Alcohol and food - Centre for Public Health

Michela Morleo Mark A. Bellis Clare Perkins Kerin L. Hannon Kirstie Clegg Penny A. Cook
January 2010
Foreword by Dr Ruth Hussey OBE
Obesity and the use of alcohol are two of the major threats to the public’s health.
Both are linked to cancer, heart disease and a variety of other major killers that
prematurely end many people’s lives and create years of poor health. All too
often we address these issues in silos with expertise in food and in alcohol but
with the overlap between the two being poorly understood by professionals and
consequently under-utilised in the pursuit of improving the public’s health. Little
professional understanding means the public are not in possession of the
information they need to make healthy choices about food and alcohol.
Encouraged by advertisements and marketing, consumers can adopt poor food and high alcohol
diets without realising both will contribute to their risks of long term disease. Individuals may also skip
food in order to get drunk more quickly or try to eat certain food types in order to delay inebriation
but have little understanding of the health consequences of either action. It is essential that we
consider food and alcohol together; improve our understanding of the substantial overlaps between
these two issues; and ensure the public are aware of the dangers and benefits that food and alcohol
together represent. This report is a first step in this process and, while it is far from comprehensive,
outlines much shared territory which we need to understand. I hope people working on food, alcohol
and generic public health issues find it of interest and that it leads to new opportunities to tackle the
burden of ill health created by the widespread over consumption of food and drink.
Dr Ruth Hussey, OBE
Regional Director of Public Health / Senior Medical Director for NHS North West and DH North West
Acknowledgements
The authors would like to thank the following individuals for their help and guidance during the
compiling of this document: Jane Thomas at Liverpool Primary Care Trust; Allan Hackett at the
Centre for Tourism, Consumer and Food Studies, Liverpool John Moores University; and Zara
Anderson, Gill Elliott, Karen Hughes, Penny Phillips-Howard and Lee Tisdall at the Centre for Public
Health, Liverpool John Moores University.
Contents
Overview
page 2
1.
Introduction
page 3
2.
Alcohol as a food
page 5
3.
Combined consumption - the positive health effects?
page 10
4.
Harms related to both food and alcohol
page 12
5.
Interventions for promoting healthy food and alcohol consumption
page 17
6.
Discussion
page 23
7.
References
page 25
1
Overview
• In the UK, food and alcohol are often viewed
as separate issues despite many of the
biggest health challenges facing the UK
relating to both. Public and professional
understanding of the links between food and
alcohol are generally poorly developed.
Inconsistent and conflicting messages can
inevitably influence choices people make
about consumption.
well as additives and other ingredients being
consumed.
• In the absence of information on calories
and other nutrient content of alcohol
products, myths about the benefits of
drinking alcohol remain. For instance, it is
widely reported that stout has a high iron
content although it may take six pints
to reach even the basic recommended daily
allowance of iron.
• Two large glasses of white wine equate to
almost a fifth of a woman’s daily calorie
requirements whilst three pints of lager
equate to about a fifth of a man’s. However,
public awareness of the calorie content of
alcohol is relatively low.
• The cardio-protective effects of alcohol when
linked with fatty food consumption are poorly
communicated. Evidence suggests that
drinking less than one unit a day will provide
protective effects and drinking more does
not significantly increase protection. In fact,
whether such protection occurs at all is still
debated.
• Drinking alcohol can affect levels of hunger
and food preferences. Even moderate
alcohol consumption may increase
preferences for fatty and high sugar foods,
with such cravings contributing to risks of
obesity.
Box 1: Government recommendations for
energy intake and alcohol consumption
• Lower risk drinking for adults is defined as
no more than 2-3 units (1 unit = 10 mls of
pure alcohol; see Table 1) per day for
women, and no more than 3-4 units of
alcohol per day for men.[2] One glass of
wine would be approximately two to three
units (depending on its volume and
strength), or one and a half to two pints of
lager for a man. Having a few days a week
where alcohol is not consumed is also
recommended.i
• Many people have multiple behavioural
health risks linked to eating, low physical
activity and alcohol consumption. Together
these are likely to reinforce and accelerate
each other’s contributions to morbidity. In
fact, a number of major diseases including
cancer, cardiovascular and liver disease
have strong links to both unhealthy eating
patterns and alcohol misuse. However,
links between these behaviours are poorly
understood.
