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Introduction

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

This unit describes some of the effects of drinking alcohol. It looks at alcohol's journey through the body and its effect on the liver. It also discusses some possible beneficial effects. This is an important health issue and should be of wide interest.

This unit is an adapted extract from the Open University course Introducing health sciences: a case study approach (SDK125)

Original Copyright © 2007 The Open University. Now made available within the Creative Commons framework under the CC Attribution – Non-commercial licence (see http://creativecommons.org/by-nc-sa/2.0/uk/).

Learning outcomes

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

By the end of this unit you should be able to:

describe the effects that ethanol in the blood has on the body – specifically the effect on drivers’ judgement at blood-alcohol concentrations near the legal limit for driving and the serious effects of blood-alcohol concentrations in excess of 200 mg/100 ml;
describe the short-term effects experienced following excessive alcohol consumption. Comment on the relationship between these complex effects and ethanol metabolites or congeners, the various ‘remedies’ adopted, and that the physiological basis for these economically important short-term harmful effects remains poorly understood;
discuss some of the long-term harmful effects of drinking excessive alcohol with specific reference to the three stages of alcoholic liver disease and central and peripheral nervous system damage;
discuss fetal alcohol syndrome, describing the main effects on the fetus and some of the factors that can make research into this disorder more complex.

1.1 The biological effects of ethanol

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

This section investigates some of the harmful effects that a high level of blood-ethanol can have on the body: both short-term problems such as ‘hangover’, and long-term health problems that are associated with regular heavy drinking. Whilst this section is primarily about the biological effects that ethanol has on various organs of the body, it is important to remember that the socioeconomic effects of heavy drinking are also very serious (Paton, 2005). Figure 1 summarises some of the increased risks a drinker faces as the ethanol concentration in their blood increases.

(Source: Paton, 2005)

Figure 1 Some of the risks associated with increasing ethanol concentrations in the blood

The main acute effects of ethanol are on the nervous system, causing increased confidence and heightened mood leading to increased risk of accidents, violence and socially inappropriate behaviour. Alcohol also disrupts the ability of the brain to coordinate between sensory input and motor output which leads to slurred speech, less controlled movement, delayed reaction times and errors of judgement. Tests on drivers have shown that steering problems begin at blood-ethanol concentrations (BAC) of about 20 mg/100 ml, and the risk of being involved in a traffic accident more than doubles at BAC of 80 mg/100 ml, which is the legal limit for driving in the UK (Table 1). If this concentration doubles to 160 mg/100 ml, the risk of being involved in an accident increases more than 10-fold.

Experiments have shown that experienced drivers misjudged gaps with a concentration of 50 mg ethanol in 100 ml of blood (BAC 50 mg/100 ml). From Table 1, in which countries would it be legal for drivers to exceed this amount?

Table 1 European drink-drive blood-alcohol limits (Source: Safe Travel, 2006)

Country	Limit (mg/100 ml)	Country	Limit (mg/100 ml)
Austria	50	Lithuania	0
Belgium	50	Luxembourg	80
Bulgaria	50	Macedonia	50
Croatia	50	Malta	0
Cyprus (North)	50	Netherlands	50
Cyprus (South)	90	Norway	20
Czech Republic	0	Poland	20
Denmark	50	Portugal	50
Estonia	0	Romania	0
Finland	50	Serbia and Montenegro	50
France	50	Slovakia	0
Germany	50	Slovenia	50
Greece	50	Spain	50
Hungary	0	Sweden	20
Ireland	80	Switzerland	80
Italy	50	Turkey	50
Latvia	50	UK	80

Answer

Drink-drive limits are set at more than 50 mg/100 ml in Cyprus (South), Ireland, Luxembourg, Switzerland and the UK.

If BAC levels increase to around 200 mg/100 ml then speech becomes slurred and coordination of movement is impaired. Coma (loss of consciousness) is likely to occur above 300 mg/100 ml, and concentrations above 400 mg/100 ml are likely to be fatal as a result of disruption of heart and lung function, or inhalation of vomit.

There are variations in the way that people respond to alcohol and some of these are described in Box 1.

