Blackwell Publishing LtdOxford, UKNBUNutrition Bulletin1471-98272006 British Nutrition Foundation? 200631?286331Original ArticleAlcohol consumption and our healthR. K. Foster and H. E. Marriott
BR IE F IN G PA P E R
Alcohol consumption in the new
millennium – weighing up the risks
and benefits for our health
R. K. Foster and H. E. Marriott
British Nutrition Foundation, London, UK.
1. Introduction
2. An introduction to alcohol and alcoholic beverages
2.1 How is alcohol produced
2.2 The production of alcoholic beverages
2.3 Calculation of alcohol content in beverages
2.4 Other measures of alcohol
3. Guidelines for sensible drinking
3.1 UK guidelines
3.2 Guidelines for sensible drinking around the world
4. Alcohol consumption
4.1 Current alcohol intakes in the UK
4.2 Recent trends in alcohol intake in the UK
4.3 Trends around the world
5. Absorption and metabolism of alcohol
5.1 Absorption of alcohol
5.2 Alcohol metabolism
6. Alcohol and nutrition
6.1 Nutrient composition of alcoholic beverages
6.2 The effect of alcohol on energy intake
6.3 Nutritional implications of chronic excessive alcohol consumption
6.4 Other components of alcoholic beverages
7. The burden of disease and mortality related to alcohol
8. Alcohol and disease risk
8.1 Methodological problems of studies assessing associations between
alcohol consumption and disease risk
8.2 Alcohol and bodyweight
8.3 Alcohol and coronary heart disease
8.4 Alcohol and blood pressure
8.5 Alcohol and stroke
8.6 Alcohol and type 2 diabetes
8.7 Alcohol and cancer
Correspondence: Rebecca K. Foster, Nutrition Scientist, British Nutrition Foundation, High Holborn House, 52–54 High Holborn, London
WC1V 6RQ, UK.
E-mail: [email protected]
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Alcohol consumption and our health
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9. Alcohol and other conditions
9.1 Adverse reactions to alcohol for some susceptible individuals
9.2 Alcohol and peptic ulcers
9.3 Alcohol during pregnancy
9.4 Alcohol, bone mineral density and fracture risk
9.5 Alcohol and renal dysfunction
10. Alcohol and social issues
10.1 Short-term psychological and psychomotor effects of alcohol intake
10.2 Crime and public disorder as a result of drinking alcohol
10.3 Alcohol-related harms and other public health issues
10.4 The economics of alcohol consumption
10.5 Population-based initiatives underway to reduce the incidence of
binge drinking
11. Conclusions
Summary
Alcohol is produced via the anaerobic fermentation of sugars by yeast and involves
glucose molecules (C6H12O6) being broken down to yield ethanol (C2H5OH), carbon dioxide (CO2) and energy. The amount of alcohol contained in different alcoholic beverages varies considerably and is referred to as the ‘strength’ of the drink,
which is expressed as the percentage of alcohol by volume (ABV). A standard unit
of alcohol in the UK equates to 8 g or 10 ml of pure alcohol. Guidelines for sensible
drinking set by the UK government are 3–4 units (24–32 g) a day or less for men,
and 2–3 units (16–24 g) a day or less for women. Specific recommendations have
been set for those planning pregnancy and pregnant women, who should drink no
more than 1–2 units of alcohol once or twice a week and should avoid heavy drinking sessions. Guidelines for sensible drinking are similar in other countries. When
taking into account the standard drink unit used to define guidelines, the most commonly recommended limit is 24 g/day for men and 20 g/day for women.
Older people are more likely to drink in line with the sensible drinking guidelines,
as they tend to consume alcohol over a period of time, as opposed to consuming
large quantities on one or two days of the week, a practice that is more popular
among younger people. Consuming double the sensible drinking guidelines in one
day is classified as binge drinking (an alternative definition is drinking until intoxicated). It has become recognised that binge drinking is a common phenomenon in
the UK, particularly among younger people. Other factors, such as income, ethnicity and region of residence, are also recognised to be predictive of the quantity of
alcohol consumed; for example, higher-income households are more likely to consume large quantities of alcohol and consume alcohol more frequently.
The quantity of alcohol consumed is an important factor in determining how it
affects health and well-being. In terms of nutritional health, chronic excessive alcohol intake is well recognised to affect an individual’s nutrient status, because it
reduces food intake and/or may interfere with the digestion, absorption, metabolism and utilisation of some nutrients. However, when consumed in moderation,
alcohol is unlikely to interfere with the metabolism of nutrients or be associated
with impaired vitamin function or depletion to an extent that may harm health,
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R. K. Foster and H. E. Marriott
provided that dietary intakes are adequate. Alcoholic beverages contain alcohol,
carbohydrate and only small amounts of some vitamins, trace elements and minerals. They are therefore unlikely to contribute significantly to micronutrient intake.
Any association that exists between moderate alcohol consumption and the absorption and metabolism of nutrients from the diet is dependant on a number of factors,
including: the nutrient in question; habitual intake of the nutrient and the nutritional status of the individual; and the quantity of alcohol consumed over a period
of time. Overall, little information exists about the implications of binge drinking
on nutrient status; but it may alter food intake, and excessive alcohol consumption
can cause disturbances to the digestive system. While infrequent binge drinking is
unlikely to have any long-term nutritional implications (although it may affect
nutrient status in the short-term), regular binge drinking may have a more negative
impact.
Although alcoholic beverages tend to have few nutrients, they can be a significant
source of energy, as alcohol provides 7 kcal per gram. Studies indicate that alcoholic
beverages are usually additive to an individual’s normal energy intake and individuals are unlikely to compensate for energy from them during the day. The aperitif
effect of alcohol may also encourage an increase in energy intake. It is therefore not
surprising that alcohol intake has been associated with weight gain and an increase
in body mass index (BMI) (with the exception of chronic excessive drinkers). However, there are a number of methodological problems that need to be considered
when comparing the findings of studies investigating the association between alcohol intake and disease risk, including: potential misreporting of total intake; the use
of an appropriate control group; and the need for comparable measurement units.
Consumption of alcoholic beverages has also been associated with increasing the
risk of ill-health associated with pre-existing conditions. For example, it may contribute to ulcer development or aggravate symptoms of existing ulcers. There is evidence that moderate alcohol consumption during pregnancy may affect the
development of the fetus’s central nervous system, and may result in low birthweight. However, there is currently no consensus as to whether alcohol should be
completely avoided during pregnancy. However, it is well recognised that excess
alcohol consumption during pregnancy can put the fetus at risk of fetal alcohol
syndrome.
Quantity of alcohol consumed is particularly important when considering the association between alcohol and chronic diseases; for example, there is now strong evidence that light to moderate (1–3 drinks per day) consumption decreases the risk of
a coronary heart disease (CHD) episode compared with abstainers (with particular
benefits in men aged over 55 years and post-menopausal women). However, heavy
drinking is associated with an increased risk of CHD. Further information is required
to determine the association between drinking patterns and heart health. However,
there is a consensus of opinion that it is the alcohol per se that influences heart health,
rather than a particular type of alcoholic beverage; and other factors that affect an
individual’s choice of drink may be important in distorting the findings from studies
that show otherwise. As with risk of CHD, light to moderate alcohol consumption
is associated with a decreased risk (of 30–40%) of type 2 diabetes, when compared
with teetotallers. Heavy drinking may be associated with an increased risk, resulting
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Alcohol consumption and our health
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in a ‘J’ or ‘U’ shaped relationship between alcohol consumption and the incidence
of type 2 diabetes. A ‘J’ shaped relationship has also been reported between alcohol
consumption and blood pressure. It is widely accepted that heavy alcohol intake is
a risk factor for high blood pressure, and evidence indicates that moderate intakes
may exert a short-term lowering effect, while abstainers/teetotallers are reported to
have a higher blood pressure. The type of stroke is important when considering the
association between stroke and alcohol, as any alcohol consumption is associated
with an increased risk of haemorrhagic stroke, but low intakes (i.e. one drink per day)
may have a protective effect on ischaemic stroke. Heavy drinking is associated with
an increased risk of both types of stroke.
Alcohol intake has also been associated with an increased risk of cancers at a
number of sites. However, a consensus for a likely causal association has only been
identified between alcohol and cancers of the upper-aero digestive tract and liver.
The mechanisms to explain the positive associations between alcohol and breast
cancer, and alcohol and colorectal cancer, have yet to be identified. It is unclear
whether some types of alcoholic beverage are more strongly associated with
increased risk of cancer than others. Mechanisms identified to date suggest that it
is the alcohol per se that exerts damage and, therefore, quantity of alcohol consumed is the most important variable.
Studies looking at the relationship between alcohol and mortality suggest that
10–80 g (approximately 1–8 drinks) of alcohol each week is optimal to reap the
health benefits, but increased risk is noted at higher intakes (thus indicating a ‘U’
shaped relationship between alcohol intake and mortality). Gender and age are
important factors when considering the association between alcohol and mortality.
For example, for younger people, the benefits of alcohol may be outweighed by the
increased risk of other diseases (e.g. alcohol-related cancers, liver cirrhosis) and
increased risk of violence and accidents. Aggressive behaviour, increased risk taking
and decreased responsiveness to social expectations, which may lead to personal
‘harm’, including accidents and violence, are usually the result of alcohol intoxication (i.e. through binge drinking).
Excess alcohol consumption may also result in a ‘hangover’, which disrupts normal life through symptoms of fatigue and increased anxiety, and has economic consequences in the workplace through poor performance or absenteeism. The extent
to which a hangover can affect an individual’s performance, including psychomotor,
recognition and managerial skills, is still being debated. Binge drinking is also associated with an increased risk of sexually transmitted diseases and unplanned pregnancies. Although the cost of binge drinking in terms of long-term health has yet to
be established, the significant economic cost is well recognised. A number of population-based initiatives are underway to try and change the ‘drinking culture’, and
thus reduce the incidence of binge drinking. Initiatives include: advertising campaigns; changes to alcohol advertising regulations; and changes to pub licensing regulations.
Keywords: alcohol, binge drinking, guidelines for sensible drinking, moderate alcohol
intake
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1. Introduction
This paper provides an overview of guidelines for sensible drinking and current drinking habits both in the
UK and around the world. Focusing on moderate alcohol consumption, the current evidence regarding the
nutritional implications of alcohol in the diet, and its
effects on disease risk are also considered. Finally, the
social implications of the topical binge drinking phenomenon are discussed, thereby providing a timely and
useful overview of the potential risks and benefits of
alcohol consumption to our health.
More than 90% of adults in Britain drink alcohol
(Strategy Unit 2004). For the majority of people who
drink alcohol, it is associated with pleasure, socialising
and relaxing (MORI 2000). When consumed in moderate amounts, it is an accepted element of a healthy, balanced diet and lifestyle, with few adverse effects to
nutritional health or risk of disease, and possibly some
benefits. However, when alcohol is consumed in excess,
for example because of chronic abuse or binge drinking,
it can adversely affect the health and well-being of the
individual, and cause detriment to society. In particular,
binge drinking is associated with an increased risk of
injury or assault of the drinker and individuals in the
vicinity. Chronic excessive consumption is associated
with an increased risk of a number of adverse health
conditions, including myopathy, liver cirrhosis, liver
cancer, pancreatitis, kidney problems and problems with
the central, peripheral and autonomic nervous system,
such as cerebral dementia. It is also likely that chronic
excessive drinkers will suffer from some nutritional deficiencies (Peters & Preedy 1999; Rajendram & Preedy
2005). Fortunately, it is only the minority of the population who are classified as chronic excessive drinkers,
and for this reason, this briefing paper will focus primarily on the risks and benefits of light or moderate alcohol
intake. Preedy and Watson (2004) provide a comprehensive overview of alcohol-related harms, including
those related to chronic excessive consumption of
alcohol.
2. An introduction to alcohol and
alcoholic beverages
Alcoholic beverages contain ethanol, which is chemically an aromatic compound containing a hydroxyl
group. Ethanol in beverages is commonly referred to as
alcohol (International Food Information Service 2005).
By law, ethanol for human consumption is only allowed
to be derived from the fermentation of agricultural
crops (e.g. cereals, grapes). Pure ethanol is also known
as absolute alcohol, the production of which is subject
to strict regulations, as is its use (e.g. in research establishments and the chemical industry). Because drinks
containing ethanol/alcohol are subject to taxation in
many countries, when sold for other purposes it is rendered unfit for consumption. For example, ethanol produced for domestic use contains a purple dye and
pyridine (which has an unpleasant smell) and is known
as methylated spirit (‘meths’) and ethanol for industrial
use contains 5% methanol (CH3OH) (which is poisonous), yielding industrial rectified spirit. As the term
‘alcohol’ has been widely adopted as a colloquial equivalent of ethanol, in this briefing paper, alcohol is used
synonymously with ethanol.
2.1 How is alcohol produced?
Alcohol is produced via the anaerobic fermentation of
sugars by yeast. In essence, the overall process involves
glucose molecules (C6H12O6) being broken down in the
absence of oxygen to yield ethanol (C2H5OH), carbon
dioxide (CO2) and energy. In wine or beer making, the
carbon dioxide bubbles off and the amount of alcohol
produced is controlled by the amount of yeast and the
duration of fermentation (i.e. a larger quantity of yeast
and longer fermentation produces more alcohol). The
net overall reaction can be summarised as:
C6H12O6 → 2C2H5OH + 2CO2 + energy
2.2 The production of alcoholic beverages
Sugar, preferably glucose, is necessary to make alcohol.
The sugars in fruit can be fermented by yeast to produce
wine and cider. Alcoholic beverages can also be made
from grains, such as barley and rye (traditionally in
Europe), corn (traditionally in the Americas) and rice
(traditionally in the Far East). As these grains do not
contain fermentable sugars, the starch in the grain has to
be hydrolysed (broken down, for example to maltose
and glucose), before fermentation can occur. Alcoholic
beverages produced in this way include ales, beers,
lagers and rice wines. Grains also form the basis of spirits such as whisky and vodka, whilst liqueurs are made
from distilled spirits (produced through the evaporation
and condensation of alcohol, which produces liquid
with a higher alcohol content), which are sweetened and
flavoured. Fortified wines, such as port and sherry, are
made by adding spirit to wine. About 10–15 years ago,
pre-mixed drinks (referred to as ‘alco-pops’) were introduced to the market, further adding to the selection of
alcoholic beverages available.
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
Alcohol consumption and our health
Methods of production of alcoholic beverages have
developed through various traditions and practices
and, more recently, large-scale production processes.
Although alcoholic fermentation is a rapid process, the
production of alcoholic beverages can take many years
because of the different processes involved and the
desired characteristics of the final products. For example, many wines are best left to ‘age’, rather than drunk
‘young’, and some types of whiskey may be left to
mature for decades. The distinctive flavours of different
types of alcoholic beverage also arise from the addition
of other specific ingredients, such as hops in beer and
juniper berries in gin.
2.3 Calculation of alcohol content in beverages
The ‘amount’ of alcohol contained in alcoholic beverages
varies considerably and is referred to as the ‘strength’ of
the drink, which, by law in the European Union (EU),
should be expressed as the percentage of alcohol by volume (ABV). This information is mandatory for beverages
containing more than 1.2% ABV. It should be noted that
percentage ABV is not the same as the percentage of alcohol by weight (percentage w/v), because alcohol is less
dense than water (relative densities 0.79 and 1.00,
respectively). For example, 5% ABV is equivalent to 4 g
of alcohol per 100 ml (4% by weight). The alcohol content of a range of strengths ‘by volume’ is shown in
Table 1, and the typical percentage ABV of different
types of alcoholic beverages is shown in Table 2.
2.4 Other measures of alcohol
Drinks containing alcohol are also ascribed a value of
‘units’, which relate to the amount of alcohol they contain. ‘Units’ were a concept developed for clinical practice in 1987 and have since been used as the basis of
sensible drinking guidelines (discussed in section 3). One
unit equates to 8 g (or 10 ml) of pure alcohol.
291
The list below shows the number of units of alcohol in
common drinks:
•
•
•
•
•
•
•
a pint of ordinary strength lager – 2 units;
a pint of strong lager – 3 units;
a pint of bitter – 2 units;
a pint of ordinary strength cider – 2 units;
a 175-ml glass of red or white wine – 2 units;
a pub measure of spirits – 1 unit;
an alco-pop – around 1.5 units.
Key points
• Ethanol in beverages is commonly referred to as
alcohol.
• Alcohol is produced via the anaerobic fermentation of
sugars by yeast, and involves glucose molecules
(C6H12O6) being broken down to yield ethanol
(C2H5OH), carbon dioxide (CO2) and energy.
• The amount of alcohol contained in different alcoholic beverages varies considerably and is referred to as
the strength of the drink, which is expressed as the percentage of alcohol by volume (ABV).
• A unit of alcohol equates to 8 g or 10 ml of pure
alcohol.
3. Guidelines for sensible drinking
3.1 UK guidelines
The Department of Health currently advises that there
are no significant health risks associated with consuming up to 3 to 4 units (24–32 g) of alcohol a day for
men, and up to 2 to 3 units (16–24 g) a day for women.
However, consistently drinking more than these levels
per day is linked with a progressive increase in risks to
Table 2 Typical percentage alcohol by volume (ABV) of alcoholic
beverages (source: Chan et al. 1994)
Table 1 Alcohol content of a range of strengths ‘by volume’
Alcoholic beverage
% ABV
% Alcohol by volume (ABV)
Alcohol (g/100 ml)
5
10
15
20
25
30
35
40
4.0
7.9
11.9
15.8
19.8
23.7
27.7
31.6
Low alcohol beer
Alco-pops
Beer, cider
Wines
Spirits
Liqueurs
Fortified wines
0–2
4–5.5
4–6
9–13*
37–45
20–40
18–25
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
*Since these data were published, wines with a higher percentage ABV have
become widely available; it is not unusual to find wines with 14.5% ABV
(average strength is about 12.5% ABV).
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R. K. Foster and H. E. Marriott
health, many of which are discussed in detail in section
8. It should be noted that these figures are guidelines,
not recommendations or targets. In 1992, the recommended maximum levels of alcohol consumption were
set at no more than 21 units (168 g) per week for men
and 14 units (112 g) for women (Department of Health
1992). However, following growing evidence that the
health implications of occasional sessions of heavy
drinking differed from the health implications of consuming the same amount of alcohol daily over the
course of a week, daily upper limits on alcohol intake
were formulated, in a bid to discourage heavy drinking
sessions (Department of Health 1995). A history of sensible drinking messages can be found in the 1995
Department of Health report, entitled: Sensible Drinking. The report of an inter-departmental working group.
