverse the harmful effects of drinking alcohol. Currently some alcoholic liver diseases may be reversed with abstinence, but cirrhosis is irreversible and treatment (Section 1.5) is focused on slowing progression and reducing complications.


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