Box 1 (Explanation) Variations in alcohol tolerance

In some individuals, the main acute effects of drinking an alcoholic drink are rather different from those just described – they rapidly become quite unwell and experience what is known as a ‘flush’ reaction. The symptoms of this reaction are redness of the face and chest, rapid heart rate, dizziness, nausea, nasal congestion and pulsating headaches. More severe reactions can cause breathing problems and low blood pressure. Individuals who experience these effects accumulate a higher level of acetaldehyde in their blood than those who do not experience these effects.

The enzyme alcohol dehydrogenase (ADH), which converts ethanol into acetaldehyde, and the enzyme aldehyde dehydrogenase (ALDH), which converts acetaldehyde into acetic acid, can each exist in a number of different isoforms which work at different rates. The particular combination of isoforms that individuals have, varies according to the population to which they belong. The production of all proteins in the body, including enzymes, is controlled by genes, individual units of the inherited genetic material, DNA. Genes are inherited from the parents, and everyone inherits a complete set of genes, including those that direct the production of ADH and ALDH. However, people from different populations have slightly different variants of each gene. This is why certain ethnic groups have a relatively high proportion of people who become quite ill after drinking small amounts of alcohol – because of increased levels of acetaldehyde in their blood. More than 75% of Japanese people who drink report flushing, compared with 5–10% of Caucasians (Arnon et al., 1995).

If unusually high levels of acetaldehyde accumulate following an alcoholic drink, how could this have been caused by (a) the rate of reaction of an ADH isoform, and (b) the rate of reaction of an ALDH isoform?

Answer

ADH promotes acetaldehyde production, so an ADH isoform with a high rate of reaction would cause more acetaldehyde to accumulate than one with a slower rate. An ALDH isoform with a slow rate of reaction removes acetaldehyde slowly, allowing high levels of acetaldehyde to accumulate.

The overall effects of ethanol metabolism depends on many factors and ranges from a decline in BAC of less than 10 mg/100 ml per hour to over 40 mg/100 ml per hour for different people.

1.2 Hangovers

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

‘Beer is the reason I get up every afternoon.’

In certain cultures, an evening of heavy drinking is a regular social activity and the ill-effects suffered the following morning are accepted as an inevitable part of life. The economic cost of alcohol-related absence is frequently caused by workers experiencing symptoms of ‘hangover’. This is the term used to describe the collection of symptoms that occur in drinkers on the day following a heavy drinking session, once the ethanol has been cleared from the blood (Figure 2). Even when a hangover is not severe enough to cause absence, it may severely impair the ability of a person to function effectively in the workplace. The economic impact of alcohol-related illness is dominated by these short-term productivity deficits, with chronic alcohol-related diseases only accounting for a small proportion of this cost.

Source: Cartoonstock.com ©

Source: Cartoonstock.com

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Figure 2

The list below shows the most reported symptoms of hangover, with the commonest first:

headache
poor sense of well-being
diarrhoea
anorexia (lack of appetite)
tremor (trembling hands) fatigue
nausea.

Symptoms vary enormously between people and episodes, making research into this condition difficult, even without considering the ethical issues of deliberately making people ill. A variety of physiological mechanisms have been proposed that could reasonably explain the occurrence of hangovers, but without much evidence to back them up. We will consider each of the possibilities briefly.

1.2.1 Physical disturbances

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

Dehydration

How can drinking alcohol result in dehydration?

Answer

Ethanol inhibits the release of vasopressin; this results in an increase in the volume of urine produced by the kidneys and can lead to dehydration.

Although vasopressin levels return to normal during hangover, once ethanol is no longer present in the blood, additional fluid loss may occur due to sweating, vomiting and diarrhoea. Symptoms of dehydration include many of those associated with hangovers (dizziness, light-headedness, weakness, thirst, etc.).

Gastrointestinal disturbances

At a high concentration, ethanol damages cells on contact (Box 2) and so can cause irritation of the stomach and intestinal lining resulting in inflammation.

Ethanol also increases the production of gastric acid and intestinal secretions, and the after-effects of these processes include abdominal pain, nausea and vomiting, all of which can be associated with hangovers.

Box 2 (Enrichment) The antibacterial action of ethanol

Ethanol can act as a disinfectant because it damages cells it is in contact with. It is an effective disinfectant and is used at 70 per cent vol. strength in hospital swabs and laboratories to kill bacteria.