The Prime Minister’s Strategy Unit (2004) has recognised that since the revised guidelines came into place in
1995, variations in the size and strength of alcoholic
drinks have been introduced, making the units unstandardised. For example, the average strength of wine is
now approximately 12.5%, whereas unit measures are
based on 9% strength. Typical pub measures have also
changed for some drinks; for example, a glass of wine is
now frequently served as a 175-ml measure. Therefore,
whereas a small 125-ml glass of 9% strength wine
would equate to one unit, wine served in today’s measures provides around two units. This report also investigated drinkers’ awareness of the alcohol guidelines.
Eighty per cent of drinkers surveyed had heard of the
term ‘alcohol units’, but only 25% understood the
meaning of ‘a unit’. Because of this poor understanding,
and the inconsistency between the strength and size of
alcoholic beverages, the government plans to reconsider
the presentation of sensible drinking guidelines to
develop a much clearer format, focusing on the types
and amounts of alcoholic drinks currently available
(Prime Minister’s Strategy Unit 2004).
who are pregnant, or trying to become pregnant, should
drink no more than 1–2 units of alcohol once or twice a
week and should avoid heavy drinking sessions (Department of Health 1995). It should also be noted that
chronic excessive consumption of alcohol has a detrimental effect on the absorption and utilisation of folate
(see section 6 for more information). Adequate folate
intakes are important before and during the first
12 weeks of pregnancy to protect the fetus against
neural tube defects. For more information on nutrition
before and during pregnancy, see Williamson (2006).
Alcohol intake and breastfeeding
Alcohol can pass to the baby in small amounts through
breastmilk. It is thought that less than 2% of maternal
alcohol intake is passed into the breastmilk, but it can
change the taste of the milk, which may influence the
baby’s acceptance and therefore short-term uptake of
breastmilk (Mennella 2004; Department of Health
2005). Current advice from the Department of Health
(2005) is that breastfeeding women should keep below
the daily limit of 2 to 3 units, and avoid drinking alcohol just before a feed.
People with diabetes
Precautions regarding alcohol intake that apply to the
general public are particularly important for people
with type 1 diabetes, in order to help manage blood glucose levels. Alcohol markedly suppresses gluconeogenesis and has a hypoglycaemic effect (Lieber 1994). For
those on insulin or sulphonylurea drugs, alcohol can
cause severe hypoglycaemia that can result in brain
damage or death. In order to manage blood glucose levels, people with type 1 diabetes are recommended to:
For some population groups, such as pregnant women
and people with diabetes, more stringent guidelines
about sensible drinking exist, some of which are outlined below.
• avoid over-consumption of alcohol (i.e. not exceed
safe drinking limits);
• choose ordinary types of lager rather than the higher
alcohol types;
• never drink on an empty stomach, and top up with a
snack if necessary;
• have a snack (such as cereal or toast) before going to
bed and check blood glucose concentrations to reduce the
risk of a hypoglycaemic event later on (Thomas 2001).
Guidelines for intake of alcohol during pre-pregnancy
3.2 Guidelines for sensible drinking around the world
Excessive intakes of alcohol have been shown to affect
reproduction in women, influencing the ability to conceive and the viability of conception (Goldberg 2002).
The Department of Health recommends that women
Guidelines for sensible drinking limits vary between
countries, and these have been outlined in table 3. Some
countries use more than one set of guidelines; for example, European wine-producing countries, such as France
Specific guidelines for population groups
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
National Health & Medical
Research Council
Federal Ministry for Labour,
Health & Social Affairs
Centre for Addiction & Mental
Health and Addictions
Research Foundation
Australia
Austria
Canada
Ministry for Agriculture &
Forestry and National
Institute for Food & Nutrition
Ministry of Education,
Psychological & Counseling
Services
Israel
National Academy of Medicine
Italy
Ministry of Health, Family &
Persons with Disability
France
Department of Health
Not to exceed 5 units/day
(60 g/day)
Oy Alko AB
Finland
Ireland
Not to exceed 20 g/day
National Board of Health
Denmark
Not to exceed 2–3 units/day
(24–36 g/day)
21 units/week (210 g/week)
Not to exceed 15 units/
week (165 g/week)
Not to exceed 21 units/
week (252 g/week)
National Institute of Public
Health
24 g/day
Not to exceed 2 units/day
(27.2 g/day) or 14 units/
week (190 g/week)
24 g/day
Not to exceed 4 units/day
(40 g/day) or 28 units/
week (280 g/week)
Men
Guidelines (grams of alcohol)
Czech
Republic
Health Canada – Sante Canada
Source
Country
Table 3 International drinking guidelines
Not to exceed 1–2 units/day
(12–24 g/day)
14 units/week (140 g/week)
Not to exceed 3 units/day
(36 g/day)
Not to exceed 20 g/day
Not to exceed 10 units/
week (110 g/week)
Not to exceed 14 units/
week (168 g/week)
16 g/day
Not to exceed 2 units/day
(27.2 g/day) or 9 units/
week (122 g/week)
16 g/day
Not to exceed 2 units/day
(20 g/day) or 14 units/
week (140 g/week)
Women
12 g
10 g
12 g
12 g/beer,
8 g/wine
11 g
12 g
13.6 g
20 g
10 g
Alcohol content
of standard drink
Recommend that pregnant women do not drink, students should not
drink more than one unit at a time and avoidance of alcohol if taking
medication.
Recommend that pregnant women should not drink and that people
should not drink and drive.
Recommend that children under the age of 15 should not drink.
Moderate drinking means no more than 1 drink a day and no more
than 7 drinks a week. More than 4 drinks on one occasion, or more
than 14 drinks a week, is a risk to health and safety. If you are
pregnant or breastfeeding, avoid alcohol.
Hazardous limit (unacceptable risk for health consequences) defined
as 60 and 40 g of alcohol per day (men and women, respectively).
Based on British ‘Sensible Drinking Guidelines’.
Guidelines recommend not drinking more than 1–2 drinks/h and
having 1–2 alcohol-free days/week. Lists special populations that
should not drink, including pregnant women and youths.
Additional comments
Alcohol consumption and our health
293
Sweden
Not to exceed 20 g/day
Not to exceed 4–5 units/day
(32–50 g/day)
Catalonia: Central Authority
Swedish Research Council
Not to exceed 70 g/day
Basque Country: Department
of Health & Social Security
Not to exceed 20 g/day
Not to exceed 4–5 units/day
(32–50 g/day)
Not to exceed 70 g/day
Not to exceed 3 units/day
(30 g/day)
Not to exceed 3 units/day
(30 g/day)
Ministry of Health and Spanish
Institute for the Investigation
of Beverage Alcohol
Spain
1–2 units/day (14–28 g/day)
1 unit/day (10 g/day) up to 5
times/week (not to
exceed 50 g/week)
Not to exceed 32.5 g beer/
day or 20.7 g wine/day
Ministry of Health
Romania
2–3 units/day (28–42 g/day)
2 units/day (20 g/day) up to
5 times/week (not to
exceed 100 g/week)
Not to exceed 2 units/day
(20 g/day) or 14 units/
week (140 g/week)
Not to exceed 32.5 g beer/
day or 20.7 g wine/day
National Council on Food and
Nutrition
Portugal
State Agency for Prevention of
Alcohol Related Problems
Allcokutt suggestions include: never drink on an empty stomach; show
respect to people who do not drink alcohol; women cannot
tolerate as much alcohol as men; adolescents should not drink.
Allcokutt
Poland
Recommend situational abstinence, such as when driving, during
pregnancy, at work or in the company of children and young people.
Directorate for Health & Social
Welfare
Norway
Not to exceed 3 units/day
(30 g/day) or 21 units/
week (210 g/week)
8–10 g
10 g
14 g (unofficial)
10 g
9.9 g
Recognise that a moderate alcohol intake may have certain positive
medical effects.
Wine officially considered as an integral part of a Mediterranean diet.
Based only on wine consumption.
Suggest two alcohol-free days/week (based on WHO
recommendations).
Should not exceed 6 units/day (60 g/day) for men, 4 units/day
(40 g/day) for women on one single occasion.
Advised not to drink on at least 2 days within a week and avoidance
of alcohol when pregnant, driving or operating machinery and if an
adolescent. Women with a low bodyweight are advised to drink less
than the recommended daily limit.
Alcohol Liquor Advisory
Council
Not to exceed 2 units/day
(19.8 g/day)
19.75 g
New
Zealand
Not to exceed 3 units/day
(29.7 g/day)
1–2 units/day (19.75–
39.5 g/day)
Stichting Verantwoord
Alcoholgebruik
Additional comments
The
Netherlands
Alcohol content
of standard drink
Ministry of Health, Labour &
Welfare
Women
Japan
Men
Source
Guidelines (grams of alcohol)
Country
Table 3 Continued
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R. K. Foster and H. E. Marriott
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
3–4 units/day (not to exceed
32 g/day)
Scottish Executive
Not to exceed 4 units/day
(56 g/day) or 14 units/
week (196 g/week)
Not to exceed 2 units/day
(28 g/day)
National Institute of Alcohol
Abuse and Alcoholism
American Heart Association
1–2 units/day (14–28 g/day),
not to exceed 14 units/
week (196 g/week)
Department of Agriculture and
Department of Health &
Human Services
Source: based on information from the ICAP (2004).
*See section 2 for information on sensible drinking guidelines.
United
States
3–4 units/day (24–32 g/day),
not to exceed 21 units/
week (168 g/week)
Department of Health
United
Kingdom
Not to exceed 2 units/day
(24 g/day)
Swiss Federal Commission for
Alcohol Problems and Swiss
Institute for the Prevention of
Alcohol & Drugs Problems
Switzerland
Men
Source
Country
Guidelines (grams of alcohol)
Not to exceed 3 units/day
(42 g/day) or 7 units/week
(98 g/week)
Not to exceed 1 unit/day
(14 g/day)
1 unit/day (14 g/day), not to
exceed 7 units/week
(98 g/week)
2–3 units/day (not to exceed
24 g/day)
2–3 units/day (16–24 g/day),
not to exceed 14 units/
week (112 g/week)
Not to exceed 2 units/day
(24 g/day)
Women
14 g
14 g
14 g
8g
8g
10–12 g
Alcohol content
of standard drink
Recognise that moderate drinking may lower the risk of coronary
heart disease among men over 45 and women over 55. Exceeding
moderate consumption can raise the risk for accidents, high blood
pressure, stroke, violence, suicide, birth defects and certain cancers.
A safe level of alcohol intake has not been established for women at
any time during pregnancy. Advise to avoid drinking before or when
driving, and to consume alcohol with food to slow absorption.
Women who are pregnant or who are trying to get pregnant should
drink no more than 1–2 units of alcohol per week. Recognises that
moderate drinking for men over 40 and post-menopausal women
confers health benefits, including lower risk of coronary heart
disease, ischaemic stroke and gallstones.
Uses ’Sensible Drinking Guidelines’* as part of national alcohol
strategy.
List exceptional drinking guidelines: not to exceed 4 units/event, not to
exceed 1 unit/h. No alcohol for youngsters; no alcohol during
sports; no alcohol while operating machinery or before driving.
Women have to be particularly cautious.
Additional comments
Alcohol consumption and our health
295
296
R. K. Foster and H. E. Marriott
and Spain, subcategorise the guidelines into different
drink types, i.e. beer and wine. Overall, most countries
have relatively similar recommendations when taking
into account the standard drink unit used, the most common recommendation being a limit of 24 g/day of alcohol for men and 20 g/day for women. The highest
recommendation originates from the Basque region of
Spain, where it is recommended not to exceed more than
70 g/day for men and women. The alcohol content of the
Japanese ‘standard drink’ (also referred to as a unit) is
the highest recorded, being over double the amount used
for a unit in the UK (19.75 g and 8 g, respectively). However, when comparing average consumption of alcohol
(litres of alcohol per adult per annum), it is evident that
Japan has a lower alcohol consumption than the UK (the
equivalent of 6 L of absolute alcohol consumption compared with an average of 9 L in the UK) (World Health
Organization 1999). One reason why the Japanese have
a lower alcohol intake could be the higher prevalence of
alcohol flushing responses, known to be particularly
prevalent in those of East Asian descent, due to a genetic
polymorphism. Symptoms, which include facial flushing, palpitations and drowsiness, are believed to discourage alcohol intake among those who suffer from the
condition (Vines 1999; Yokoyama et al. 2003).
Key points
• The standard drink unit in the UK equates to 8 g of
alcohol. Guidelines for sensible drinking set by the UK
government are 3–4 units (24–32 g) a day or less for
men, and 2–3 units (16–24 g) a day or less for women.
• Specific recommendations have been set for those
planning pregnancy and pregnant women, who should
drink no more than 1–2 units of alcohol once or twice a
week and should avoid heavy drinking sessions.
• Guidelines for sensible drinking are fairly similar
between other countries. When taking into account the
standard drink unit used to define guidelines, the most
commonly recommended limit is 24 g/day for men and
20 g/day for women.
4. Alcohol consumption
4.1 Current intakes in the UK
In the UK, average consumption of alcohol is assessed
(via self-reporting) from national surveys, including the
National Diet and Nutrition Survey (NDNS), the Health
Survey for England (HSE) and the General Household
Survey (GHS). The most recent NDNS revealed that,
over 7 days, 60% of men and 44% of women consumed
more than the recommended amount of alcohol on at
least one day of the week [i.e. men consumed more
than 4 units (32 g) and women more than 3 units (24 g),
per day] (Hoare et al. 2004). On average, men obtained
a significantly higher proportion of total energy from
alcohol than women (6.5% and 3.9%, respectively);
however, the median values were much lower, suggesting that a small proportion of respondents were deriving
a much larger percentage of energy from alcohol (Henderson et al. 2002). When interpreting the findings of surveys used to estimate alcohol intake, it is important to
recognise that under-reporting is a particular problem.
Other difficulties associated with measuring alcohol
intake are discussed in more detail in section 8 of the
briefing paper.
Official UK dietary surveys often subcategorise respondents’ intake of alcohol into the following categories:
• low: drinking less than 7 units (approximately 56 g)
for women and 10 units (80 g) for men in 1 week;
• moderate: drinking 8–14 units (64–112 g) for women
and 11–21 units (88–168 g) for men in 1 week;
• fairly high: drinking 15–25 units (120–200 g) for
women and 22–35 units (176–280 g) for men in 1 week;
• high: drinking 26–35 units (208–280 g) for women
and 36–50 units (288–400 g) for men in 1 week;
• very high: drinking more than 36 units (288 g) for
women and more than 51 units (408 g) for men in
1 week;
• binge drinking: exceeding twice the advised daily
limits on one single occasion.
It is these definitions that are used throughout this
section.
Data from the GHS (ONS 2001) estimate that:
• half the adult UK population (26.3 million) are low to
moderate drinkers;
• 6.4 million adults are fairly high to high drinkers;
• 1.8 million adults are very high drinkers.
Overlapping these categories are binge drinkers, who
drink more than twice the daily guidelines on a single
occasion (Strategy Unit 2003). According to the most
recent GHS, 22% of men and 9% of women drink more
than double the recommended alcohol intake on at least
one day of the week (ONS 2006a). These figures are substantially lower than those from other surveys, thus
emphasising the difficulty in collecting accurate information in this area. For example, reports of binge drinking from the NDNS identified that 39% of men and 22%
of women exceed the daily guidelines by more than double on at least one day of the week (Hoare et al. 2004).
The 2004 HSE found that a larger percentage of younger
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
Alcohol consumption and our health
men had a binge drinking occasion in the week before the
survey; for example, 39% of men aged 16–24 years,
compared with 13% of those aged 35–44 years, could be
classified as binge drinkers (Department of Health
2006a). The same trend was evident among women, with
27% of 16–24-year-olds compared with 15% of those
aged 35–44 years having had a binge drinking occasion
during the week before the survey (Department of Health
2006a). The survey found that respondents in the older
age groups tended to binge drink less but, in contrast,
drank on a more frequent basis; for example, 52% of
men and 32% of women aged 55–64 years consumed
alcoholic beverages on three or more days a week compared with 29% of men and 14% of women in the age
group of 16–24 years (Department of Health 2003).
Regional variations
Few regional variations in drinking habits have been
identified from the dietary surveys, although the NDNS
found that people living in northern regions were more
likely than those in the south-east and London to consume alcohol (83% and 71%, respectively) (Henderson
et al. 2002). Similar trends were found in the GHS: Scotland is the most likely area in which heavy drinking
occurs on at least one day of the week, compared with
England or Wales (Walker et al. 2002). Evans et al.
(2000) propose that the effects of heavy drinking at
weekends have been reflected in trends in coronary heart
disease (CHD)-related mortality, with deaths being
more common on Mondays in Scotland. The associations between alcohol intake and risk of disease are considered in more detail in section 8.
Economic variations
Percent age
Dietary surveys have generally found that higher-income
households are likely to consume more alcohol and consume alcohol more frequently. For example:
Figure 1 Alcohol consumption (units per week)
among women aged 16–24 years, 1993−2002.
Source: Department of Health (2006a).
• the GHS estimated that respondents with a gross
weekly income of more than £1000 were almost twice
as likely to exceed the daily limits on at least one day per
week than those with a gross weekly income of £200 or
less (Walker et al. 2002);
• the latest NDNS found that men and women in
receipt of benefits were significantly less likely than
those in non-benefit households to have recorded consuming alcohol during the survey week (59% of men
and 55% of women compared with 84% of men and
71% of women, respectively) (Henderson et al. 2002).
Ethnicity
The HSE (Department of Health 2006c) found that all
minority ethnic groups (black Caribbean, Indian, Pakistani, Bangladeshi and Chinese) consumed less alcohol
than the general population, with the exception of the
Irish, who drank more frequently and were more likely
to drink more than the guidelines. Among ethnic minority groups, Pakistani and Bangladeshi groups most commonly reported not consuming alcohol in the last
12 months, or being a non-drinker, and this was more
commonly reported in women than men.
4.2 Recent trends in alcohol intake in the UK
In the past 10 years, surveys have continued to show an
increase in alcohol consumption, particularly among
certain subgroups of the population. For example, in
young women (aged 16–24 years), the prevalence of
fairly high alcohol intakes has increased significantly,
from 9% of women drinking more than 21 units per
week in 1993 to 21% in 2002 (as figure 1 indicates),
with fewer women drinking lower quantities (Department of Health 2003).