• The NHS recommends an average daily
calorie intake of 2,000 per day for women
and 2,500 for men.ii Typically, a beef
casserole with mash and vegetables would
equate to approximately 500 calories.iii
• Failure to recognise alcohol as a food
(together with resistance from the alcohol
industry) has meant that most alcoholic
drinks are exempt from normal food labelling
requirements. Consumers are, therefore,
unaware of the calorie content of drinks as
i
ii
iii
See http://www.nhs.uk/chq/Pages/846.aspx?CategoryID=87&SubCategoryID=87.
See http://www.nhs.uk/chq/Pages/1126.aspx?CategoryID=51&SubCategoryID=165.
See http://www.nhs.uk/Livewell/Loseweight/Pages/Healthyfoodswaps.aspx.
2
• Eating food before or while drinking alcohol
appears to reduce the rate of alcohol
absorption into the bloodstream, potentially
reducing the immediate risk of drunkenness.
However, such information, rather than
being used by nightlife patrons to reduce
drunkenness, is often used to increase
inebriation through fasting before drinking via
an Eating is Cheating attitude.
alcohol-related violence and generally
provide high fat and calorie foods.
• Off trade measures to combine alcohol and
food typically focus on increasing sales of
both. Offers such as a meal for two and a
bottle of wine for £10 can suggest half a
bottle of wine is a safe and acceptable
amount to consume with a meal at night when consumption at such levels would
actually mean exceeding the recommended
daily maximums.
• Coffee consumption appears to reduce the
risk of developing alcoholic liver cirrhosis in
drinkers. However, both coffee and alcohol
may contribute to hypertensive disease and
lowering alcohol consumption is a safer and
more effective way of reducing risk.
• UK policy must address the links between
alcohol and food in order to maximise the
effectiveness of public health responses and
enable people to make better informed
choices about eating and drinking. We
urgently need to move away from seeing
alcohol as a means to achieve inebriation to
regarding it as an accompaniment to food
with both being consumed in moderation.
• Those on calorie controlled diets may
dangerously reduce nutritious food intake to
save calories that they wish to use for
alcohol consumption. This has been termed
drunkorexia.
• The roots of food and alcohol problems have
been linked to similar early life experiences.
Poor education has been linked to low levels
of activity, obesity and alcohol consumption
problems in later life. Further, the ACE
(Adverse Childhood Experiences) study has
linked negative childhood experiences with
early onset of alcohol,[1] higher levels of
alcohol abuse as an adult and risk of obesity.
1 Introduction
• Nightlife settings provide some key
challenges for tackling food and alcohol
issues. Although tapas-like food in bars may
help reduce the rate at which individuals
become intoxicated, the UK's typical
provision of salty snacks (crisps and nuts)
may (deliberately or otherwise) increase thirst
and consequently alcohol consumption.
Alcohol has been consumed for millennia both
as a catalyst for social enjoyment at meals,[3]
and as part of daily nutrition.[4] Until the
seventeenth century, wine was the only storable
drink as water was often unsafe and ale
deteriorated quickly.[5] However, wine was an
unaffordable luxury for most, leaving ale as one
of the only safe drinks available to the masses
until the widespread establishment of clean
public water systems.