In previous centuries, weak beers and ciders were often brewed by, or given as a ration to, the peasant workforce, and were the drink of choice. Because of the antibacterial action of the ethanol, they were safer to drink than the often-contaminated water.

Low blood sugar

The level of glucose which is present in the blood is carefully maintained in order to ensure that cells receive a continuous supply of fuel for metabolic processes. Excess glucose from the diet is stored in the liver and released in a carefully regulated manner to maintain the level in the circulation. Ethanol consumed in large amounts disrupts this balance and this can result in low blood sugar levels a few hours later. Since glucose is the primary source of energy for cells in the brain, this could explain hangover symptoms such as fatigue, weakness, and mood disturbances.

1.2.2 Psychological and sleep disturbances

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

The severity of hangover symptoms has also been associated with particular personality traits. For example, some research has indicated that individuals with personality traits that predispose them to a risk of alcoholism, experience more severe hangover symptoms than other people.

Although alcohol acts as a sedative, the sleep it induces can be of poorer quality and shorter duration than normal. Ethanol interferes with the action of key neurotransmitters, in particular GABA and glutamate, to cause an overall sedative effect. The body counterbalances this by changing the number of GABA and glutamate receptors present at the synapses, increasing the number of glutamate receptors and decreasing the number of GABA receptors. Ethanol is removed relatively quickly from the body, but it takes longer for the number of receptors to return to normal, leaving the nervous system in a temporary unbalanced, over-excited state.

What are the physiological signs associated with alcohol withdrawal?

Answer

Elevations in heart rate and body temperature, tremor, insomnia and anxiety.

Because the symptoms of hangover share many of the characteristics of alcohol withdrawal symptoms, a possible interpretation is that hangover may be a mild form of alcohol withdrawal.

1.2.3 Chemical factors

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

Ethanol metabolites

The suggestion that acetaldehyde accumulation is involved in hangovers is largely due to the observation that high concentrations of acetaldehyde in the blood give rise to toxic effects which resemble hangovers (rapid pulse, sweating, nausea, etc.).

Why would acetaldehyde accumulate in the body after heavy drinking?

Answer

Ethanol is converted into acetaldehyde by the enzyme ADH, and then ALDH catalyses the breakdown of acetaldehyde into acetic acid. If the first reaction occurs at a faster rate than the second, then acetaldehyde accumulates.

However, high concentrations of acetaldehyde in the blood are not detected during hangovers in most people, so there is no direct evidence that acetaldehyde is the root cause.

Other chemicals

Studies have shown that purer drinks (such as vodka and gin) cause fewer hangover symptoms than drinks rich in congeners (whisky, brandy, red wine). Congeners are the chemicals that provide characteristic taste, aroma and colour. However, pure ethanol can cause hangovers, so congeners can only be a contributing factor. One chemical that has been identified as potentially important in hangover is methanol.

Methanol is absorbed and metabolised by the same mechanisms as ethanol, but ethanol is preferentially metabolised when both substances are present. Methanol levels in the blood therefore remain high after ethanol levels decrease, possibly explaining the delayed onset of hangover (Jones, 1987). The products of methanol breakdown are formaldehyde and formic acid, both of which are very toxic: high concentrations can cause blindness and death. Drinks which are associated with increased hangover symptoms contain high levels of methanol (e.g. brandy, whisky).

Methanol poisoning is treated by administering large doses of ethanol; the methanol is thus metabolised more slowly, preventing the build-up of toxic formaldehyde and formic acid. This approach might form the basis for theories that consuming more alcohol is a way to overcome a hangover.

Hangover treatments

There are numerous treatments reputed to alleviate the symptoms of hangover, ranging from anecdotal folklore to costly pharmaceutical products. Hangover symptoms abate with time, but vary widely between individuals and occasions, so trials of remedies are of limited reliability. Whilst these remedies may not have been subject to systematic scientific testing, some are reasonable approaches based on what is understood about hangover physiology:

Consumption of food containing the sugar fructose, such as fruit or fruit juices, or bland food rich in carbohydrates, may help to counter symptoms arising from low blood sugar.
Sleeping is likely to relieve symptoms associated with fatigue.
Drinking copious volumes of water reduces dehydration.
Anti-inflammatory drugs, such as aspirin, are commonly used to relieve the symptoms of headache, but there is a risk that since they can irritate the gut lining they might compound alcohol-induced stomach disturbances.
Caffeine is traditionally widely used and may counteract fatigue symptoms.
More alcohol (Box 3) may alleviate mild withdrawal symptoms, and/or allow methanol time to clear the system without producing high concentrations of formaldehyde and formic acid. However, any immediate relief would be overshadowed by the reinitiation of the whole process.