Among all women, the average number of units consumed per week has increased by just over 1 unit since
1993, and in 2002, the majority of women were con-
45
40
35
30
25
20
15
10
5
0
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
297
Estimated
units per
week
<1
1–7
7–14
14–21
1993
1994
1995
1996
1997
1998
Year
1999
2000
2001
2002
>21
R. K. Foster and H. E. Marriott
298
35
% of c onsum ers
30
16–24
25
25–34
35–44
20
45–54
15
55–64
65–74
10
75 and over
5
0
1993
1994
1995
1996
1997
1998
1999
2000
2001
Year
suming 1–7 units per week. Among men, the intake of
alcohol has also remained steady in the past 10 years,
with the average alcohol intake increasing by less than 1
unit. There has been a slight increase in the percentage
of men consuming more than the weekly guideline maximum alcohol intake, in all age groups (as figure 2 indicates). However, it should be noted that the largest
increase has been among the youngest age group (16–
24 years). It is not possible to confirm that the trends
among young women and men are due to binge drinking
alone, owing to the way the data are collected over a
period of time and averaged out, rather than being dayspecific. However, high alcohol consumption over the
week, or on one day, is associated with adverse health
consequences as outlined in section 8, and therefore this
is a worrying trend.
The proportion of people aged 16 years or below consuming alcohol is also a concern; the Office for National
Statistic (ONS 2006a) reported that 23% of boys and
girls aged 11–15 years drank alcohol during any week.
The survey also reports that the quantity of alcohol
being consumed is increasing; for example, in 1990
young drinkers (aged 11–15) were consuming on average of 5.3 units per week, but in 2004 this had increased
to 10.4 units per week (ONS 2006a). In each year,
among those who drank, boys consumed more than
girls, although recently the greatest increase has been
among girls aged 14 years. The types of alcohol
consumed by underage drinkers varies depending on a
number of factors, including experience of drinking.
Research by McKeganey et al. (1997) and by Alcohol
Concern (2001) suggests that alco-pops may ‘introduce’
alcohol to under 18 year olds who then go on to consume stronger alcoholic beverages (McKeganey 1998).
Despite these worrying trends, studies suggest that
drinking at a young age does not necessarily reflect
drinking patterns in adult life (Strategy Unit 2003).
However, the effects of alcohol consumption are wide
ranging, impacting on society, as well as on individuals’
2002a
Figure 2 Percentage of men consuming more
than 28 units per week, by age group, 1993−2002.
Source: Department of Health (2006b).
health as outlined in section 8, and the potential implications of drinking at such a young age should not be
overlooked.
4.3 Trends around the world
Overall, Europe has the highest alcohol consumption
worldwide, with rates increasing year on year, which is
mainly associated with the increased alcohol consumption among the younger European population (Health
Promotion Agency 2001). When comparing per capita
alcohol intake in the UK with other European countries,
it is evident that the UK has an annual per capita intake
close to the European average (fig. 3). However, if consumption continues to rise among the younger population at its current rate, the UK population could be the
highest consumers on a per capita basis within the next
10 years (Strategy Unit 2003).
In the past, wine-producing countries have tended to
have the highest per capita alcohol intake, although this
is now stabilising compared with non-wine-producing
countries, presumably due to increased accessibility and
lower costs. People from countries in the Mediterranean
region tend to drink more wine-based beverages, in
comparison with those from countries in the north of
Europe, that tend to drink more beer-based alcoholic
drinks (Health Promotion Agency 2001; Sieri et al.
2002; Strategy Unit 2003). It has been suggested that
this may be one of the reasons that CHD is less common
in these areas, a phenomenon referred to as the ‘French
paradox’, which is discussed in more detail in section 8.
As figure 3 indicates, Turkey and Israel have considerably lower intakes than any other European country,
which could be due to religious and cultural practices
that prohibit alcohol (Neumark et al. 2001). The highest per capita consumption is recorded for Luxembourg,
but it is accepted that a significant proportion of alcohol
bought in Luxembourg is for consumption by visitors
from outside the country (Rehm et al. 2001). The meth-
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
Alcohol consumption and our health
299
Figure 3 Alcohol consumption by country, adults aged 15 years and above, 2002, Europe. Reproduced with kind permission of the British Heart Foundation
(BHF) (2006).
odology used to collect the data and variations between
countries in the way the data are presented are also
likely to account for at least some of the apparent differences in alcohol consumption.
Key points
• On average, men obtain a significantly higher proportion of total energy from alcohol than women.
• Half of the adult UK population are low to moderate
drinkers. Despite high and very high drinkers being a
minority, evidence from the GHS suggests that this figure is growing.
• In the UK, some variations in drinking habits between
subgroups of the population have been identified by the
NDNS, for example:
people living in northern regions of England are
more likely than those in the south-east and London
to consume alcohol;
higher-income households are more likely to consume large quantities of alcohol and consume alcohol more frequently;
compared to other ethnicities, the Irish drink the
most alcohol; all other minority ethnic groups
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
consume less alcohol than the average for the
general population.
• It has become recognised that binge drinking is a
common phenomenon in the UK, particularly among
younger people. The NDNS found that 39% of men
and 22% of women exceed the daily guidelines by more
than double on at least one day of the week.
• Data from the HSE indicate that the percentage of
men and women who binge drink decreases with
increasing age, but in contrast, older people drink on a
more frequent basis.
• The proportion of people aged 16 years or below consuming alcohol is also rising.
• The UK has an average per capita alcohol intake close
to that of the European average.
• Overall, Europe has the highest alcohol consumption
worldwide, with rates increasing year on year.
5. Absorption and metabolism of alcohol
5.1 Absorption of alcohol
Alcohol is a water-soluble molecule. It is absorbed
throughout the entire gastrointestinal tract, and this is
300
R. K. Foster and H. E. Marriott
mainly controlled by gastric emptying. Once absorbed, it
circulates in the blood and is distributed through the
water in the body by the process of diffusion. Alcohol will
diffuse more rapidly into organs with a rich blood supply,
such as the lungs, but little alcohol enters body fat, owing
to its poor solubility in fat. Exposure to alcohol is greatest
in the liver, as blood is received directly from the stomach
and small bowel via the hepatic portal vein (Paton 2005).
Factors affecting absorption of alcohol and blood
alcohol concentrations
Absorption of alcohol is quickest when drinks containing alcohol are drunk on an empty stomach. The type of
alcoholic beverage will also affect the rate of absorption;
drinks with a concentration of alcohol of 20–30% ABV
are most rapidly absorbed (e.g. fortified wines). Aerated
drinks are also recognised to get into the system more
quickly, owing to easy absorption (Paton 2005). The
amount of alcohol that has been absorbed can be measured by the blood alcohol concentration. The rate of
absorption will vary between individuals and, therefore,
after two individuals have drunk the same amount and
type of any one drink, they may have different blood
alcohol concentrations. This will be due to a number of
factors, such as the speed at which the drink was consumed and whether food was eaten while drinking, as
this may interfere with the absorption from the stomach
and affect the rate of gastric emptying. Some drugs are
also known to inhibit or enhance the rate of gastric emptying, thus slowing down or increasing the rate of
absorption, and subsequently affect the concentration of
alcohol in the blood. Gender and body size are also recognised to be important determinants of the rate at
which alcohol is absorbed. For example, an average
woman drinking the same amount as an average man of
the same size will become intoxicated more quickly,
because she has a higher percentage of body fat. As alcohol is poorly soluble in fat and women have a lower percentage of lean tissue, there is consequently a higher
concentration of alcohol found in the lean tissue. Moreover, as women tend to be of smaller stature, they will
also have a smaller volume of blood, resulting in a higher
concentration of alcohol in the blood (Paton 2005).
5.2 Alcohol metabolism
Once absorbed, alcohol must be metabolised immediately, for two reasons. First, the body has no capacity to
store alcohol, in contrast to the other energy-yielding
macronutrients (protein, fat and carbohydrate), and
second, alcohol has toxic properties. The liver is the
principal site of alcohol metabolism, but some alcohol is
also immediately metabolised in the stomach by alcohol
dehydrogenase (the enzyme responsible for breaking
down alcohol), found in the gastric mucosa (James &
Ralph 2000). Some alcohol (2–5%) is excreted
unchanged in the urine, sweat or breath.
In a healthy person, the majority of alcohol consumed
is metabolised, and therefore removed from the blood at
a constant rate; on average, about 6 g per hour (James &
Ralph 2000). However, the rate at which alcohol is
metabolised varies considerably between individuals and
is affected by a number of factors, including drug intake,
frequency (and usual quantity) of alcohol consumption,
age, bodyweight and liver size, and some differences may
be genetic (Truswell 1998). Gender has also been found
to be associated with the speed at which alcohol is
metabolised. Women have less alcohol dehydrogenase
activity in the gastric mucosa, and so they metabolise
alcohol more slowly and have a steeper rise in blood
alcohol concentration when drinking. It has also been
suggested that the microsomal ethanol-oxidising system
(MEOS) pathway (another mechanism of breaking alcohol down, see below) operates more slowly in women
(Frezza et al. 1990).
Metabolic pathways of ethanol utilisation
Most of the absorbed alcohol (C2H5OH) is oxidised to
acetaldehyde (CH3CHO). Three separate enzymes or
enzyme systems have been identified to catalyse this
reaction, as outlined in figure 4 (and explained in more
detail below). Although quantitative data on their
respective roles are difficult to obtain, it is thought that
the different systems are involved in different ways in
the metabolism of alcohol.
The principal route of alcohol metabolism is via the
Nicotinamide adenine dinucleotide (NAD)-linked
enzyme alcohol dehydrogenase (ADH), which is in the
cytoplasm of liver cells and in the gastric mucosa and
which catalyses the reaction:
C2H5OH + NAD+ → CH3CHO + NADH + H+
Low levels of alcohol are metabolised to acetaldehyde
by ADH. The hepatic MEOS is induced in the liver and
other tissues by repeated ingestion of alcohol and, as a
result, alcoholics are thought to have an induced MEOS,
whereas for the general population, the role of this system in ethanol metabolism is small. This system alters
the energy coupling of alcohol oxidation to oxidative
phosphorylation and heat is generated. The MEOS
requires the co-enzyme NADPH and oxygen to catalyse
the reaction as shown:
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
Alcohol consumption and our health
301
Cytoplasm
NAD
1.
NADH
C2H5OH
CH3CHO
Ethanol
Alcohol dehydrogenase
Acetaldehyde
Endoplasmic reticulum
NADPH
NADP
Acetate
2.
Ethanol
Acetaldehyde
MEOS
Peroxisomes
H2O2
Figure 4 The three main pathways of alcohol
metabolism. Adapted from: James and Ralph
(2000).
3.
H2O
Ethanol
C2H5OH + NADPH + H+ + 2O2 → CH3CHO +
2H2O2 + NADP+
This reaction also involves a cytochrome similar or
identical to cytochrome P450, which is also involved in
other inactivation or detoxification reactions, including
those linked with some drugs. Ethanol can, therefore,
compete with drugs for this enzyme, which may be why
alcohol ingestion can increase the circulating concentration of many drugs and why for many drugs alcohol is
contra-indicated.
The third pathway that is thought to exist is an indirect one. This pathway is not thought to play a major
role in alcohol metabolism, but it may be used under
certain physiological conditions. Catalase, in addition
to catalysing the breakdown of hydrogen peroxide
(H2O2), can also catalyse the oxidation of alcohols,
including ethanol, as the chemical formula shows:
C2H5OH + H2O2 → CH3CHO + 2H2O
Oxidation of acetaldehyde to acetate (CH3COO–)
Acetaldehyde is the product of all three systems outlined
above; it is toxic (more so than alcohol) and has to be
metabolised further to acetate. This reaction is catalysed
by the enzyme acetaldehyde dehydrogenase (ALDH),
and can be represented as:
Acetaldehyde
Catalase
oxidised via the tricarboxylic acid cycle (TCA cycle)
(Krebs cycle). This process provides most of the
adenosine triphosphate (ATP) that results from ethanol
oxidation.
Generation of energy
Finally, there are biochemical reactions in the liver
which are involved in the regeneration of co-enzymes
required for efficient ethanol metabolism. Most of the
NADH is reoxidised to NAD+ by the mitochondrial
electron transfer chain, which ultimately results in the
production of more energy. NADP+ is reduced by the
pentose phosphate pathway, thus alcohol-derived
energy is merely a by-product of alcohol detoxification.
Whether these detoxification mechanisms simply dissipate the energy provided by alcohol, or whether the
energy in alcohol is incorporated into the energy budget
in the same way as protein, fat and carbohydrate, has
been the subject of some considerable debate. One theory has suggested that the energy produced as a result of
alcohol detoxification is wasted as heat, rather than
used for biochemical work, a so-called ‘futile cycle’
(Lieber 1991a). However, as discussed in section 8, evidence indicates no significant wastage of energy when
alcohol is metabolised via the principal route.
CH3CHO + NAD+ + H2O → CH3COO– + NADH
+ 2H+
Genetic differences in alcohol and acetaldehyde metabolism, alcohol sensitivity and alcoholism
A large proportion of acetate is rapidly converted in
other tissues to non-toxic acetyl co-enzyme A (acetyl
CoA) by the enzyme acetyl-CoA synthetase, then further
In the past few years, several studies have been published about the polymorphisms of the genes that code
for enzymes responsible for the breakdown of acetalde-
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
302
R. K. Foster and H. E. Marriott
hyde – the alcohol dehydrogenase family (see Couzigou
1999). In humans, there are at least four or five isoenzyme classes of ALDH, of which ALDH2 is one. Individuals homozygous for the ALDH2*2 allele have no
ALDH2 activity. This results in an elevated level of acetaldehyde after alcohol consumption, which causes
unpleasant side effects, such as facial flushing and
headaches. A high percentage of individuals of Asian
origin (e.g. up to 50% of Japanese and Chinese people)
are recognised to have a mutation of the acetaldehyde
dehydrogenase ALDH2 gene, and alcoholism has been
found to be lower among these individuals, perhaps
because they avoid alcohol consumption (Truswell
1998). It has been hypothesised that this is also the reason for lower intake of alcohol among this subgroup of
the population, which was illustrated in section 4.
there are three potential pathways in the first stage
of alcohol metabolism, in which alcohol is oxidised
to acetaldehyde. The most commonly used route is
via the NAD-linked enzyme ADH;
acetaldehyde is more toxic than alcohol, and therefore is oxidised quickly to acetate via the enzyme
ALDH;
acetyl CoA synthetase converts a large proportion
of acetate to acetyl CoA, where it is further oxidised
to provide energy, via the Krebs cycle.
• Due to a genetic polymorphism, some individuals are
unable to oxidise acetaldehyde efficiently. Therefore,
when they consume alcohol, they are exposed to high
levels of acetaldehyde, which causes unpleasant side
effects, such as headaches and facial flushing. This is a
particular problem among the Asian population.
Key points
6. Alcohol and nutrition
• The rate at which alcohol is absorbed from the digestive tract varies between individuals, as it is dependent
on many factors, such as gender, body size, the speed at
which the drink was consumed or whether food was
eaten while drinking.
• Once absorbed, alcohol must be detoxified and
metabolised immediately, as it has toxic properties. The
liver is the principal site of alcohol metabolism.
• The rate at which alcohol is metabolised also varies
considerably between individuals. On average, it is
metabolised at a rate of about 6 g per hour (a little less
than one unit/hour), but this depends on a number of
factors, e.g. gender, frequency of alcohol consumption,
age and stature.
• Alcohol is metabolised in three stages:
6.1 Nutrient composition of alcoholic beverages
Alcohol is the second highest source of energy, on a per
gram basis, of all the macronutrients, providing 29 kJ/g
(7 kcal/g). As table 4 indicates, most alcoholic beverages
contain only small amounts of nutrients – primarily carbohydrate and very small amounts of protein. Beers also
contain small amounts of some micronutrients, primarily
B vitamins and some minerals, and wines contain several
trace elements, including iron, potassium, copper and
sodium. As with beer, the quantity of vitamins, minerals
and trace elements in wine varies considerably and
depends on a number of factors, including the raw ingredients and production method. For example, in wine the
micronutrient content will be affected by the type of
Table 4 Nutrient content of specific alcoholic beverages, per 100 ml
Bitter
Lager
Guinness
Cider
Red wine
White wine
Port
Spirits (37.5% ABV)
Alco-pops
Cream liqueurs
Alcohol (g)
Carbohydrate (g)
Energy (kcal)
Protein (g)
Vitamins/minerals per 100 ml
2.9
4.0
3.3
3.8
9.6
8.9
15.9
29.6
3.2
13.5
2.2
Tr
1.5
2.6
0.2
3.0
12.0
Tr
3.6
22.8
30
29
30
36
68
74
157
207
37.9
325
0.3
0.3
0.4
Tr
0.1
0.1
0.1
Tr
0
Tr
Small amounts of B vitamins and minerals
Small amounts of B vitamins
Small amounts of B vitamins and 0.2 g of iron
Small amount of some minerals
Small amount of some minerals and B vitamins (riboflavin and B6)
Small amount of some minerals and B vitamins (riboflavin and B6)
Small amount of some minerals
Variable
Information not available
Contains 16.1 g of fat from the cream, which also contributes some
fat-soluble vitamins and small amounts of minerals
Source: Chan et al. (1994); personal correspondance.
ABV, alcohol by volume; Tr, trace.
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
Alcohol consumption and our health
grape and its harvest time, production method, additives
to the wine (e.g. vitamin C is added to some wine to stabilise it), storage, and yeast variety used in the fermentation process (yeast contains high levels of some B
vitamins). As shown in table 4, liqueurs may also contain
protein and fat owing to the addition of egg or cream.
Values for alcoholic beverages given in food tables are
expressed per 100 ml, rather than the usual method of
per 100 g. This is because alcoholic beverages are normally measured by volume (see section 2). To determine
nutrient composition per 100 g, values should be divided
by specific gravity. The precise specific gravity varies
according to the composition of the drink, and generally
increases with the amount of solids (mainly sugars) and
decreases with the amount of alcohol. For example, the
specific gravity of 40% volume spirits is 0.95, that of
medium white wine is about 1.005, and that of draught
bitter is about 1.004. For comparison, the specific gravities of ethanol and water are 0.79 and 1.00, respectively.
For more information, see Chan et al. (1994).
6.2 The effect of alcohol on energy intake
As well as being a source of energy, it has been suggested
that consuming alcohol may affect an individual’s food
intake, thereby having an indirect, as well as direct,
effect on overall energy consumption. The effects of
alcohol on food intake have been investigated in two
ways. First, laboratory-based studies have been used to
measure physiological indicators associated with food
intake, such as appetite, hunger or satiation, following
various pre-loads and test meals. Second, observational
studies of free-living people have considered trends in
energy intake according to levels of alcohol consumption. Overall, these studies have demonstrated that
energy derived from alcohol is additive to the individual’s normal diet, i.e. individuals are unlikely to reduce
their food intake to compensate for the energy from
alcohol during the day (Westerterp et al. 1999). Interestingly, reports of small laboratory studies (Foltin et al.
1993; Westerterp-Plantenga & Verwegen 1999) have
indicated that alcohol can have an aperitif effect (i.e. act
as an appetite stimulant), resulting in a greater overall
intake of energy from a test meal after consumption of
alcohol. The duration of this effect has been found to
vary, along with the extent to which it affects subsequent food intake (i.e. amount of food consumed) (Yeoman 2004). The mechanism by which alcohol stimulates
appetite is not yet known; however, as alcohol intake
affects many neurotransmitters, hormonal and other
afferent signals (such as leptin, a hormone involved in
appetite regulation), changes to any one or all of these
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303
could affect food intake (Yeoman et al. 2003). Yeoman
(2004) also reported that the disinhibition of restrained
eating or decreased satiation from foods may be another
possible mechanism for the short-term stimulation of
appetite following an alcoholic beverage.
6.3 Nutritional implications of chronic excessive
alcohol consumption
Chronic excessive consumption of alcohol is well recognised to affect an individual’s nutritional status and is
well documented to be associated with nutrient deficiencies and malnutrition. It is believed that this is for two
reasons: first, alcoholics are recognised to have a poor
diet, perhaps due to a disturbance in normal eating
behaviour resulting from a disruption to ‘normal life’,
which may result in primary malnutrition (Santolaria &
González-Reimers 2004); and second, when consumed in
large quantities, alcohol interferes with the digestion,
absorption, metabolism and utilisation of some nutrients
(Lieber 2000; Santolaria & González-Reimers 2004).
This malabsorption of nutrients from the diet may result
in secondary malnutrition, as figure 5 illustrates.
Poor utilisation of nutrients because of inefficient
metabolism or retention may also be a consequence of
alcohol-related diseases, such as chronic pancreatitis and
liver disease. Although it was once thought that diseases
of alcoholics, such as liver cirrhosis, were the result of
poor nutrition alone, it is now recognised that poor nutrition is usually an effect, rather than the cause (James &
Ralph 2000; Santolaria & González-Reimers 2004).
Deficiencies of particular nutrients, such as thiamin
and folate, are well recognised among chronic excessive
consumers of alcohol. For example, thiamin deficiency
due to excessive alcohol intake is referred to as
Wernicke–Korsakoff syndrome and is characterised by
Direct Toxicity
Stomach
and
Intestine
Alcohol
Liver
‘Empty Calories’
- Impaired
Utilisation
of Nutrients
- Increased
Degradation
of Nutrients
Malnutrition
Maldigestion
Malabsorption
Functional Impairment
Figure 5 The process of secondary malnutrition due to alcohol-related
malabsorption common amongst chronic excessive alcohol drinkers. Source:
Lieber (1991b).
304
R. K. Foster and H. E. Marriott
mental confusion and short-term memory loss (James &
Ralph 2000). A more severe form, Wernicke’s encephalopathy, starts suddenly and features areas of bleeding in
the brain, resulting in states of confusion, loss of bodily
co-ordination and abnormal eye movements (Youngson
2001). A large amount of information outlining the
implications of chronic excessive alcohol intake on
nutritional status exists. However, a detailed overview of
this is beyond the scope of this report, which focuses primarily on the implications of moderate alcohol intake.
The nutritional implications of moderate
alcohol consumption
Few studies have been undertaken to assess the impact
of moderate alcohol intake on nutritional status, and
there is a lack of consistency in the results of those studies that have taken place (Jacques et al. 1989; Guillard
et al. 1994; Lecomte et al. 1994; Walmsley et al. 1998).
Three possible scenarios, or a combination of all of
them, should be considered when exploring the nutritional implications of low/moderate alcohol intake:
• Moderate alcohol consumption may increase intakes
of some nutrients, either because of the contribution of
nutrients found in alcohol (such as B vitamins in beer),
or because of interactions between alcohol and nutrients. For example, Walmsley et al. (1998) report higher
intakes of B vitamins with increasing alcohol consumption, which was partially explained by the high content
of certain B vitamins in beer;
• Even at low intakes, alcohol may adversely affect the
digestion, absorption, metabolism or utilisation of nutrients, which could have adverse consequences on nutritional status when alcohol is consumed on a regular
basis. It is well recognised that chronic excessive alcohol
exposure impairs folate absorption, for example by
inhibiting expression of the reduced folate carrier and
decreasing the hepatic uptake and renal conservation of
circulating folate (and subsequent excretion in urine),
although it is less clear to what extent moderate alcohol
intake affects folate absorption (Halsted et al. 2002;
Mason & Choi 2005). A study by Laufer et al. (2004)
demonstrated that moderate alcohol intake may have
adverse effects on vitamin B12 status, which has been
attributed to intestinal malabsorption and altered binding of intrinsic factor (Shaw et al. 1990). Previous studies in this area have found inconsistent results, which
Laufer et al. (2004) attributed to methodological weaknesses (Jacques et al. 1989; Van der Gaag et al. 2000);
• Substituting food with drink, which in turn reduces
nutrient intake, is a common problem among alcoholics.
However, conclusions from a number of studies to date
have found that alcohol does not habitually substitute
food intake among light to moderate alcohol consumers,
and therefore nutrient loss should not be expected from
reduced food intakes (Colditz et al. 1991; Veenstra et al.
1993; Männistö et al. 1996; Walmsley et al. 1998).
The variation in results of studies that have looked at
nutrient status and moderate alcohol intake may be
because the likelihood of any of these scenarios occurring will vary depending on a number of factors, including: the nutrient in question; an individual’s habitual
intake of the nutrient; the quantity of alcohol consumed
and over what period of time; and the nutrient status of
the individual (van den Berg et al. 2002). So many confounding factors make it particularly difficult to disentangle relationships between moderate alcohol intake
and nutritional status for any one nutrient.
The nutritional implications of binge drinking
There is little published information available about the
implications of binge drinking on nutritional status.
Due to the potential complications of carrying out studies in this area, it is difficult to know the true effects of
binge drinking on our diet and nutrient status. Taking
account of common drinking behaviours, there are perhaps a number of factors that will affect the nutrient
intake of binge drinkers, and for regular binge drinkers,
this may lead to a compromised nutrient status. For
example, it is common among individuals who go out to
drink in order to get drunk (i.e. binge drink) to avoid
eating before going out (in order to get drunk more
quickly) and forget to eat after the evening out. Excessive alcohol intake over a short period of time may also
lead to adverse gastrointestinal conditions, such as vomiting or diarrhoea, following the drinking episode,
which may reduce the absorption of nutrients. This may
be the result of fluid overload, as alcohol passes rapidly
into the colon, or the effect of microorganisms inducing
an acetaldehyde-stimulated colonic response. The
metabolism of nutrients may also be affected by the
large quantities of alcohol consumed. Bearing in mind
these possible implications of binge drinking, infrequent
binge drinking is unlikely to have any long-term consequences on nutrient status. However, regular binge
drinking may have a more negative impact.
6.4 Other components of alcoholic beverages
Phenolic and polyphenolic compounds
Some beverages contain plant-derived bioactive phenolic compounds such as flavonoids. Plants produce
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Alcohol consumption and our health
thousands of phenolic and polyphenolic compounds as
secondary metabolites. These bioactive compounds are
essential to the plant’s physiology, being involved in
diverse functions, such as structure, pigmentation, pollination, pathogen and predator resistance, and growth
and development. These phenolic and polyphenolic
compounds have a diverse range of effects in vitro that
are suggestive of a putative role in the prevention of
chronic diseases, such as cardiovascular disease (CVD)
and cancer. However, their precise role remains largely
unclear, and research has been made more difficult by
the fact that absorption of the parent compounds is generally low and it has been necessary to study the fate following absorption of a diverse range of metabolites.
Many of these polyphenols can be found in alcoholic
beverages. For example, red wines, and to a much lesser
extent, white wines, are a rich source of a variety of phenolic and polyphenolic compounds. In the making of
red wine, with prolonged extraction, the fermented
‘must’ may contain up to 40% of the phenolics originally present in the grapes. The production of white
wine results in either low levels or an absence of skinand seed-derived phenolics, so the overall level of phenolics is much lower than that found in many red wines.
The range of concentrations also differs according to the
geographical origin of the grapes.
Whiskies also contain complex mixtures of phenolic
compounds. These include quercetin, vanillin, and
ellagic, gallic and syringic acids, which are extracted
from the wooden casks during maturation (Duthie &
Crozier 2003). The phenolic profile depends on how
long the spirit has been matured, the species of oak from
which the casks are made, the pre-treatment of the cask,
e.g. charring the wood, prior use of the cask for bourbon or sherry storage, and the number of times the cask
has previously been used for maturation. Phenolics may
also arise from derivatives of malt and from peat smoke,
and from the breakdown of wood lignin during cask
charring and whisky maturation. In in vitro studies, the
presence of phenolics conveys considerable anti-oxidant
activity to whiskies. However, there appear to be few
epidemiological studies that have attempted to relate
whisky consumption per se to the incidence of heart disease and cancer, and as noted in section 8, the type of
drink consumed may be predictive of lifestyle factors,
which can cause problems with confounding in epidemiological studies.
Beer contains a range of phenolic and polyphenolic
compounds which come from the barley and hops used
in beer production. Total phenolic concentrations are
comparable to those found in white wine and may
approach levels found in phenolic-rich red wines
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305
(Duthie & Crozier 2003). Consequently, beer exhibits
considerable antioxidant activity in model systems, and
the phenolics and/or their metabolites appear to be
readily absorbed, resulting in increases in antioxidant
capacity of plasma after consumption (Fantozzi et al.
1998; Bourne et al. 2000; Ghiselli et al. 2000). However, relevance of this to health still remains unclear
(Duthie & Crozier 2003).
Congeners
Alcoholic fermentation (i.e. the fermentation of fruits
and grains to produce alcohol) produces about 95%
alcohol and 5% fusel oil, a mixture of organic acids,
higher alcohols (propyl, butyl and amyl), aldehydes and
esters. These bioactive compounds are known collectively as congeners and distil over with the alcohol. On
maturation of the liquor, fusel oil changes and imparts
the special flavour to the spirit, and therefore it is understood that congeners contribute to the taste, smell and
appearance of alcoholic beverages (Swift & Davidson
1998). Many of the symptoms of a hangover (see section
10) are attributed to congeners in alcoholic beverages,
and therefore they may have some short-term effects on
health (Bender & Bender 2000; Wiese et al. 2000).
Key points
• Once absorbed and metabolised, alcohol contributes
to an individual’s energy balance, providing 7 kcal per
gram.
• Most alcoholic beverages contain alcohol, carbohydrate and only small amounts of protein, some vitamins,
trace elements or minerals.
• Overall, studies have demonstrated that energy
derived from alcohol is additive to the individual’s normal diet, and individuals are unlikely to compensate for
energy from alcohol during the day. The aperitif effect
of alcohol may also encourage an increase in energy
intake.
• Chronic excessive alcohol intake is well recognised to
affect an individual’s nutrient status; because it reduces
food intake, and/or as a result of alcohol interfering
with the digestion, absorption, metabolism and utilisation of some nutrients. Deficiencies of some nutrients,
such as thiamin and folate, are more common among
alcoholics, because these nutrients are particularly sensitive to the effects of alcohol.
• Any association that exists between moderate alcohol
consumption and nutrient absorption and metabolism,
is likely to be dependant on a number of factors, including: the nutrient in question; habitual intake of the
R. K. Foster and H. E. Marriott
306
nutrient and the nutrient status of the individual; and
the quantity of alcohol consumed over a period of time.
• Overall, when consumed in moderation, alcohol is
unlikely to interfere with the metabolism of nutrients, or
be associated with impaired vitamin function or depletion, to an extent that may harm health, provided that
dietary intakes are adequate.
• Little information exists about the implications of
binge drinking on nutrient status; but it may alter food
intake, and excessive alcohol consumption can cause
disturbances to the digestive system. Although infrequent binge drinking is unlikely to have any long-term
nutritional implications, regular binge drinking may
have a more negative impact.
• Wine, beer and whiskies all contain a range of phenolic and polyphenolic compounds in varying quantities. These bioactive compounds have potential healthpromoting attributes, but their precise roles remain
largely unclear.
7. The burden of disease and mortality
related to alcohol
Age-standardised rate per 100 000 population
The number of alcohol-related deaths in England and
Wales has been rising since the 1980s, with a more substantial increase in recent years, as figure 6 indicates.
Alcohol-related deaths are more common among men
than among women; for example, in 2004 the male
death rate was 17.7 per 100 000 population, compared
with the rate for women of 8.5 deaths per 100 000 population (Office for National Statistics 2006b). The proportion of deaths related to alcohol and the most
20
18
16
14
12
10
8
6
4
2
0
2004
2003
2002
2001
2000
1999
1998
1997
1996
1995
1994
1993
1992
1991
Men
Women
Figure 6 Alcohol-related death rates across England and Wales, 1991−
2004. Source: ONS (2006b).
common causes of alcohol-related death vary by age.
For example, among the young, road traffic accidents,
suicide and alcoholic liver disease are more common
causes of alcohol-related death (Britton & McPherson
2001). A number of published papers have tried to
establish the relationship between alcohol consumption
and risk of death. For example, using data from the
Whitehall cohort following more than 10 000 civil servants for 11 years, a ‘U’ shaped relationship between
alcohol intake and mortality was reported. Non-drinkers and those drinking more than 248 g per week had
approximately a twofold increased risk of mortality,
compared with moderate drinkers, consuming 10–80 g
of alcohol each week (Britton & Marmot 2004). The
optimal frequency of drinking was between once/twice a
week and daily, after adjustment for average volume
consumed per week (Britton & Marmot 2004).
The Copenhagen Heart Study, involving more than
12 000 individuals (aged 30–79 years) followed for
12 years, reported an increase in risk of mortality with
increasing alcohol consumption, with a significant relative risk of 1.44, for 42–69 drinks (approximately 400–
700 g) per week, which increased to a relative risk of
2.29 for 70+ drinks per week. However, individuals
drinking 1–6 drinks (10–60 g) per week had a 35%
lower death rate compared with those who never drank
(Grønboek et al. 1994). Data from more than 490 000
participants of the US Cancer Prevention Study II
have been analysed to assess alcohol consumption and
mortality among middle-aged and elderly adults (Thun
et al. 1997). The study concluded that moderate alcohol
consumption slightly reduced overall mortality, with
overall death rates of those reporting about one drink/
day (approximately 10 g) being 20% below those of
non-drinkers; but above one drink per day, the overall
death rate among drinkers increased (Thun et al. 1997).
All these studies included participants aged 30 years and
over only, and as noted, age is particularly important
when considering the balance of adverse and beneficial
effects of alcohol intake.
Analysis by Britton and McPherson (2001) concluded
that there is only likely to be a net favourable mortality
balance associated with light/moderate alcohol consumption among men aged 55 years and over and
women aged 65 years and over, who have a much higher
risk of CVD. There is also a pronounced gender effect on
CHD-related mortality, with women reaping the benefits, and harms, of alcohol at a much lower level of intake,
as discussed in section 8. The relationship between mortality and alcohol consumption is also affected by choice
of the control population (i.e. light drinkers or abstainers) which is discussed further in section 8.1.
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Alcohol consumption and our health
It should be noted that none of the studies cited above
have considered the effect of the pattern of alcohol consumption, which is particularly important to some
causes of alcohol-related death, such as accidents and
violence, but also possibly stroke and some cases of
CHD (as discussed in section 8), and this may account
for some of the variation in alcohol-attributed deaths
between European countries reported by Britton et al.
(2003). The Whitehall II Cohort Study also reported
that drinking only once a month, or on special occasions, had a 50% increased risk of mortality (Britton &
Marmot 2004).
For the younger age groups, the benefits may be outweighed by the increased risk of other diseases (e.g.
alcohol-related cancers, liver cirrhosis) and increased
risk of violence and accidents. White et al. (2002) have
considered the younger population in their analysis,
based on population data and relative risk of mortality
from published systematic reviews, and made some recommendations for sensible drinking limits depending on
age, assuming that no more than a 5% increase in risk of
mortality is an acceptable compromise. A limit of 1 unit
per day for women up to the age of 44 years, 2 units per
day for women aged 45–74 years and 3 units per day for
those aged over 75 years are recommended. More tiers
have been recommended for men: those up to 34 years –
1 unit per day; 35–44 years – 2 units per day; 45–
54 years – 3 units per day; 55–84 years – 4 units per day,
and 85+ years – 5 units per day (White et al. 2002).
Mortality data have commonly been used as a source
of information to identify health problems for a population. However, as medical techniques have become
more advanced, death is more easily averted, and therefore the mortality statistics are unable to provide a comprehensive picture of the health problems in a country.
Other measures to summarise population health have
been introduced, such as disability-adjusted life years
(DALYs). DALY is a measure of the years ‘lost’ to premature death and the years of healthy life ‘lost’ to living
in a poor state of health. This means that, if a condition
is associated with morbidity, rather than mortality (such
as chronic excessive alcohol intake), the DALY measure
will be larger. For example, Connor et al. (2005) calculated that 17 200 years of life were lost from premature
deaths due to alcohol in New Zealand in 2002, while
26 000 DALYs were lost. DALYs due to alcohol are in
some cases greater compared with other common diseases; for example, alcohol accounted for 4% of DALYs
for the USA in 1996, compared with only 0.4% of
deaths; whereas ischaemic heart disease accounts for
11% of DALYs, and a substantial 24.7% of deaths
(McKenna et al. 2005). This emphasises the potential
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307
harm that alcohol can have on poor health and subsequent quality of life.
Key points
• Studies looking at the relationship between alcohol
intake and mortality suggest that 10–80 g (approximately 1–8 drinks) of alcohol each week is optimal to
reap the health benefits; thus indicating a ‘U’ shaped
relationship between alcohol intake and mortality.
• Gender and age are important factors when considering the association between alcohol intake and CHDrelated mortality.