Box 3 (Enrichment) ‘Hair of the dog’

This phrase is used to describe the consumption of a small alcoholic drink in order to cure hangover. The expression alludes to an old belief that an antidote to having been bitten by a mad dog was to place some burnt hair from the same dog onto the wound. The phrase is also used in Hungary ‘kutya harapást szörével’ translated as (you may cure) ‘the dog's bite with its fur’.

Phrases to describe the concept of drinking to alleviate hangover symptoms are also found elsewhere, such as the French ‘rallumer la chaudière’ (re-light the boiler) or the Danish ‘rejse sig ved det træ, hvor man er faldet’ (you should get up next to the tree where you fell).

A recent study concluded that ‘no compelling evidence exists to suggest that any complementary or conventional intervention is effective for treating or preventing the alcohol hangover’ and suggested that an effective intervention would remain elusive until the underlying biology was better understood (Pittler et al., 2005). Hangovers are unpleasant experiences that cause disruption to people's lives and can impair their ability to perform tasks such as working or driving effectively. The most effective way of reducing hangover symptoms is to avoid drinking excessive amounts of alcohol, especially drinks containing the highest levels of congeners.

1.3 Long-term problems from chronic alcoholism

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

Chronic alcoholism, the excessive and habitual consumption of alcohol, results in many health problems. Three are discussed here – the damage caused to the drinker's liver and to the nervous system, and the effect of alcohol consumption during pregnancy on the fetus. Other health problems include cardiovascular disease and cancer.

1.3.1 Alcoholic liver disease

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

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 women (21 units for men).

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:

C	Have you ever felt the need to cut down your drinking?
A	Have you ever felt annoyed by criticism of your drinking?
G	Have you ever felt guilty about your drinking?
E	Have 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 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

Long description

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 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)

Long description

Why might there be nutritional deficiencies in chronic alcoholism?

Answer

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

Long description

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.

1.4 Nervous-system damage

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

Chronic consumption of high levels of alcohol can cause irreversible damage to the nervous system. The majority of people with chronic alcoholism have some degree of dementia, which is a general loss of intellectual abilities including memory, judgement and abstract thinking, as well as personality changes. The general effect seems to be a shrinkage of brain tissue, as revealed by brain imaging techniques (Figure 6) or post-mortem studies, the extent of which correlates with the amount of alcohol consumed (National Institute on Alcohol Abuse and Alcoholism, 2000). In particular shrinkage is extensive in the prefrontal cortex, PFC, which has responsibility for choice, decision-making and regulation of behaviour. It is also present in deeper brain regions associated with memory, and in the cerebellum which is involved in movement and coordination.

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Figure 6 MRI (magnetic resonance imaging) image showing how the brain structure is affected in a person with chronic alcoholism. (a) Images taken in three places in a healthy brain – these are ‘slices’ taken through the front, middle and back of the head (see inset). (b) Shows the shrinkage of the brain in images taken at the same three positions in a person with chronic alcoholism (Photo: Daniel Hommer/National Institute of Alcohol Abuse and Alcoholism)

Long description

Alcoholism is also associated with damage to the peripheral nerves (i.e. those connecting the central nervous system, CNS, with the rest of the body). This causes symptoms such as sensory disturbances (numbness or pain), motor disturbances (weakness and muscle wasting) and some problems with speech, swallowing, heart rate, pupil function, erectile function, breathing during sleep, etc. The mechanism of nerve damage is not clear and could be associated with a direct toxic effect of ethanol on nerves, or indirectly via nutritional deficiencies.

1.5 Fetal alcohol syndrome

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

There are a range of disorders associated with maternal alcohol consumption during pregnancy which are collectively known as fetal alcohol spectrum disorders, FASDs. The best characterised is fetal alcohol syndrome, FAS. FAS is defined by four criteria, the first of which is excessive maternal alcohol intake during pregnancy, the other three being:

a characteristic pattern of minor facial abnormalities and other malformations (in particular of the limbs and heart); the characteristic facial features are illustrated in Figures 7 and 8;
growth retardation;
central nervous system abnormalities in the fetus/infant.

Figure 7 Characteristic facial features in a child with fetal alcohol syndrome. Findings may include a smooth philtrum (the vertical groove between the base of the nose and the border of the upper lip), thin upper lip, upturned nose, flat nasal bridge, skin folds covering the inner corner of the eye, small openings between the eyelids and small head circumference (Source: American Academy of Family Physicians)

Long description

Figure 8 Characteristic facial features in children of different ethnicities with fetal alcohol spectrum disorders illustrating the facial features described in Figure 14. (a) Northern European descent. (b) Black. (c) Native American, (d) Biracial (white, black) (Photos: American Academy of Family Physicians)

Long description

FAS is considered to be the leading cause of mental retardation in the world and is linked to impaired learning, attention problems, slower reaction times and impaired problem solving, planning and ability to keep track of things (National Institute on Alcohol Abuse and Alcoholism, 2000). Studies from the 1970s and 1980s estimated the incidence rate of FAS in the USA as 1–2 cases per 1000 children born each year. In a population-based study in Seattle in 1997 the rate was nearly 1 per 100 live births. The highest rates to date report 4.6 per cent of 6-year-old children in one community within the Western Cape Province in South Africa (Strömland, 2004).

The mechanisms that result in FAS are complex. Ethanol and acetaldehyde present in the mother's circulation cross the placenta and circulate freely through the blood vessels of the developing fetus. Fetal development involves the division and migration of cells in a carefully orchestrated manner, a process that is disrupted by substances such as ethanol. The developing nervous system is particularly sensitive to disruption.

Not all children who are exposed to alcohol during fetal life are born with FASDs, and there may be several risk factors, involving genetic as well as environmental factors. There are also likely to be many other contributing factors such as nutrition, parental care, drug abuse and smoking which make research into FAS complicated. There are no treatments to reverse the damaging effects of alcohol on the developing brain, although the characteristic facial features lessen during adolescence. A safe threshold of alcohol consumption or critical period during pregnancy when alcohol must be avoided has not been identified. Women who are pregnant, or even those who are just likely to become pregnant, are advised to abstain from drinking alcohol. Whilst FAS is entirely preventable by avoiding alcohol during pregnancy, in reality a significant number of women of childbearing age in all western cultures are dependent on alcohol to a certain extent. Treating alcohol dependence in these women is therefore a health care priority for the protection of any future children, as well as for their own health.

1.6.1 What works in helping people to stop or reduce their alcohol intake?

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

There is at the moment no known cure for alcoholism. Both psychological and drug treatments are used in treating excessive alcohol intake (Buonopane and Petrakis, 2005). The plethora of different types of treatment in itself may indicate that there are no guaranteed results, and the condition remains hard to resolve.

Throughout England a mapping exercise (Alcohol Concern, 2002) estimated that there were over 300 advice and counselling services, 100 day programmes and nearly 200 residential programmes specifically established to treat alcohol addiction. The range of treatments available at these centres is very diverse and can be baffling to people seeking help. Many of the non-drug-related forms of support have not been subjected to clinical trials that would be able to demonstrate whether or not they are effective. This is not to say that the therapies and supportive interventions do not work, but just that it is difficult to demonstrate their effectiveness in an objective ‘scientific’ way.

A proportion of people with alcohol dependency are able to stop using alcohol without the assistance of outside agencies or formal types of help (Klingemann and Sobell, 2001). For Rachael the shock of the realisation that she was harming her own health might be sufficient for her to resolve to make this major change to her behaviour (Vignette 2).

Vignette 2 Rachael needs treatment

When she was first given the diagnosis of ‘alcoholic fatty liver’, Rachael was determined to find out as much as she could about this condition. After several sessions on the internet and following a further consultation with her own doctor she was able to find out the following information:

Fatty liver always occurs if alcohol consumption exceeds 100 ml of ethanol each day (just over a bottle of wine). (Rachael was drinking three-quarters of a bottle of spirits, about twice this amount).
The condition is usually reversible if no more alcohol is consumed.
The condition may progress to cirrhosis and possibly liver failure if the person continues to drink alcohol (Teli et al., 1995).