• For younger people, the benefits of alcohol intake
may be outweighed by the increased risk of other diseases (e.g. alcohol-related cancers, liver cirrhosis) and
increased risk of violence and accidents.
• Alcohol is commonly associated with morbidity,
rather than mortality.
• DALYs due to alcohol are in some cases greater compared with other common diseases.
8. Alcohol and disease risk
There is now a large body of scientific literature that
supports the hypothesis that consuming alcohol modifies the risk of several diseases. The extent to which it
affects the risk of disease will vary, depending on a number of factors relating to the alcohol consumed, such as
the quantity and type of drink, and individual characteristics such as genetic susceptibility. Chronic excessive
alcohol drinkers are also susceptible to a number of conditions not commonly seen among the general population, such as alcoholic neuropathy. Fortunately, it is only
a minority of the population who can be classified as
chronic excessive drinkers, and therefore, this section
will focus on the relationship between light/moderate
alcohol consumption and risk of common noncommunicable diseases, including obesity, heart disease,
stroke, high blood pressure (hypertension) and cancer.
8.1 Methodological problems of studies assessing
associations between alcohol consumption and
disease risk
There are many methodological problems facing
researchers attempting to investigate the association
between alcohol consumption and chronic disease risk.
In particular, it is very difficult to assess alcohol consumption accurately. Many studies rely on self-reported
intakes, and misclassification is common as respondents
may misreport their intakes either intentionally (e.g. for
fear of being stigmatised) or unintentionally (e.g. from
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R. K. Foster and H. E. Marriott
over- or underestimation) (ILSI 1999). Inappropriate
classification of drinkers could lead to erroneous associations between measured intake and risk of disease.
The problems in reliably assessing individuals’ alcohol
intake also make it difficult for studies to ensure a heterogenous sample with representation from all drinking
‘categories’.
‘Non-drinkers’ or ‘abstainers’ are usually the selected
reference population. The appropriateness of this has
been debated, as individuals may choose not to drink
because of ill-health (these people are sometimes
referred to as ‘sick quitters’), or may follow a ‘healthier’
diet and lifestyle, as illustrated among those taking part
in the European Prospective Investigation into Cane and
Nutrition (EPIC) Heidelberg study (Ruf et al. 2005).
Either of these factors may put the reference sample at
an increased or decreased risk of certain diseases (ILSI
1999).
Drinking habits may also change substantially over
time, which creates a problem for prospective studies
that measure intake on one occasion and follow up subjects for prolonged periods. It is possible that drinking
patterns (i.e. daily, drinking with meals, binge drinking,
etc.) influence associations between alcohol consumption and disease risk. It was once thought that the type
of drink consumed might also be relevant in considering
disease risk, although there is now a consensus that it is
the alcohol content per se that is important. However,
what is becoming increasingly apparent is that the type
of drink is a predictor for specific lifestyle factors that
need to be considered. For example, studies have found
wine drinkers to have a healthier diet than people who
drink beer or spirits (McCann et al. 2003; Johansen
et al. 2006). Therefore, investigations into this area need
to adjust sufficiently for lifestyle factors such as diet,
smoking and physical activity, because variations in lifestyle may account for at least some of the differences in
disease risk (Grønboek 1999; Tjønneland et al. 1999).
Comparing findings from different studies can also be
difficult, as studies use different measurement units.
Respondents may recall the number of drinks they
drank, but information on the size of the drink and its
alcoholic strength may not be available. Some studies
may translate the information into grams of alcohol,
while others refer to ‘standard units’ as discussed in section 3. The latter is a particular problem when comparing international studies, as standard units of alcohol
vary across the world. A further complication with
regards to measurement units is the inconsistent use of
‘categories’ of drinker (i.e. heavy, moderate and light)
between studies. The categories used to describe weekly
drinking habits (e.g. fairly high, high, etc.) in the UK
dietary surveys were outlined in section 4; however,
these terms are not consistent with the terminology used
in the majority of studies discussed below.
8.2 Alcohol and bodyweight
Most prospective data support the conclusion that
heavy alcohol intake (classified as >30 g or >3 drinks
per day) is associated with an increased risk of weight
gain and obesity, while light to moderate drinking is not
(Wannamethee & Shaper 2004). The findings of crosssectional studies have not been as consistent, except that
very heavy consumers (consumption of >49 g/day) have
a low body mass index (BMI) (reasons for which were
discussed in section 4) (Suter 2005). These inconsistent
findings may be due to the various methodological
problems linked to studies measuring alcohol, as outlined at the beginning of this section, particularly the
misreporting of intake, which is recognised to be a particular issue in overweight/obese subjects. Other factors
that cannot be controlled for in epidemiological studies
may also influence the relationship between alcohol
consumption and bodyweight. For example, it has been
suggested that much of the inconsistency between these
studies may have arisen from the confounding effects of
cigarette smoking (i.e. stimulation of energy expenditure, effect on decreasing appetite and subsequent food
intake). This has been demonstrated by findings from
the British Regional Heart Study, which found current
smokers to have a lower mean BMI than non- (and
ex-) smokers at almost every level of alcohol intake, and
the strongest influence of alcohol on bodyweight was
seen in non-smokers (Wannamethee & Sharper 1992;
2003). According to Suter (2005), other factors may
influence the relationship between alcohol intake
and bodyweight, including: the frequency of drinking
(affecting the amount of alcohol consumed and the
metabolism of alcohol and other macronutrients);
gender; genetic background; and the composition of the
diet.
A number of studies have reported associations
between alcohol intake and distribution of bodyweight,
particularly abdominal obesity; however, the exact relationship is unclear and is complicated by a variety of
factors. For example, analysis of data from the large US
prospective male Health Professionals’ Follow-up Study
reported that changes in alcohol consumption over
time were not significantly related to waist gain (KohBanerjee et al. 2003). However, the reported alcohol
intake among this cohort was only approximately 11.5–
14.9 g/day, and small-scale prospective studies suggest
that quantity and frequency of alcohol intake may be an
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Alcohol consumption and our health
important factor. For example, a case–control study by
Dorn et al. (2003), involving approximately 2000 participants (with a mean age of 52 years), reported alcohol
consumption to be associated with lower levels of centrally located fat, compared with abstinence, and in particular, small amounts of alcohol on a regular basis were
associated with the smallest abdominal measurements.
Participants with the most intense drinking (3–4 drinks/
day) on a sporadic basis had some of the largest
abdominal measurements.
Greenfield et al. (2003) also reported that a moderate
alcohol intake (equated to 1–2 drinks per day) was significantly associated with less abdominal fat, compared
with abstainers. This case–control study investigated the
association between alcohol intake and abdominal fat
among approximately 400 monozygotic twins to minimise genetic and environmental effects. Finally, some
research has suggested that the relationship between
alcohol and fat distribution may alter according to the
type of alcoholic beverage, but the data are inconsistent
(Sakurai et al. 1997; Dallongeville et al. 1998; Dorn
et al. 2003).
As alcohol often seems to supplement, rather than displace, food-derived energy intake, as discussed in section
6, the lack of a clear relationship between alcohol consumption and bodyweight has led to the suggestion that
energy from alcohol may have an effect on normal energy
regulation. Possible explanations for this have considered the low biological efficiency of alcohol as an energy
source, the thermogenic effects of alcohol and the interaction of alcohol with lipid metabolism. These possible
explanations are considered in more detail below.
Thermogenic effect of alcohol
A review of studies considering the thermogenic effect of
alcohol has shown that in non-alcoholic subjects, the
extra energy expenditure associated with alcohol ingestion ranges from 10% to 15% of the energy content of
the alcohol ingested (Westerterp et al. 1999). This is
entirely in keeping with the thermogenesis associated
with the other macronutrients. However, a recent review
by Suter (2005) states that the thermic effect of alcohol
among moderate consumers is 15–25% of the energy
content of the alcohol intake, which would result in
alcohol contributing less energy to the overall energy
balance. It should also be noted that alcohol has a different thermogenic effect in heavy alcohol consumers, as
the mechanism by which the alcohol is metabolised
leads to increased thermogenesis (see below for more
discussion) (Suter 2005). The alcohol-related ill-health,
common to heavy drinkers, such as liver cirrhosis, may
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309
also have an impact on the thermogenesis of the alcohol
consumed (Suter 2005).
Biological efficiency of alcohol
As explained in section 5, among heavy alcohol consumers (and habitual daily moderate alcohol consumers), a
larger fraction of the alcohol energy will be metabolised
via the MEOS. This system alters the coupling of alcohol oxidation to oxidative phosphorylation, by using
NADPH, thus generating heat and reducing the amount
of energy available (James & Ralph 2000; Suter 2005).
It is suggested that this is a contributing factor for the
lower BMIs of very heavy alcohol consumers compared
with moderate drinkers or abstainers, and this has been
supported by experimental studies with alcoholics,
which found that when substituting 50% of dietary
energy from carbohydrate with energy from alcohol,
subjects lost weight (Lieber 1991a). These findings support the idea of alcohol inducing energy wastage among
very heavy alcohol consumers, as the thermogenic effect
of alcohol is higher than its biological efficiency. The
dose of alcohol required for induction of the MEOS varies from one individual to another, which may provide a
further explanation for the variability in results of
studies of alcohol and bodyweight (Suter 2005). No
significant wastage of energy is reported when
alcohol is metabolised through the principal route, i.e.
via the NAD-linked enzyme ADH (Lieber 1991a)
(see section 4).
Alcohol and lipid oxidation
There are three possible mechanisms by which alcohol
may interfere with lipid metabolism to encourage
weight gain. First, it is well recognised that ingestion of
alcohol leads to the suppression of fat oxidation by
approximately 30%, while the alcohol is metabolised;
this in turn inhibits fat mobilisation (Feinman & Lieber
1999; Jéquier 1999; Santolaria & González-Reimers
2004). A study by Siler et al. (1999) also indicated that
moderate alcohol consumption led to an increase in
hepatic de novo lipgenesis, thus increasing the fat mass
directly. Therefore, the interaction of ethanol and lipid
metabolism is relevant to the effect of alcohol consumption on bodyweight and body composition, because it
favours lipid storage (Feinman & Lieber 1999).
Summary
As discussed in section 5, studies indicate that alcoholderived energy is usually additive to the normal diet and
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therefore promotes an increase in energy intake; therefore, one would expect alcohol intake to be associated
with weight gain and a higher BMI (with the exception
of chronic heavy drinkers whose diet and metabolism
may be altered). Recent prospective studies considering
weight gain and alcohol consumption have demonstrated that people who drink more than 3 drinks a day
tend to be heavier, compared with low alcohol drinkers
or abstainers. No association has been demonstrated at
lower intakes, but other confounding factors may be
obscuring the relationship.
8.3 Alcohol and coronary heart disease
In the past decade, there have been many epidemiological
studies providing evidence that low to moderate intakes
of alcohol may reduce the risk of heart disease, with one
of the largest prospective cohort studies reporting an
adjusted relative risk of 0.69 for angina and 0.65 for
myocardial infarction among middle-aged men consuming one drink per day, compared with non-drinkers and
occasional drinkers (<1 drink per week) (Camargo et al.
1997). It is evident from these studies that the amount of
alcohol consumed is important when considering this
relationship, along with gender. A comprehensive metaanalysis looking at the average volume of alcohol
consumed in relation to CHD mortality risk found consumption of 0–20 g/day to be associated with a decrease
in risk; this inverse association was noted for those consuming up to 72 g/day in both genders. Consuming 89 g/
day or more was associated with an increased risk of
CHD (Corrao et al. 2000). However, the major protective effect occurred at 10 g/day for women compared
with 25 g/day for men, thus emphasising that gender is
an important determinant. The meta-analysis noted that
the estimates of degree of protection, based on the findings of 28 good quality cohort studies, were smaller than
estimates based on all studies combined.
Other factors that may influence the association
between alcohol intake and risk of CHD
More recently, it has been recognised that the pattern of
alcohol consumption (amount of alcohol consumed per
session or number of drinking occasions per week) may
influence CHD risk (Agarwal 2002; Rehm et al. 2003b;
Warner Kershner et al. 2004). To date, ‘drinking patterns’ have not been considered in many epidemiological
studies, and therefore the influence of this factor may
have been underestimated (Rehm et al. 2003a). A
review of studies by Puddey et al. (1999) indicates an
increased risk of major coronary events among drinkers
with episodic heavy drinking patterns, thus adding to
the current public health concern around people binge
drinking.
This relationship still exists when comparing individuals who undertake heavy drinking sessions with those
who consume similar amounts of alcohol spread over
1 week. For example, findings from the Health Professionals’ Study found that, for a given level of weekly
alcohol consumption, spreading alcohol consumption
across the week was potentially more beneficial to cardiovascular health than restricting it to a smaller number of days (Mukamal et al. 2003). These findings are
generally in line with those from other large prospective
cohort studies, although Tolstrup et al. (2006) reported
that drinking patterns may be important to CHD risk
among men, independent of total alcohol intake (i.e. the
lowest hazard ratio was among men consuming 21 units
or more per week over 7 days). Whereas among postmenopausal women, total alcohol intake may be more
important, with the lowest risk reported among those
consuming 14 drinks or more per week over 2–4 days.
Ecological studies, paradoxically indicating a low
CHD mortality rate in populations with high smoking
rates and consuming a diet high in saturated fat (e.g. the
French), have led to the suggestion that some alcoholic
beverages, namely red wine, are more protective than
others. This concept has been supported by the presence
of bioactive compounds, namely polyphenols, found in
red wine (see section 6 for more discussion). A number
of observational case–control and cohort studies have
considered whether consuming one type of alcoholic
beverage compared with another impacts on CHD risk.
Current consensus is that it is the alcohol per se that is
responsible for the positive heart health effects (Rimm
et al. 1996; Burns et al. 2001; Wollin & Jones 2001;
Rehm et al. 2003b; Warner Kershner et al. 2004); and
this has been demonstrated by data from the Health
Professionals’ Follow-up Study (Mukamal et al. 2003).
Studying some of the mechanisms recognised to be
involved in the protective effect of alcohol, including
changes in concentrations of high density lipoprotein
(HDL) cholesterol, fibrinogen and triglycerides, Rimm
et al. (1999) calculated that 30 g of alcohol a day should
reduce risk of coronary disease by 24.7%. These mechanisms and others are discussed in more detail later in
this section.
8.4 Alcohol and blood pressure
An association between blood pressure and alcohol
intake is widely accepted, with heavy drinking patterns
(in particular, binge drinking) being a risk factor for high
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blood pressure, or hypertension (Dyer et al. 1981; Witteman et al. 1990; Marmot et al. 1994). Evidence indicates that a reduction in alcohol intake among heavy
drinkers can reduce systolic and diastolic blood pressure
among hypertensive or non-hypertensive people (Xin
et al. 2001). For example, findings from a meta-analysis
of randomised controlled trials indicated alcohol intake
reduction in heavy drinkers (those consuming 3–6 drinks
per day) results in a 3.31-mmHg reduction in systolic
blood pressure and 2.04-mmHg reduction in diastolic
blood pressure. Therefore, those diagnosed with hypertension should reduce their intake of alcohol in order to
improve their condition (Dickinson et al. 2006).
However, there is much debate about the overall relationship between alcohol and blood pressure. For example, evidence indicates that moderate intakes of alcohol
may lead to short-term lowering of blood pressure
(Witteman et al. 1990; Gillman et al. 1995), whereas
abstainers/teetotallers have a higher blood pressure, suggesting a ‘J’ shaped relationship (Papadakis et al. 2000;
Agarwal 2002). Reviews have also described a threshold
phenomenon, whereby the risk of high blood pressure
increases if intake exceeds 3 standard drinks per day
(Beilin et al. 1996; Keil et al. 1998; Grobbee et al. 1999;
Klatsky 2003). A consensus view on this issue has yet to
be agreed. The variation in findings may be due to methodological differences. For example, a systematic review
of nine studies by McFadden et al. (2005) suggested a
potential reduction in blood pressure in the hours after
exposure to alcohol, followed by a rise in blood pressure, thus indicating the importance of the timing of the
blood pressure measurement. A review by Lip and
Beevers (2003) summarises other factors that have been
found to influence the possible relationship between
alcohol and blood pressure, including type of beverage
and pattern of drinking. For example, heavy ‘weekend
drinkers’ have been found to have a higher blood pressure when compared than those who drink the same
quantity over a week (Wannamethee & Shaper 1991).
8.5 Alcohol and stroke
A number of epidemiological studies have investigated
the relationship between alcohol intake and stroke.
These have shown alcohol to both reduce and increase
the risk of stroke, depending on the quantity of alcohol
consumed, drinking habits (e.g. binge vs. regular drinking), and the type of stroke (i.e. ischaemic stroke or
haemorrhagic stroke). The variation in results is not surprising, as different types of stroke have different causes:
ischaemic stroke is caused by a blockage in a blood vessel in the brain, commonly arising from a blood clot
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311
formed somewhere else, and therefore has a similar aetiology to that of CHD; haemorrhagic stroke is caused by
a rupture of a blood vessel supplying the brain, thus
releasing blood into the brain (see Stanner 2005 for
more information). Therefore, it is unlikely that the
effect of alcohol would be the same for both types of
stroke. It is now believed that findings from earlier studies, which did not differentiate between the different
type of stroke and the quantity of alcohol consumed,
obscured the relationship between alcohol intake and
stroke (Grobbee et al. 1999; Mazzaglia et al. 2001).
Although a recent comprehensive review reported a
lack of association between light to moderate drinking
and haemorrhagic stroke (Warner Kershner et al. 2004),
meta-analyses that have explored this relationship have
reported a positive, linear relationship between alcohol
intake and haemorrhagic stroke (Corrao et al. 1999;
Reynolds et al. 2003). In line with these findings, the
most recent systematic review undertaken by Mazzaglia
et al. (2001) concluded that there is a causal association
between haemorrhagic stroke and heavy drinking (classified as more than 40 g/day).
Turning to ischaemic stroke, although there is a variation in the findings of studies, the consensus of opinion
is that there is a positive association between ischaemic
stroke and heavy alcohol intake. However, as illustrated
by the meta-analyses and reviews, results from studies
investigating the association between moderate alcohol
consumption and ischaemic stroke are inconsistent
(Puddey et al. 1999; Britton & McPherson 2001; Mazzaglia et al. 2001; Reynolds et al. 2003). In the most
recent meta–analysis considering this association, those
consuming 12 g or less of alcohol each day had a significantly lower risk of ischaemic stroke (Reynolds et al.