For many people, indeed for Rachael herself, the use of alcohol is firmly embedded into social structures that are hard to dislodge. If Rachael stopped drinking how would she relieve the stresses and strains of her life? How could she remain at the core of her organisation when so much ‘business’ is conducted by her peers in the bar? If Rachael doesn't stop drinking, what might happen?

Research studies that have compared groups of problem drinkers with those in treatment have found that amongst the people not receiving recognised forms of treatment a proportion modify their own drinking habits. A major study in the USA (Weisner et al., 2003), found that 12 per cent of the problem drinkers followed up as a ‘control group’ and who had received no formal counselling or psychological help, reported that they were still abstinent of alcohol after 12 months, but this is much less than the 57 per cent under formal treatment who were not using alcohol after 12 months.

If stopping drinking alcohol is difficult in the short term, it becomes even more difficult for people to remain abstinent in the longer term. Many people with dependency on alcohol seem to go through several cycles that include periods of controlled drinking or abstinence, followed by problem drinking that leads to further treatment episodes and so on through their lives. Research in Germany (Mann et al., 2005) followed 96 problem drinkers over 16 years, and confirmed that people drift in and out of problem drinking over many years. Indeed only 22 per cent reported abstinence for the entire 16 years.

Research findings collected from a large number of trials have also indicated which people can be predicted to have the best outcomes from various types of treatment for their problem drinking (Weisner et al., 2003):

Women seem to do better than men, although they often enter treatment later than men and may have more associated mental health problems.
Although some young people ‘mature’ out of their problem drinking behaviour, in general very young people entering treatment have a worse outcome than more mature people.
Lower socio-economic status is associated with less improvement over time.
The worse the problem drinking at the start of treatment and the presence of psychiatric problems, the poorer the outlook for the success of treatment.
Networks and family support can be important predictors of the outcome of treatment. If the person's family and friends are also involved in addictive types of behaviour, the chances of successful treatment are poorer. However, the presence of a supportive family environment is associated with improved chances of successful treatment (Copello et al., 2005).

1.6.2 Treating alcohol-related liver disorders

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

Although considerable progress has been made in the treatment of many other chronic medical conditions, scant progress has been made in the treatment of cirrhosis. In over 8000 people admitted to hospitals in the Oxford region of the UK with liver cirrhosis during a 30-year observation period, 34 per cent had died one year after their admission and this death rate remained more or less constant (Roberts et al., 2005).

The largely pessimistic view of the failure of treatment of liver damage may change as there is evidence (Iredale, 2003) that the underlying processes, such as inflammation, are becoming increasingly understood, and may potentially be reversible in the future. However, it is clear that at the moment, no really effective medication currently exists to reverse the damage produced by alcohol and the best hope for long-term health for Rachael and other problem drinkers remains abstinence from drinking alcohol.

Liver transplantation

If Rachael continues to drink alcohol the fatty infiltration of her liver may progress to cirrhosis (Teli, 1999). When cirrhotic liver damage becomes severe, liver transplantation might be possible. Because of the limited availability of livers for transplantation some specialist units have a rule that people should demonstrate their resolve and not drink alcohol for a fixed period of time (perhaps six months), before the transplant is considered. This type of rule, with its rather moralistic overtones, has been challenged by Webb and Neuberger (2004). Other people may be not considered suitable for liver transplant because they have other physical or psychological problems (Walsh and Alexander, 2000).

Transplantation is a simple idea but replacing a diseased organ with a fully functioning one from a donor can be complicated in practice. As you can imagine there are many ethical dilemmas involved in taking organs from heart-beating but brain-dead people. Many of the potential medical problems arise after transplantation because the host person's body will consider the new organ to be ‘non-self’ and attempt to reject it. Although rejection can be controlled by immunosuppressive drugs, these often have side-effects. Despite these difficulties many people with a liver transplant lead entirely normal, active lives (Prasad and Lodge, 2001).