2003). However, more prospective studies are needed to
clarify this association, as findings from the Health Professionals’ Follow-up Study indicated no association
between 0.1–9.9 g of alcohol a day and risk of ischaemic
stroke (Mukamal et al. 2005a). As ischaemic stroke is
the most common type in Western countries, accounting
for 75–85% of all strokes, any reduction in its risk
could have a significant impact on public health.
Other factors that may influence the association
between alcohol intake and risk of stroke
A small number of studies have considered whether the
type of alcohol has any effect on the risk of stroke. To
date, evidence indicates that wine (in moderation) may
have protective effects, while other beverages do not
(Constant 1997; Truelsen et al. 1998; Malarcher et al.
2001; Mukamal et al. 2005a). For example, the large
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R. K. Foster and H. E. Marriott
prospective Copenhagen City Heart Study found no
association between risk of stroke and intake of spirits
and beer, yet daily, weekly and monthly intakes of wine
(mode = 1–7 units/week), compared with no wine, were
associated with a lower risk of stroke (Truelsen et al.
1998). Assuming that studies have used appropriate
methods to control for confounding lifestyle factors, this
relationship may not be due to the difference in wine
and beer composition, but could be due to wine being
more commonly consumed with a meal, thus slowing
down its metabolism. Although not always taken into
consideration, patterns of drinking may be an important
factor in understanding the relationship between alcohol consumption and stroke. For example, consumption
of a large quantity of alcohol in a few hours is associated
with an increased risk of both haemorrhagic and
ischaemic stroke (Grobbee et al. 1999; Mazzaglia et al.
2001). Drinking pattern could therefore account for
some of the variation in the results of different studies,
and hence recent reviews recommend that future
research should ensure this factor is considered.
Hypertension (as discussed above) is one of the most
important risk factors for stroke and, therefore, alcoholinduced fluxes in blood pressure might be in part
responsible for the association between alcohol consumption and stroke (Reynolds et al. 2003; Frayn
2005). Some studies have controlled for hypertension
when assessing the relationship between alcohol intake
and stroke, which Puddey et al. (1999) suggest may
attenuate any association; however, a consensus on this
issue has yet to be met. Other possible explanations for
the variation in findings include possible racial and gender inter-relationships (Puddey et al. 1999). Alternatively, it is feasible that raw data (e.g. death certificates)
used by the researchers may have been inaccurate, as
there are few reliable methods of distinguishing between
different forms of stroke (Mazzaglia et al. 2001).
Sudden death
Although findings have varied, some studies have
reported an association between cardiovascular death
and heavy episodic drinking (Britton & McKee 2000;
Malyutina et al. 2002; Mukamal et al. 2005b). Those
studies that did not account for drinking patterns found
no significant results (Wannamethee & Shaper 2002;
Marques-Vidal et al. 2004). A systematic review by
McKee and Britton (1998) suggests that heavy drinking
occasions are mainly associated with physiological mechanisms, increasing the risk of sudden cardiac death and
other related conditions, such as increased blood clotting
and reduced threshold for ventricular fibrillation. This
association between heavy drinking occasions and cardiac deaths, particularly sudden cardiac deaths, came to
light from experiences in Eastern Europe, where heavy
episodes of binge drinking are common. In particular, an
observational study by Chenet et al. (1998) reported a
significant increase in sudden cardiac death at weekends,
which is markedly similar to the pattern of deaths that are
seen from alcohol poisoning and from accidents and violence, commonly associated with binge drinking.
Proposed mechanisms for how light/moderate alcohol
intake may increase the risk of cardiovascular
conditions
Two mechanisms are considered here to explain how
light to moderate alcohol intake may increase the risk of
hypertension. It is well recognised that hypertension can
increase the risk of stroke through various mechanisms,
as reviewed by Frayn (2005). However, the different
dose-dependant effects and divergence between acute
and chronic intake makes the mechanism of the interaction between alcohol and hypertension complex.
Grobbee et al. (1999) suggest that the pressor effect
caused by a high alcohol intake could be due to a neurogenic mechanism, a humoral mechanism or caused
directly through the actions on the vessels that maintain
peripheral resistance, resulting in hypertension induced
by alcohol.
Alcohol has been found to have anti-coagulant
effects, which may play an important role in increasing
the risk of haemorrhagic stroke. However, overall, the
mechanisms associating moderate alcohol consumption
and increased risk of haemorrhagic stroke, and heavy
alcohol intake and both haemorrhagic and ischaemic
stroke, are unclear.
Recognised mechanisms for light/moderate alcohol
intake reducing the risk of cardiovascular conditions
A number of mechanisms have emerged from both experimental and observational epidemiological studies that
may explain the reported associations between alcohol
consumption and CVD, and these are outlined below.
Blood lipids Reviews of the relationship between alcohol intake and blood lipids indicate that moderate alcohol intake has been shown to lead to an increase in high
density lipoprotein (HDL) cholesterol (a lipoprotein
that binds with cholesterol and brings it back to the liver
for elimination or re-processing), and a decrease in low
density lipoprotein (LDL) oxidation (which is involved
in the development of atherosclerotic plaques) (Grobbee
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et al. 1999; Puddey et al. 1999; Papadakis et al. 2000;
Mazzaglia et al. 2001; Agarwal 2002; Warner Kershner
et al. 2004). There has been some debate as to whether
the pattern of drinking may be important in determining
the effects of alcohol on blood lipids. Evidence indicates
that this is not the case (Peasey et al. 2005; Puddey et al.
1999).
Antioxidant properties As alcoholic beverages are
originally derived from plants, they contain some bioactive substances found in plants and plant-derived
foods (Duthie & Crozier 2003). Of all the alcoholic beverages, wine has the highest concentration of bioactive
substances, and in particular, polyphenols. Polyphenols
are thought to have anti-oxidant activity which may be
beneficial in protecting against the oxidation of LDLcholesterol. Although studies have confirmed that
polyphenolic compounds, from red wine in particular
have antioxidant activity in vitro, it has been less clear
whether such antioxidant effects occur in vivo. Furthermore, the bioavailability of polyphenols is an area of
particular uncertainty (see section 6). There is also large
individual variation in the absorption of bioactive substances between subjects.
Haemostatic factors The process of blood clotting
(known as haemostasis) functions as a careful balance
between blood flowing and stopping, and between
clotting and clots dissolving. If blood is prone to clot
too little, then there is a risk of haemorrhage; too much,
and there is a risk of blood clots forming where they are
not wanted, such as in an artery supplying blood to the
brain, causing a stroke, or to the heart, causing a heart
attack. Moderate alcohol consumption is recognised to
have anti-coagulant effects as it causes:
• a decrease in levels of plasma fibrinogen (the precursor of the insoluble blood-clotting protein, fibrin),
which reduces the risk of blood clots;
• a decrease in platelet adhesiveness, and a subsequent
decrease in platelet aggregation;
• changes in the concentration of fibrinolytic factors,
including clotting factor VII and tissue plasminogen
activator, thus reducing platelet aggregation.
Homocysteine High levels of homocysteine in the blood
(above those considered normal) are associated with an
increased risk of CHD and stroke. Homocysteine is an
amino acid produced as the body metabolises protein.
Although alcoholics have been shown to have raised
homocysteine levels, levels have been found to be lower
in individuals who are moderate alcohol drinkers (Bree
et al. 2002).
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313
Several of the B vitamins are involved in homocysteine metabolism, and studies have found that supplementation, particularly with folic acid, can lower
homocysteine levels (see Clarke 2005). Folate intake is
also recognised to be of particular importance when
assessing the association between alcohol intake and
risk of chronic disease. For example, findings from the
large prospective cohort Nurses’ Health Study indicate
that higher dietary folate intakes (above 400 µg/day)
can diminish the risk of CVD associated with high
intakes (30 g/day) of alcohol, but the expected benefit of
moderate alcohol intake was not observed when folate
intake was low (Jiang et al. 2003). This finding could be
due to the relationship between folate and serum
homocysteine. However, there appears to be a variation
in the association between folate, alcohol and risk of
CVD with age, as the positive association between
heavy alcohol intake, low folate and risk of disease
seems to be most apparent in younger women below the
age of 60 years (Jiang et al. 2003).
Endothelial function The endothelium forms the interface between the artery wall and constituents of the
blood. It plays an important role in the regulation of
vascular tone, for example by inhibiting platelet aggregation and adhesion. Endothelial dysfunction is thought
to presage atherosclerosis; therefore, healthy functioning of the endothelium is important. There are some
human studies linking moderate alcohol intake, particularly red wine, with better endothelial function
(Teragawa et al. 2002).
Other emerging risk factors for CVD Moderate alcohol consumption (up to 40 g/day), compared with nondrinking and heavy drinking, has been found to have
anti-inflammatory and immunomodulatory effects,
which may influence the inflammatory processes that
characterise the development of atheroma (Imhof et al.
2004). See Stanner (2005) for more information.
Associations between alcohol intake and
CVD-summary
It is evident that there are disparities in the relationships
between alcohol consumption and various cardiovascular conditions, with complex inter-relationships between
conditions. For example, alcohol is associated with an
increased risk of haemorrhagic stroke, but may have a
protective effect on ischaemic stroke. Heavy drinking
(more than 40 g/day), however, is associated with an
increased risk of both types of stroke. As the majority of
cases of stroke are ischaemic in nature, it is important to
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identify the true characteristics of the relationship
between stroke and alcohol intake. Drinking patterns
also may be important in relation to the risk of stroke,
and future studies in this area should consider this factor.
The impact of drinking patterns on heart health is
also unknown, although there is now strong evidence
that moderate consumption (10 g/day for women, and
25 g/day for men) decreases the risk of a CHD episode,
with particular benefits to men aged over 55 years and
post-menopausal women; however, heavy drinking
(classified as more than 89 g/day) is again associated
with an increased risk. In particular, a number of studies
indicate a positive association between heavy episodic
drinking and CVD-related death. The consensus of
opinion among scientists is that it is the alcohol per se
that influences heart health, rather than the type of alcoholic beverage, and other factors that affect an individual’s choice of drink may be important in distorting the
findings from studies that show otherwise.
A number of potential mechanisms have been identified to account for the risk reduction associated with
moderate alcohol intake and CHD, and the possible
benefits associated with ischaemic stroke. However,
there are fewer explanations to account for the
increased risk of CVD conditions associated with heavy
consumption of alcohol, or the positive linear relationship between alcohol and haemorrhagic stroke.
8.6 Alcohol and type 2 diabetes
Evidence indicates that moderate alcohol consumption
(1–3 drinks/day) is associated with a decreased risk (of
30–40%) of type 2 diabetes, when compared with teetotallers or the lowest consumers (Conigrave & Rimm
2003; Zilkens & Puddey 2003; Howard et al. 2004;
Van de Wiel 2004; Carlsson et al. 2005; Koppes et al.
2005). However, heavy alcohol consumption appears to
be associated with an increased risk; therefore, the association between alcohol and type 2 diabetes is thought
to be ‘J’ or ‘U’ shaped, with risk beginning to rise at
around 4 drinks per day (Conigrave & Rimm 2003;
Howard et al. 2004; Carlsson et al. 2005; Koppes et al.
2005). It should be noted that a number of confounding
factors may complicate the relationship between alcohol
intake and risk of diabetes; gender, BMI, frequency of
drinking and type of alcoholic beverage have all been
found to be important.
Possible mechanism
Although the acute effects of alcohol may induce a state
of insulin resistance, studies indicate that a moderate
amount of alcohol intake results in enhanced insulin
sensitivity in the long-term, and therefore this may
account for the possible beneficial effect of moderate
alcohol consumption on risk of type 2 diabetes, as
reported in a number of review papers (Zilkens & Puddey 2003; Van de Wiel 2004; Koppes et al. 2005). This
effect on insulin sensitivity may also be one of the mechanisms involved in the protective effect of alcohol with
regard to atherosclerotic disorders. The cardio-protective effects of alcohol are particularly relevant to people
with type 2 diabetes, for whom coronary risk factors are
highly prevalent. Similarly, heavy alcohol consumption
should be avoided by those with diabetes because of its
detrimental effects on lipid metabolism (see section 8.2),
blood pressure (see section 8.4) and other cardiovascular risk factors (see section 8.5).
8.7 Alcohol and cancer
There is strong and consistent convincing evidence from
epidemiological and experimental studies that alcohol is
an independent risk factor for oral, pharyngeal, oesophageal and liver cancers (WCRF 1997; Department of
Health 1998; Key et al. 2004). There is also considerable evidence to show a small increase in risk of breast
cancer with increasing alcohol consumption (Key et al.
2004). Reviews by Pöschl and Seitz (2004) and MorrisBrown (2005) have supported a weak association
between increasing alcohol consumption and increased
risk of colorectal cancer. Alcohol has also been considered to cause an increased risk of cancer of certain other
organs, such as the stomach, lung and cervix (Bagnardi
et al. 2001); however, this briefing paper will focus on
cancers of the upper digestive tract, the liver, breast and
colorectal cancer.
The increase in cancer risk appears to be primarily due
to alcohol per se, rather than specific alcoholic beverages, although some studies have found that a stronger
relationship exists between cancers of the upper digestive tract and distilled spirits (Longnecker 1995; Pöschl
& Seitz 2004). Pattern of alcohol intake has been found
to affect the association between alcohol and some
chronic diseases, although very limited information is
available on drinking pattern and cancer risk. A large
prospective study showed that consumption of wine outside a meal was associated with a relative risk of cancer
death of 1.7 for women and 3 for men, compared with
those consuming wine with a meal. Also, one study indicated that subjects who drank outside of meals were at
a higher risk of cancers of the upper aero-digestive tract,
after allowance for drinking status and number of drinks
per day. The association was particularly marked for
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Alcohol consumption and our health
cancers of the pharynx (odds ratio 1.8), oesophagus
(odds ratio 1.7) and oral cavity (odds ratio 1.5) (Dal
Maso et al. 2002). A detailed discussion of the mechanisms by which alcohol affects these organs/sites is
beyond the scope of this briefing paper, but some of the
most likely are briefly considered later in this section.
Cancers of the upper aero-digestive tract
Alcohol has a carcinogenic dose–response effect at sites
of the upper aero-digestive tract, which is independent
from smoking, and in some studies, smoking and
alcohol have been found to interact in a multiplicative
fashion (Department of Health 1998; Doll et al.
1999; Bagnardi et al. 2001). In Westernised countries,
alcohol and tobacco are the main risk factors for 75%
of oral and pharyngeal cancers (International Agency
for Research on Cancer 1988). However, the incidence
of these forms of cancer is relatively low in the UK, even
among people who both smoke and drink alcohol;
therefore, other mechanisms (e.g. genetics) are probably
responsible, with alcohol and smoking playing a contributory role (Morita et al. 2002; Ogden 2005).
Liver cancer
Chronic excessive alcohol consumption can lead to liver
cirrhosis, which can develop into hepatocellular carcinoma (Boffeta & Hashibe 2006). Excessive alcohol consumption is the main diet-related risk factor for liver
cancer in Western countries. A meta-analysis by Corrao
et al. (2004) reported a relative risk of 1.8 for hepatocellular carcinoma for the heaviest consumers (100 g/
day). However, the direct correlation between alcohol
consumption and the development of hepatocellular carcinoma is not straight forward, as the disease does not
develop in all patients with cirrhosis. There is evidence
that alcohol, the metabolism of alcohol, or both, affect
cell signalling pathways that regulate normal and abnormal hepatocyte function, proliferation and apoptosis
(McKillop & Schrum 2005). It is thought that the specific
effect of ethanol on hepatocyte signalling integrity varies
according to acute or chronic exposure to alcohol.
Breast cancer
A large number of epidemiological studies indicate that
alcohol intake increases the risk of breast cancer, and the
risk rises with increasing consumption of alcohol, even
in small amounts (i.e. one drink per day) (WCRF 1997).
Breast cancer is the most commonly diagnosed cancer
among women across the UK. Although a number of
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315
other factors (e.g. family history, hormonal factors, age)
contribute to the risk of breast cancer, alcohol is one of
the few recognised dietary risk factors. The mechanism
is unknown but may involve increased levels of circulating oestrogen. Various reviews and meta-analyses
have been undertaken to assess the potential risk of
breast cancer associated with alcohol intake (Longnecker 1994; Corrao et al. 1999; Bagnardi et al. 2001;
Collaborative Group on Hormonal Factors in Breast
Cancer 2002; Hamajima et al. 2002; Boffetta & Hashibe 2006). Longnecker (1994) reported a 10% increase
in the risk of breast cancer with every 10 g of alcohol
consumed each day (about one drink per day). Yet more
recently, a collaborative reanalysis of data from 53
epidemiological studies found a smaller increase in the
risk of breast cancer, of 7%, with every additional 10 g
of alcohol consumed per day (Collaborative Group on
Hormonal Factors in Breast Cancer 2002).
Colorectal cancer
Epidemiological studies have generally reported a positive association between alcohol consumption and risk
of colorectal cancer. The most recent meta-analysis in
this area reported a pooled multivariate risk of 1.16
(bordering on significance) with 30–44 g/day of alcohol,
and a significant multivariate risk of 1.41 for those consuming 45 g/day of alcohol or more, when compared
with non-drinkers (Cho et al. 2004). This meta-analysis
indicated a dose–response, with alcohol intake of about
30 g/day (3 drinks) increasing the risk of colorectal cancer, while two other meta-analyses reported an increased
risk from about 2–3 drinks per day (Longnecker et al.
1990; Bagnardi et al. 2001). However, findings related
to specific alcoholic beverages or different anatomic
sites in the large bowel have been inconsistent.
Proposed interactions between alcohol and cancer-causing mechanisms
Multiple (possibly site-specific) mechanisms may be
involved in the associations between alcohol and cancer,
although, perhaps most importantly, an individual’s risk
of alcohol-related cancer is modulated by genetic factors
(Boffetta & Hashibe 2006).
In animal models, alcohol does not initiate cancer, but
can increase the effect of substances that are carcinogenic. However, when alcohol is metabolised to acetaldeyhyde, it becomes highly toxic, and is believed to be
mutagenic and carcinogenic, and subsequently, it is
thought that it is acetaldehyde that is responsible for the
carcinogenic effect associated with alcohol consump-
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R. K. Foster and H. E. Marriott
tion. Binding to DNA and the formation of stable
adducts are possible mechanisms by which acetaldehyde
could trigger the occurrence of replication errors, or
mutations in oncogene or tumour suppressor cells. See
Pöschl & Seitz (2004) for further information.