If Rachael's liver damage becomes so severe that she has to have a liver transplant then the outlook is surprisingly good. Approximately 75 per cent of people with a new liver will be alive five years after the transplant surgery (Iredale, 2003), and progress with new surgical techniques and immunosuppressive drugs continues to improve the chances of survival. However, research has shown that between 8 per cent and 22 per cent of people are found to drink alcohol within six months of their transplant, and overall between 10 per cent and 30 per cent; relapse in due course (Webb and Neuberger, 2004). Let us hope that Rachael is able to get the right information, treatment and support to help her live a long and happy life.

Summary

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

The main acute effects of ethanol are on the nervous system, causing characteristic changes in behaviour and judgement. There are particular issues with regard to driving, with different countries setting various ‘safe’ limits for blood-ethanol concentration. Very high blood-ethanol concentrations can be fatal.
Hangovers are unpleasant and are poorly understood. Various mechanisms have been proposed including direct effects of ethanol on organs, ethanol withdrawal, accumulation of acetaldehyde and the effects of other chemicals present in alcoholic drinks. Many treatments are in common usage but there is little evidence of any particular intervention being beneficial.
Alcoholic liver disease results from excessive drinking and includes fatty liver (which is the early reversible stage) and the more serious alcohol-induced hepatitis and cirrhosis.
Excessive drinking can also lead to nervous-system damage resulting in dementia, and shrinking of central nervous system tissue.
Fetal alcohol syndrome can result from maternal alcohol consumption during pregnancy. It involves disruption of fetal development causing CNS abnormalities, growth retardation and characteristic facial features.
Treatment of liver disorders is difficult other than by abstinence.

Revision questions

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

Question 1

Drinking alcohol produces a complex set of effects on a number of body systems.

(a) On which system are the main acute effects most likely to lead to sudden death, and why?
(b) Name some possible causes of death from drinking alcohol.

Answer

(a) The main acute effects are on the nervous system, causing mood changes and impairment of judgement and reaction time, etc.
(b) Possible causes of death are a fatal traffic accident due to poor judgement; other accident due to uninhibited behaviour; inhalation of vomit; heart or lung failure; liver cirrhosis; suicide due to depression. You may be able to think of others.

Question 2

Explain two different ways whereby some individuals could have higher levels of acetaldehyde in their system than others, after drinking identical alcoholic drinks.

Answer

(a) Acetaldehyde is produced from ethanol more rapidly in some individuals than in others.
(b) Acetaldehyde is converted into acetic acid more slowly in some individuals than in others.

Question 3

If the reaction catalysed by ALDH to form acetic acid is faster than the production of acetaldehyde (catalysed by ADH), how will this affect the drinker?

Answer

There will be no build-up of acetaldehyde because it will metabolise to acetic acid as soon as it is made. So, the drinker will not experience the flushing, increased heart rate, dizziness or nausea associated with a build-up of acetaldehyde.

Question 4

The proportion of fat per body weight increases with age. How might this affect older drinkers?

Answer

The increased proportion of fat to muscle in older people will result in a decrease in total body water. As ethanol is water-soluble, the same amount of ethanol will be dissolved in a smaller amount of water, resulting in a higher BAC in an older person than a younger. Unless the body responds by making more enzymes, this will result in higher levels of intoxication after smaller amounts of ethanol.

Question 5

(a) Why is it impossible to be precise about what is a safe drinking limit? (b) Why in particular are pregnant women advised to avoid drinking any alcohol at all?

Answer

(a) People inherit genes that direct production of ethanol-metabolising enzymes, and will therefore process ethanol at different rates. People also vary greatly in weight and in their muscle to fat ratios. It is therefore impossible to do more than give very broad guidelines on what might be a safe level of drinking.
(b) Pregnant women are advised to abstain from drinking alcohol because of the risk of fetal alcohol syndrome (FAS). No safe limit has been identified for this because the mechanisms by which alcohol consumption causes FAS in some individuals are poorly understood.

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References

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

Alcohol Concern (2002) Report on the Mapping of Alcohol Services in England, London, Alcohol Concern.

Arnon, R., Degli Esposti, S. and Zern, M. A. (1995) ‘Molecular biological aspects of alcohol-induced liver disease,’ Alcoholism: Clinical and Experimental Research, vol. 19, pp. 247–256.

Buonopane, A. and Petrakis, I. (2005) ‘Pharmacology of alcohol use disorders’, Substance Use and Misuse, vol. 40, pp. 2001–2020.