The publication of the review on food, nutrition,
physical activity and the prevention of cancer in 2007 by
the World Cancer Research Fund, will provide a much
needed, detailed overview of the evidence base in this
area (for more information, see http://www.wcrf.org/
research/second_wcrf_aicr_report. lasso).
Summary
Risk of cancer at a number of sites has been associated
with alcohol intake. A consensus for a likely causal association has been identified between alcohol and cancers
of the upper aero-digestive tract and the liver. However,
mechanisms to explain the positive association between
alcohol and breast cancer, and between alcohol and colorectal cancer, have yet to be identified. There is a linear
dose–response relationship between alcohol intake and
risk of cancer, although the magnitude of the risk varies
depending on cancer site. However, it is likely that
smoking will have a multiplicative effect at all sites.
Although the mechanisms identified to date suggest
that it is the alcohol per se that exerts damage and therefore the quantity of alcohol consumed is the most
important variable, it remains unclear whether the type
of alcoholic beverage consumed is an important factor
in determining the association between alcohol intake
and cancer.
Key points
• There are a number of methodological problems that
need to be considered when exploring the associations
between alcohol consumption and disease risk, including: misreporting of total intake; the use of an appropriate control group; and the need for comparable
measurement units.
• Alcohol intake is associated with weight gain and an
increase in BMI (with the exception of chronic excessive
drinkers), and this is supported by recent prospective
studies. However, a number of other factors may
obscure the relationship, and may account for the variation in findings from studies.
• Alcohol is associated with an increased risk of haemorrhagic stroke, but low intakes (i.e. one drink per day)
may have a protective effect on ischaemic stroke. Heavy
drinking is associated with an increased risk of both
types of stroke, and this has been the predominant find-
ing of studies. Drinking patterns also may be important
in relation to the risk of stroke.
• There is now strong evidence that light to moderate
(1–3 drinks per day) alcohol consumption decreases the
risk of a CHD episode, compared with abstainers, with
particular benefits in men aged over 55 years and postmenopausal women; however, heavy drinking is once
again associated with an increased risk.
• Further information is required to determine the association between drinking patterns and heart health.
However, there is a consensus of opinion that it is the
alcohol per se that influences our heart health, rather
than a particular type of alcoholic beverage; and other
factors that affect an individual’s choice of drink may be
important in distorting the findings from studies that
show otherwise.
• Light to moderate alcohol consumption is associated
with a decreased risk (of 30–40%) of type 2 diabetes,
when compared with teetotallers. Heavy drinking may
be associated with an increased risk, resulting in a ‘J’ or
‘U’ shaped relationship between alcohol consumption
and the incidence of type 2 diabetes (similar to that seen
with CHD).
• Cancers at a number of sites have been associated
with alcohol intake; however, a consensus for a likely
causal association has only been identified between alcohol and cancers of the upper-aero digestive tract and the
liver. The mechanisms to explain the positive associations between alcohol and breast cancer, and evidence
for the positive association between alcohol and colorectal cancer, have yet to be identified.
• There is a linear dose–response relationship between
alcohol intake and risk of cancer, although the magnitude
of the risk varies depending on cancer site. However, it
is likely that smoking will have a multiplicative effect at
all sites. It is unclear whether some types of alcoholic beverage are more strongly associated with an increased risk
of cancer than others. Mechanisms identified to date suggest that it is the alcohol per se that exerts damage.
9. Alcohol and other conditions
Experience from clinical cases suggests that consuming
even moderate amounts of alcohol may cause an adverse
reaction in some individuals. Alcohol should also be
avoided in certain circumstances, such as pregnancy.
9.1 Adverse reactions to alcohol for some
susceptible individuals
A small number of studies have investigated why red
wine may cause headaches and migraines among those
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susceptible, when other alcoholic beverages do not.
Although small scale, these studies have confirmed that
alcohol per se is not the cause of these adverse reactions
(Littlewood et al. 1988). The UK Committee on Toxicity of Chemicals in Food, Consumer Products and the
Environment (2000) reported on the potential ‘allergic’
response to red wine, and suggested that the phenolic
flavonoid content of the wine may be responsible. The
report also noted that the headaches may be mediated
by histamine, a vasoactive amine, which has been suspected of causing headaches. Jarisch and Wantke (1996)
verified this association among those suffering histamine
intolerance, but other explanations are needed to
account for those individuals who suffer headaches and
migraines from alcoholic beverages other than wine.
9.2 Alcohol and peptic ulcers
It was previously thought that an association existed
between alcohol consumption and benign digestive disorders, such as peptic ulcer. However, it is now thought
that diet does not have a significant role, as duodenal
ulcers are primarily due to a Helicobacter Pylori infection, or intake of non-steroidal inflammatory drugs
(Cummings 2000; Yamada et al. 2005). However, alcohol can be a ‘problem food’ for anyone with an ulcer, or
at risk of an ulcer, and should be avoided or consumed
sparingly. Alcoholic beverages typically increase the
acidity of the stomach and therefore can contribute to
ulcer development or aggravate symptoms of existing
ulcers (NHS Direct 2006).
9.3 Alcohol during pregnancy
The potentially damaging consequences of heavy alcohol intake during pregnancy for the embryo have been
discussed in the scientific literature since the early
1970s, with the most widely recognised consequence
being fetal alcohol syndrome (FAS). FAS is characterised
by reduced birthweight and length, including a small
head size and an underdeveloped brain, a variety of congenital abnormalities, e.g. of the heart or joints, and a
characteristic facial appearance. Affected children are at
a high risk of mental retardation and generally have
stunted physical growth. However, FAS is not the only
outcome of pre-natal alcohol exposure, and it has been
suggested that it can present as a spectrum of disorders.
Fetal alcohol spectrum disorder (FASD) is an umbrella
term to describe a range of effects that can occur due to
the presence of alcohol during the pre-natal stage. FASD
is characterised by the presence of some of the criteria
for FAS and is associated with lesser degrees of harm
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317
from maternal alcohol consumption. It is thought that a
number of factors affect the severity of the condition,
including the amount of alcohol that the fetus is exposed
to, the timing of exposure, patterns of drinking and
genetic factors (although FASD is non-hereditary, genes
may be an important determinant of the degree of the
risk) (Riley & McGee 2005). There is little known about
the long-term development of affected children; however, experts in this field suggest that appropriate early
care and interventions for children with heavy pre-natal
alcohol exposure may improve the mental development
of children born with FAS (Spohr et al. 1993; Riley &
McGee 2005).
Today, there is a growing body of evidence suggesting
that moderate alcohol intake during pregnancy may
have an adverse affect on the fetus, and subsequently the
infant and child, and binge drinking in early pregnancy
may be particularly harmful. For example, alcohol
consumption during pregnancy is associated with an
increased risk of miscarriage, although it is unclear
whether this is related to the quantity consumed or
drinking habits in relation to the stage of pregnancy
(Royal College of Obstetricians and Gynaecologists
2006). Alcohol intake during pregnancy is also believed
to affect fetal growth and development; for example,
using prospectively collected data from more than
31 000 pregnancies, Mills et al. (1984) showed that
those consuming under one drink each day had an odds
ratio of producing a small-for-date newborn of 1.11,
compared with an odds ratio of 1.62 for those drinking
1–2 units/day and 1.96 for those drinking 3–5 units/day.
However, it is unclear how drinking habits in relation to
the stage of pregnancy affect birthweight. One study
showed that among women who continued to drink
more than 2 units/day during the third trimester, 45%
had an infant with a birthweight below the tenth percentile, whereas those who had reduced or discontinued
their alcohol consumption during this period had no
excess of low-birthweight babies (Rossett et al. 1980).
More recently, there have been a number of studies
reporting a possible association between maternal alcohol intake during pregnancy and neurological development of the fetus. For example, Hepper et al. (2005)
found that among pregnant mothers consuming an average of 4.2 units/week, spontaneous startles in fetuses
were higher, compared with those not exposed to alcohol; thus suggesting that alcohol exerts a delaying effect
on the natural decrease in the incidence of spontaneous
startles, and as fetal startles have been linked to brainstem function and central nervous system (CNS) development, they may be an important indicator of delayed
development of the CNS. Earlier studies have found
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R. K. Foster and H. E. Marriott
other effects of mothers’ alcohol intake during pregnancy on the fetus, such as altered breathing movements
(Fox et al. 1978; McLeod et al. 1983), although the significance of these findings is uncertain (Royal College of
Obstetricians and Gynaecologists 2006).
Long-term implications, such as aggressive behaviour
among children whose mothers drank alcohol during
pregnancy, have also been noted (Sood et al. 2001). A
long-term prospective study on pre-natal alcohol intake
and offspring development observed neurobehavioural
effects from the first day of life through to 14 years of
age. The stratified cohort sample of more than 1500
women drank on average one drink per day before
pregnancy and less than one drink per day during midpregnancy. The study found that learning problems
were more commonly observed among children aged
from 7 to 14 years, but problems with attention and
speed of processing information were observed across
the 14-year period. The effects were dose-dependent and
generally without a threshold (Streissguth et al. 1994).
However, other studies considering child developmental
outcomes have found no relationship at approximately
one drink per day during pregnancy (Jacobson et al.
1998, 1994).
From the research undertaken to date, it is not clear
whether the effects of alcohol intake during pregnancy
fit a threshold or dose–response model, or may be
related to the stage of development of the fetus during
exposure. The stage of pregnancy at which the mother
consumes alcohol may be particularly important as the
brain passes through some developmental phases during
which it is more vulnerable to teratogenic agents, such
as alcohol (Coles 1994). The pattern of drinking is also
thought to be important; for example, alcohol may be
less harmful if consumed with a meal, but most harmful
when consumed in excess in one session (Plant et al.
1999). Genetic factors affecting maternal or fetal metabolism, as well as interaction with other harmful behaviours, may also be important (Autti-Rämö 2002).
Furthermore, differences in outcome may be accounted
for by differences in study design and in particular outcome measures. It is therefore an area in which further
research is needed.
Recommendations for intake during pregnancy
There is currently no consensus of opinion across the
world on what is a safe level of alcohol consumption
during pregnancy. In the USA, pregnant women have
been advised not to drink alcoholic beverages and alcohol (US Surgeon General’s Office 2005). Currently, the
Department of Health recommends that women should
drink no more than 1–2 units of alcohol, once or twice
a week at any stage of pregnancy, and should avoid
binge drinking (Department of Health 1995). The Midwives’ Information and Resource Service (2003), supports this advice for pregnant women, and reassures
women that light, infrequent drinking constitutes no
risk to their baby. Most recently, clinical guidance on
antenatal care published in the UK by the National Institute of Clinical Excellence (1997) stated that women
should limit their alcohol consumption to no more than
one standard unit per day, noting that alcohol has an
adverse effect on the fetus.
9.4 Alcohol, bone mineral density and fracture risk
A number of studies have considered the effects of alcohol consumption on bone health in terms of bone mineral
density (BMD) and risk of fracture. In relation to moderate alcohol intake and BMD, some studies indicate a
beneficial effect, while others report no association
(Ganry et al. 2000; Tudor-Locke & McColl 2000; Bainbridge et al. 2004) [see Jugdaohsingh et al. (2006) for a
recent review]. Evidence for a beneficial effect of moderate alcohol intake on bone health has mainly been
observed in studies among post-menopausal women;
however, Jugdaohsingh et al. (2006) suggest that this
may be primarily because such studies have focused on
this subgroup of the population, rather than a specific
protective effect in this group. Proposed mechanisms for
this positive association include a reduction in bone
remodelling via decreases in parathyroid hormone
concentrations and an increase in calcitonin production
(a hormone involved in the metabolism of bone); the production of endogenous hormones, including oestrogen;
the high silicon (which may promote bone formation)
content of beer; and the phenolic constituents of alcoholic beverages (Dickerson et al. 2003; Jugdaohsingh
et al. 2004).
Although studies are indicating a beneficial effect of
moderate alcohol intake on BMD, Jugdaohsingh et al.
(2006) report that there are only limited data suggesting
a decreased risk of fracture. Indeed, some studies report
an increased risk (usually associated with an increase in
alcohol intake) predominately; although the data suggest no overall risk (Iich & Kerstetter 2000; Dickerson
et al. 2003; Holick & Dawson-Hughes 2004;
Jugdaohsingh et al. 2006). The association between
high alcohol intake and fracture risk has been put down
to an increased risk of falls and other types of trauma
(Holick & Dawson-Hughes 2004).
Chronic alcohol abuse has been recognised as a risk
factor for low bone density, associated with osteoporo-
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Alcohol consumption and our health
sis and an increased risk of fractures (Holick & Dawson-Hughes 2004). Once again, the mechanism for these
associations is not clearly understood. However, some
potential factors include: poor nutrition and malabsorption of critical nutrients; alterations in the metabolism
of vitamin D and calcium; potential toxic effects of
excessive alcohol intake on osteoblasts, thus impairing
their function; and an increased risk of falls, due to
reduced co-ordination (discussed in more details in section 6) (Iich & Kerstetter 2000).
9.5 Alcohol and renal dysfunction
Chronic excessive alcohol intake is recognised to
adversely affect the kidneys. However, when considering
moderate alcohol intake and renal function (measuring
creatinine levels and glomerular filtration rates), the
association is less clear. For example, data from the
Nurses’ Health Study cohort have suggested no adverse
effect of alcohol (with intakes up to 60 g/day) on renal
function among women, when compared with nondrinkers (Knight et al. 2003). However, data from the
large US male Physicians’ Health Study cohort found an
inverse relationship between moderate alcohol consumption (7 drinks/week) and the risk of developing
renal dysfunction (Schaeffner et al. 2005). Drinking less
than 2 drinks per day also appeared to be protective of
end-stage renal disease in a case–control study, while
drinking more than 2 drinks per day was associated
with an increased risk (Perneger et al. 1999).
Key points
• Some individuals are susceptible to adverse reactions
to alcohol, although there is no clear cause; it is not
thought that alcohol per se is responsible.
• Although it is well recognised that alcohol is not a
cause of peptic ulcers, it may contribute to ulcer development or aggravate symptoms of existing ulcers.
• Excess alcohol consumption during pregnancy can
put the fetus at risk of fetal alcohol syndrome, while
lesser degrees of harm to the fetus may result in FASD.
• There is also evidence that moderate alcohol consumption during pregnancy may affect the development
of the fetus’s CNS. Aggressive behaviour and delayed
neurobehavioural development have also been reported
among children of mothers who drank in moderation
during pregnancy, along with low birthweight. However, there is no consensus regarding the impact of moderate alcohol intake during pregnancy, to the fetus or to
the child in later life.
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
319
• The most recent advice from an authoritative source
in the UK states that women should limit their alcohol
consumption to no more than one standard unit per day,
noting that alcohol has an adverse effect on the fetus.
• Some studies have reported that moderate alcohol
intake is positively associated with BMD, while others
have shown no effect. Moderate alcohol intake may
have a greater effect on BMD in post-menopausal
women.
• It is unclear whether there is any association between
alcohol intake and risk of fracture, over and above that
due to an increased risk of falls and other types of
trauma.
• Evidence indicates no adverse effect of moderate alcohol intake on renal function, although it is less clear
whether there is a beneficial effect.
10. Alcohol and social issues
Many of the adverse social consequences related to alcohol are linked to drinking alcohol in excess, through
either binge or chronic excessive drinking. It has
recently been recognised that binge drinking has become
popular among teenagers and young adults, and in particular among men, although women’s drinking has
been rising in the past 10 years, and therefore received
more attention from the media (Strategy Unit 2004).
Binge drinking has been defined as consuming double
the daily sensible drinking guidelines (i.e. at least 6 and
8 units per day for women and men, respectively), or in
some cases, drinking until inebriation. It is difficult to
confirm the long-term health effects of binge drinking,
primarily because it is difficult to identify this pattern of
drinking among individuals taking part in epidemiological studies. However, data are available on the economic cost of binge drinking to society, and the personal
costs are easy to identify. For example, alcohol intoxication induces a range of short-term psychological and
psychomotor effects that increase an individual’s risk of
injury, or assault, which subsequently involves the use of
public services, such as police and ambulance. As outlined at the end of this section, the UK government is
taking a population approach to discourage binge
drinking, and this is set out in the Alcohol Harm Reduction Strategy (Strategy Unit 2004), along with ways in
which to manage and help chronic excessive drinkers.
10.1 Short-term psychological and psychomotor
effects of alcohol intake
Consumption of alcohol may result in changes in mood
and emotion, and alcohol intoxication may induce a
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R. K. Foster and H. E. Marriott
Table 5 Effects of specific quantities of alcohol on blood ethanol concentrations and mental function
Number of drinks
Blood alcohol level
Possible effects (mg/100 ml)
1 pint of beer
2 glasses (125 ml) of wine
1 double measure whisky
30
Increased likelihood of having an accident
1.5 pints of beer
3 whiskies
Half a (75 cL) bottle of wine
50
Increased cheerfulness, impaired judgement and loosening of inhibitions
2.5 pints of beer
5 whiskies
5 glasses (125 ml) of wine
80
Loss of driving licence if caught
5 pints of beer
10 whiskies
1 L of wine
150
Loss of self-control, exuberance, quarrelsomeness, slurred speech
6 pints of beer
Half a bottle of spirits
2 bottles of wine
200
Stagger, double vision, loss of memory
0.75 bottles of spirits
400
Sleepiness, oblivion, coma
1 bottle of spirits
500+
Death
Adapted from: Royal College of Physicians (1987).
range of short-term psychological and psychomotor
effects. As table 5 indicates, these may result in
increased aggressive behaviour, increased risk taking
and decreased responsiveness to social expectations.
Therefore, for some individuals, in certain situations the
effects of alcohol consumption, particularly to intoxication, can lead to personal ‘harm’, including accidents,
violence, assault and risky sexual behaviour.
Acute ill health as a result of drinking excessive amounts
of alcohol
Excess alcohol intake can cause short-term adverse
effects to health and well-being, colloquially termed as a
‘hangover’. Although this does not impinge on National
Health Service (NHS) resources, work and normal life
will be disrupted because of fatigue and increased anxiety (Finnigan et al. 1998, 2005; Wiese et al. 2000;
McKinney & Coyle 2004, 2006). The extent to which
excess alcohol will affect psychomotor and cognitive
function is debatable, following inconsistent results
from a number of studies that have explored this topic.
In particular, aviation research has examined the performance of pilots in flight simulators, and found
increased errors on some tasks after consumption of alcohol the night before (Morrow et al. 1990; Taylor et al.
1994). However, other studies that have measured vigilance, dual tasks, including reaction times and probed
memory tasks, found no significant differences between
those who had consumed excess alcohol the night before
and those who had not (Lemon et al. 1993; Finnigan
et al. 1998, 2005). Studies considering executive- or
managerial-type cognitive functions after drinking the
night before, have also been inconsistent (Streufert et al.
1995; Verster et al. 2003; Weissenborn & Duka 2003).
This may be a result of differences between studies, in
terms of the alcohol dosage, test method and specific tests
of performance. However, studies have consistently
found that participants feel tired and anxious after excess
alcohol consumption the night before, and this could
account for poor performance and absenteeism in the
workplace, costing in the region of £6.4 billion per year
in the UK (including absenteeism from alcohol-related
injuries) (Strategy Unit 2003).
Although some research has investigated the implications of excess alcohol consumption on the body, little is
known about the physiology underlying the conditions
(Swift & Davidson 1998; Slutske et al. 2003). To date,
hangover symptoms have been attributed to several factors, including the direct effects of alcohol on the body
(see table 6), the effects of alcohol metabolites and other
ingredients of alcoholic drinks (such as congeners, see
section 6), and the effects of alcohol withdrawal, which
result from compensatory changes in the CNS that take
place in response to heavy consumption of alcohol
(Swift & Davidson 1998).
There is no consensus definition of a hangover and
few published estimates of the incidence of hangovers. A
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Alcohol consumption and our health
321
Table 6 Direct effects of alcohol on the body
Dehydration and electrolyte imbalance: Alcohol is a diuretic and therefore promotes urinary output by inhibiting the release of anti-diuretic hormone (vasopressin).
Reduced levels of anti-diuretic hormone prevent the kidneys from reabsorbing water, and therefore increase urinary output. Meanwhile, other possible
symptoms of excess alcohol intake (e.g. vomiting) can cause loss of body fluids, and result in further dehydration.
Gastrointestinal disturbances: Alcohol directly irritates the stomach, causing inflammation of the stomach lining and delayed stomach emptying, which may contribute
to the abdominal pain, nausea and vomiting sometimes experienced during a hangover.
Low blood glucose: The effect of alcohol consumption and hangover on glucose metabolism is incompletely understood. Alcohol seems to inhibit the availability
of glucose through an insulin-mediated mechanism. This reduction in available glucose can lead to hypoglycaemia, which is thought to contribute to hangover
symptoms, including fatigue, weakness and mood disturbances.
Biological rhythms: Sleep is just one of the biological rhythms adversely affected by alcohol intake, and subsequently accountable for the symptoms of a hangover.
Swift and Davidson (1998) explained the fatigue experienced during a hangover to be the result of the alcohol having a disruptive effect on an individual’s sleep.
The alcohol results in a shorter duration of sleep, and poorer quality, for example by decreasing the time spent in the dreaming state. Furthermore, drinking
time may interrupt sleeping time.
Headaches: Headaches are a common symptom of hangovers. Although the aetiology remains unknown, it is thought that a number of factors contribute to the
onset of a headache resulting from excess alcohol consumption the night before, including several neurotransmitters and hormones.The vasodilation associated
with alcohol intake and dehydration may also be factors.
Source: Swift and Davidson (1998)
review undertaken by Wiese et al. (2000) identified common symptoms of hangover as: headache; poor sense of
overall well-being; diarrhoea; anorexia; tremulousness;
fatigue; and nausea; and defined a hangover as at least
two of these symptoms, occurring after the consumption
and full metabolism of alcohol. Increased sympathetic
nervous system activity, including increased systolic
blood pressure, rapid heartbeat, tremor and sweating,
may also accompany a hangover (Finnigan et al. 2005).
Swift and Davidson (1998) report that hangover
symptoms may be influenced by the type of alcoholic
beverage consumed and the amount drunk, and symptoms usually peak when the blood alcohol concentration returns to zero and may continue for up to
24 hours after that. Overall, the greater the amount and
duration of alcohol consumption, the more likely it is
that several symptoms will occur. However, results from
studies considering this relationship vary and, therefore,
it is difficult to reach a consensus.
Injury as a result of drinking excessive amounts
of alcohol
According to research commissioned by the Strategy
Unit (2003), on any one night 41% of attendees at accident and emergency (A&E) departments tested positive
for alcohol consumption, and 14% were intoxicated.
Furthermore, between midnight and 5 am, 70% of
attendances were alcohol related. Thus, the consumption of alcohol places a significant burden on A&E services. Violent assaults, road traffic accidents, psychiatric
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
emergencies or deliberate self-harm episodes are all
commonly identified reasons for attendance among
those who have consumed alcohol (Strategy Unit 2003).
The interim analytical report from the Strategy Unit
(2003) suggests that about £0.5 billion of A&E costs are
alcohol related; however, this does not take account of
follow-up treatment that individuals may require or hospital admissions, and therefore is only a small proportion of true costs. A number of these cases are a result of
anti-social behaviour, public disorder and violence, thus
creating work for the police, as well as the NHS staff.
10.2 Crime and public disorder as a result of
drinking alcohol
Richardson and Budd (2003) reported that more than
half of alcohol-related violence between strangers and
acquaintances occurs in or around pubs, clubs or discos.
It is not possible to identify/record the causes of such
events, but it is recognised that impaired cognitive skills
may lead to intoxicated individuals misreading social
cues and responding inappropriately to social situations
with ill-treatment of others. The situation may be made
worse as consumption of alcohol results in an increased
probability of aggressive behaviour. Room et al. (2005)
report that this is due to altered messaging through brain
receptors and neurotransmitters, which may also result
in impaired motor skills, causing a reduction in co-ordination, thus resulting in individuals knocking into other
people or causing victims to be less able to defend themselves (Sumner & Parker 1995; Strategy Unit 2003).
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R. K. Foster and H. E. Marriott
In particular, excessive drinking is associated with an
increased risk of partner violence; approximately a third
of incidents of partner violence were committed when
the perpetrator had been drinking alcohol (Strategy Unit
2003). Partner violence is frequently linked to chronic
alcohol misuse; for example, rates of alcohol abuse and
alcohol dependence among perpetrators may be 2–7
times higher than in the general population (Strategy
Unit 2003).
Surveys suggest that alcohol is a factor in more than
30% of city centre arrests. Detainees under the influence
of alcohol also cause problems for custody officers in
terms of noise, hygiene and disruptive behaviour, and
therefore need close supervision. This is reflected in the
increase in costs of £59 to process an alcohol-related
arrestee (as at 2003), compared with an arrestee who
has not been drinking alcohol (Maguire & Nettleton
2003; Strategy Unit 2003), thus emphasising the economic burden of binge drinking on public services. The
overall costs of alcohol-related crime are significant;
Leontaridi (2003) has estimated that £1.7 billion is
spent on alcohol-related offences and a further £30 million is spent on alcohol-specific offences, taking account
only of costs incurred by the police, the Crown Prosecution Service, Magistrates and Crown courts, legal
costs and costs to the prison and probation services.
Particular crimes commonly related to drinking in
excess include drink driving and sexual assaults.
Although drink driving has been declining, along with
the number of casualties from road accidents involving
alcohol, 5% of all road accidents in 2000 and 17% of
deaths were associated with drivers over the legal
alcohol limit. An estimated 85 000 cases of drink driving each year cost crime-related public services £0.5 billion a year (including legal costs) (Strategy Unit 2003).
Fewer cases of alcohol-related sexual assaults are
brought to the attention of the police, than actually take
place (19 000 cases in 2003). Intoxicated victims are less
likely to report their victimisation, and a large number
of victims of sexual attacks are unreported, making the
true burden unclear. Experience suggests that offender
drinking increases the likelihood and severity of victim
injury, and reported alcohol-related sexual assaults are
more likely to occur between people who do not know
each other well, when compared with other sexual
assaults.
10.3 Alcohol-related harms and other public health
issues
Excessive alcohol consumption is also linked to other
public health issues, e.g. sexually transmitted diseases
and unplanned pregnancies, as consumption of alcohol
is recognised to increase the likelihood of unsafe sex
(Cooper 2002; Rassool & Winnington 2003). This
could be because consuming too much alcohol makes it
more difficult to make judgements and assess risks; it
lowers inhibitions and reduces the sense of self-control.
Furthermore, alcohol has also been found to increase
perceived attractiveness of the opposite gender and is
also associated with contexts in which people are more
likely to meet potential sexual partners, such as parties,
pubs and clubs, thus increasing the chance of a sexual
encounter (Alcohol Concern & Drugscope 2002; Jones
et al. 2003; Strategy Unit 2003; Paton 2005).
Alcohol consumption can also be linked to another
prominent public health concern, namely obesity. Obesity is the result of energy intake being higher than
energy expenditure for an extended period of time. As
noted in section 6, alcohol is the second most energydense nutrient and, in most cases, the energy derived
from alcohol is consumed in addition to energy from
food. Therefore, it could be considered that moderate to
heavy alcohol consumption may increase the risk of
obesity. This is discussed in more detail in section 8.
10.4 The economics of alcohol consumption
The total cost of alcohol-related harm was calculated by
the Strategy Unit (2003) at £20 billion per annum.
However, these costs (and all of the costs considered in
this section) are related to the consumption of alcohol in
excess (i.e. through binge drinking and chronic excessive
drinking). The value of the alcoholic drinks market is
more than £30 billion per annum (Strategy Unit 2003),
and it is estimated that in the UK, one million jobs are
linked to the production and sale of alcohol (ONS
2001). Money is also generated from taxes on alcohol
purchases; however, with £20 billion per annum being
spent on dealing with alcohol-related harm, and more
money being spent on prevention efforts, the net profit
for the economy is debatable.
10.5 Population-based initiatives underway to reduce
the incidence of binge drinking
As outlined in section 4, the phenomenon of binge
drinking is not just affecting the UK; all over Europe, the
younger population are drinking more. Like the UK,
other EU governments have undertaken education campaigns to warn people of the risks of drinking in excess
to their personal safety. For example (see figure 7), in
The Netherlands, a confrontational image of an unconscious, partially dressed young girl has been used to
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Alcohol consumption and our health
remind girls of the potential consequences of drinking
too much (Sheldon 2006).
Figure 7 One poster from the Dutch advertising campaign to discourage
drinking in excess. (Source: www.dekaterkomtlater.nl)
A similar type of advertising campaign has been used
in the UK: a cinema advertisement highlighting the
‘Jekyll and Hyde’ effect that binge drinking can have on
women who drink to get drunk was shown in cinemas
across the UK in 2004 (Portman Group 2006). The public health White Paper (Department of Health 2004b)
made a commitment to work with the Portman Group
Figure 8 Poster from the UK advertising campaign to discourage binge
drinking, entitled ‘Jekyll and Hyde’ effect of binge drinking. Reproduced with
kind permission from the Portman Group.
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
323
(http://www.portmangroup.org.uk) to develop a new
information campaign with the aim of cutting down
binge drinking. It is difficult to evaluate the effectiveness
of these types of campaigns, but it is suggested that they
have generally been found to be ineffective (World
Health Organization 2001; Room et al. 2005). The
White Paper also committed to support action by Office
of Communications (Ofcom) to strengthen the rules of
broadcasting, particularly to protect under-18s, based
on the idea that advertising has some influence on young
viewers’ attitudes to drinking (DCMS 2006). Since January 2005, new rules forbid alcohol commercials that
have a strong appeal to under-18s, and prevent adverts
for alcohol that include even subtle links between sex
and drinking (or a brand of alcohol), or drinking and
daring, aggressive, irresponsible or anti-social behaviour (DCMS 2006).
Other government-led initiatives to reduce the
adverse impact that alcohol can have on society include
tougher enforcement measures by the Police and Trading Standards against irresponsible drinkers and vendors who are fuelling anti-social behaviour, including
issuing £40 fixed penalty notices for being drunk and
disorderly, and naming and shaming off-licences, bars
and clubs after conviction of selling to underage drinkers. Such measures were tested for 8 weeks over the
2005 festive season as part of a wider Alcohol Harm
Reduction Strategy for England. It was thought that
such measures would kick-start a culture change where
it will be less acceptable to get drunk and behave in an
anti-social or violent manner (Department of Health
2006a). It is hoped that the option to sell alcohol 24hours-a-day will also make changes to the drinking culture in England and Wales. New licensing laws came
into force in November 2005, superseding those from
1964, with the aim of bringing Britain more in line with
other European countries, to allow for more responsible
drinking and to avoid the rush to make last orders at the
bar. It is hoped that the variation in closing times of
establishments in the same area will also avoid confrontation flashpoints, and therefore prevent crime and disorder and improve public safety (DCMS 2006).
As outlined by the World Health Organization
(2004), the prevention of alcohol-related problems
requires a comprehensive approach, combining preventative policies at a national and local level. Other activities and initiatives to reduce the incidence of harm
caused by excess consumption of alcohol are outlined in
the Alcohol Harm Reduction Strategy for England
(Strategy Unit 2004), including local initiatives, education to children, and liaison and co-operation with the
drinks industry.
324
R. K. Foster and H. E. Marriott
Key points
• Alcohol intoxication, such as through binge drinking,
may induce a range of short-term psychological and psychomotor effects that may cause increased aggressive
behaviour, increased risk taking and decreased responsiveness to social expectations, and may lead to personal
‘harm’, including accidents, violence, assault and risky
sexual behaviour. Consequently, binge drinking places a
significant burden on A&E services and the police.
• Excess alcohol consumption may also result in a
‘hangover’ that disrupts normal life, due to symptoms of
fatigue and increased anxiety, and has economic consequences in the workplace through poor performance or
absenteeism. The true extent to which a hangover can
affect an individual’s performance, including psychomotor, recognition and managerial skills, is still being
debated.
• Common symptoms of a hangover are: headache;
poor sense of overall well-being; diarrhoea; anorexia;
tremors; fatigue; and nausea. Hangover symptoms have
been attributed to several factors, including: dehydration and electrolyte imbalance; gastrointestinal disturbances; low blood glucose; and disruption to normal
biological rhythms.
• Binge drinking is also associated with an increased
risk of public health issues, including sexually transmitted diseases and unplanned pregnancies.
• Although the cost of binge drinking in terms of longterm health has yet to be established, the significant economic cost is well recognised.
• A number of population-based initiatives are underway to try and reduce the incidence of binge drinking.
These include: advertising campaigns; changes to alcohol advertising regulations; and changes to pub licensing regulations.
11. Conclusions
Alcohol has been produced for thousands of years, via
the anaerobic fermentation of sugars by yeast, and
involves glucose molecules (C6H12O6) being broken
down to yield ethanol (C2H5OH), carbon dioxide (CO2)
and energy. Alcoholic beverages primarily consist of
alcohol and carbohydrate, and offer few other nutrients;
yet per gram, alcohol is the second highest source of
energy of all the macronutrients, therefore alcoholic
drinks make a notable contribution to energy intakes.
Fortunately though, when consumed in moderation,
alcohol does not seem to interfere with the absorption
and metabolism of nutrients and, therefore, in moderation can be part of a healthy, balanced diet. This is par-
ticularly important, as more than 90% of adults in
Britain drink alcohol (Strategy Unit 2004).
For the majority of people who drink alcohol, it is
associated with pleasure, socialising and relaxing
(MORI 2000). When consumed in moderate amounts, it
is an accepted element of a healthy diet and lifestyle,
with few adverse effects to nutritional health or risk of
disease, and possibly some benefits. Guidelines for sensible drinking have been set by the UK government, and
take account of the risks to health and society. The
guidelines are 3–4 units (24–32 g) a day or less for men,
and 2–3 units (16–24 g) a day or less for women, which
are fairly similar to those of other countries.
The UK has an overall alcohol intake close to that of
the European average. Half of the adult UK population
are classified as low to moderate drinkers. Despite high
and very high drinkers being a minority, evidence from
the GHS suggests that this figure is growing. This is of
concern to public health professionals, as alcohol poses
a considerable threat to health if consumed in excess.
Unfortunately, it is all too easy to consume in excess;
humans lack biological curbs on alcohol intake, and the
biological effects of alcohol consumption increasingly
impair the capacity for judgement about how much we
should consume. Furthermore, the effects of excess consumption (i.e. the hangover) are too far removed in time
from the triggering behaviour, to act as conditioning.
Taking these factors into account, it is not surprising
that many people drink until they ‘get drunk’, or binge
drink. Binge drinking is a common phenomenon in the
UK, particularly among younger people, whereby violence and accidents pose a greater threat to health and
well-being, and are the main cause of alcohol-related
mortality. The ‘older’ binge drinking population are at a
higher risk of cardiovascular death, such as a stroke or
sudden cardiac death.
Individuals who do not necessarily binge drink but
drink more than the government-recommended limits
on a daily basis (i.e. more than 3 drinks a day for men,
and 2 drinks a day for women) are also putting themselves at an increased risk of chronic conditions, such as
CVD, high blood pressure, diabetes and weight gain.
Alternatively, light to moderate alcohol consumption
(i.e. consuming alcohol in line with the recommendations) can reduce the risk of these diseases, with the
most benefits being seen in men aged over 55 years and
post-menopausal women. However, there is an inverse
association between alcohol intake and risk of cancer,
and for some cancers, such as breast cancer, just one
drink a day can increase an individual’s risk by about
7%. For younger people, the benefits of alcohol may be
outweighed by the increased risk of other diseases (e.g.
© 2006 British Nutrition Foundation Nutrition Bulletin, 31, 286–331
Alcohol consumption and our health
alcohol-related cancers, liver cirrhosis) and increased
risk of violence and accidents.
Looking at alcohol consumption more holistically, it
provides a focus for social gatherings and relaxation,
particularly for young adults, and therefore assists in
integration and social development. However, when
consumed in excess, it can accentuate emotions and may
result in aggressive behaviour, which poses another risk.
Given the current levels of intake and, in particular, the
rise in binge drinking, action is required to encourage a
shift in the drinking culture, to discourage drinking in
excess. Targeted publicity of the potential harms of
excess drinking is already underway, although farreaching dissemination is essential to ensure that this is
effective.
Acknowledgements
This briefing paper has been written by Rebecca Foster
and Helen Marriott. The British Nutrition Foundation
(BNF) wishes to thank the members of the Foundation’s
Scientific Advisory and Industrial Scientists Committees
who have helped to shape the contents of this briefing
paper. The BNF also wishes to thank Dr Gail Golberg
and Professor Victor Preedy for their helpful comments.
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