Copello, A., Velleman, R. and Templeton, L. (2005) ‘Family interventions in the treatment of alcohol and drug problems’, Drug and Alcohol Review, vol. 24, pp. 368–385.

Iredale, J. (2003) ‘Cirrhosis: new research provides a basis for rational and targeted treatments’, British Medical Journal, vol. 327, pp. 143–147.

Jones A. W. (1987) ‘Elimination half-life of methanol during hangover’, Pharmacology and Toxicology, vol. 60, pp. 217–220.

Klingemann, H. and Sobell, L. (2001) ‘Introduction: natural recovery research across substance use’, Substance Use and Misuse, vol. 36, pp. 1409–1416.

Mann, K., Schafer, D., Ackermann, K. and Croissant, B. (2005) ‘The long-term course of alcoholism, 5, 10 and 16 years after treatment’, Addiction, vol. 100, pp. 797–805.

National Institute on Alcohol Abuse and Alcoholism (2000) [online] Alcohol Alert 50: Fetal Alcohol Exposure and the Brain. Available from: http://pubs.niaaa.nih.gov/publications/aa50.htm (Accessed 18 February 2008).

Paton, A. (2005) ‘ABC of alcohol: Alcohol in the body’, British Medical Journal, vol. 330, pp. 85–87.

Pittler, M. H., Verster, J. C. and Ernst, E. (2005), Interventions for preventing or treating alcohol hangover: systematic review of randomised controlled trials. British Medical Journal, vol. 331, pp. 1515–1518.

Prasad, K. and Lodge, J. (2001) ‘Transplantation of the liver and pancreas’, British Medical Journal, vol. 322, pp. 845–847.

Reuben, A. (2006) ‘Alcohol and the liver’, Current Opinion in Gastroenterology, vol. 22, pp. 263–271.

Roberts, S., Goldacre, M. and Yeates, D. (2005) ‘Trends in mortality after hospital admission for liver cirrhosis in an English population from 1968 to 1999’, Gut, vol. 54, pp. 1615–1621.

Strömland, K. (2004) ‘Fetal alcohol syndrome – a birth defect recognized worldwide’, Fetal and Maternal Medicine Review, vol. 15, pp. 59–71.

Teli, M., Day, C. and Burt, A. (1999) ‘Determinants of progression to cirrhosis or fibrosis in pure alcoholic fatty liver.’ The Lancet, vol. 346, pp. 987–990.

Walsh, K. and Alexander, G. (2000) ‘Alcoholic liver disease’, Postgraduate Medical Journal, vol. 76, pp. 280–286.

Webb, K. and Neuberger, J. (2004) ‘Transplantation for alcoholic liver disease’, British Medical Journal, vol. 329, pp. 63–64.

Weisner, C., Matzger, H. and Kaskutas, L. (2003) ‘How important is treatment? One year outcomes of treated and untreated alcohol-dependent individuals’, Addiction, vol. 98, pp. 901–911.

Acknowledgements

The Open University — Thu, 16 Jun 2011 09:11:58 GMT

>Except for third party materials and otherwise stated (see terms and conditions), this content is made available under a Creative Commons Attribution-NonCommercial-ShareAlike 2.0 Licence

Grateful acknowledgement is made to the following sources for permission to reproduce material in this unit:

The content acknowledged below is Proprietary and is used under licence.

Text

The content is from Book 3, ‘Alcohol and Human Health’ (ed Lesley Smart) (2007) published by Oxford University Press in association with The Open University. Copyright © The Open University. This book is part of a series which forms part of the course materials for course SDK125 Introducing Health Sciences: a case study approach.

Figures

Figure 1 Paton, A. and Touquet, R. (2005), ‘Risks associated with concentrations of alcohol in the blood’, ABC of Alcohol, Oxford, Blackwell Publishing Limited;

Figure 2 Cartoontock

Figure 4 Courtesy of Hilary MacQueen;

Figure 5 Author Glauberman/Science Photo Library;

Figure 6 Daniel Hommer M.D., National Institute on Alcohol Abuse and Alcoholism;

Figures 7 and 8 Wattendorf, D. J. and Muenke, M. (2005) ‘Fetal alcohol spectrum disorders’, American Family Physician, Academy of Family Physicians.

Unit image

Mike O'Dowd: [Details correct as of 28th February 2008]

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