• The design of many town and city centre
bars is not conducive to the sale of more
substantive food products or more relaxed
drinking rates (with an absence of tables and
seating). Fast food outlets, which can offer
more substantive food, can be the focus of
3
‘It [wine] makes the perfect drink with food,
adding its own seasoning, cutting the richness
of fat, making meat seem more tender and
washing down dry pulses and unleavened
bread without distending the belly.’
intrinsically linked to local culture. For many,
alcohol is considered as a means to intoxication
with food sometimes avoided either to hasten
inebriation[15,16] or limit calorie intake whilst
drinking.[16] There is no equivalent history of
tapas provision in UK bars and it has even been
suggested that the salty snacks (e.g. nuts and
crisps) or meals frequently on sale in these
establishments are a method of increasing
thirst,[17] and therefore sales. However, some
pubs are now allowing takeaways to be brought
into and eaten in the pub primarily in an attempt
to retain custom.[18]
Johnson: The story of wine (1991; p: 5[3])
Patterns of consumption of food and drink
should be considered as part of a healthy diet
and lifestyle. Yet today, in Europe alone, there
are marked differences in the extent to which
alcohol and food are viewed as separate issues
or considered together as an integral part of diet
and lifestyle. The ‘Mediterranean’ approach to
eating and drinking (which is caricatured as
moderate
alcohol
consumption;
low
consumption of meat and meat products; and
high consumption of vegetables, fruits, nuts and
olive oil) has been seen as an ideal for a healthier
society [6,7] and is associated with reduced
mortality.[8] Consumption of non-processed
Mediterranean foods including olive oil, fish,
fresh fruit and vegetables has contributed to
lower levels of chronic illnesses such as heart
disease among older populations.[9,10] Alcohol
may also play a role. In general, European wines
have lower alcohol contents than those from the
New World,[11] and their complex taste and
higher tannin levels may encourage
consumption
with
food.[12]
Combined
consumption of alcohol and food is customary
in the Mediterranean[6,13,14] and in Spain,
licensed premises have traditionally served small
plates of food (tapas) with alcoholic drinks to
avoid the effects of consumption on an empty
stomach.
The Government strategy for improving health
and reducing health inequalities focuses on the
wider determinants of health and seeks to
address food and alcohol behaviour, along with
physical activity and smoking. Despite
recognition that these behaviours are
inextricably linked, the relevant policies and
interventions to improve health are often not.
For example, national policies for reducing
cancer and coronary heart disease either handle
alcohol and obesity as separate issues [19] or
mention them as contributory factors but do not
suggest how prevention could follow a more
combined approach.[20, 21] Equally, alcohol policy
does not address the links with other foods.[2] In
order to examine the public health potential in
the UK for utilising intelligence on the
relationship between food and alcohol, this
review explores:
• how consumption of food and consumption
of alcohol are interrelated;
• the benefits and consequences of combined
consumption;
In the United Kingdom, the definition of food
encompasses all foodiv and drink products
including those containing alcohol, and thus
alcohol should be subject to basic food
regulations. However, food and alcohol are often
viewed as being separate issues by individuals,
health professionals and policy-makers, and are
not considered in the context of a lifestyle
iv
• the relationship between harms associated
with alcohol consumption and unhealthy
eating; and
• interventions that aim to promote both
healthy eating and lower risk alcohol
consumption.
“Food” is defined as any substance or product, whether processed, partially processed or unprocessed, intended to be, or reasonably expected to be, ingested by humans
(see http://www.food.gov.uk/consultations/ukwideconsults/2004/foodsafetyuk2004).
4
2 Alcohol as a food
2.1
Box 2: Some factors affecting the speed
of alcohol processing in the body
1. Weight: On average the liver processes
around 0.1g of alcohol per hour per kilogram of
body weight.[25] Thus, an average male of
83.6kg [26] would metabolise 8.4g of alcohol per
hour (equivalent to approximately one unit).
Processing alcohol in the body
The process of breaking down or metabolising
most food products (including alcohol) begins in
the stomach but occurs throughout the
digestive system until items are absorbed.
Whilst the bloodstream exposes all tissues and
organs to the alcohol absorbed, the liver is
disproportionately exposed as it receives blood
straight from the digestive tract.[22] A whole
range of factors affect the rate of metabolism of
alcohol such as body weight and food
consumed (see Box 2). Thus, certain individuals
may be more vulnerable to excessive
consumption of alcohol and related harms, and
the propensity for inebriation is not static.
2. Tolerance: Heavier drinkers process alcohol
more quickly than occasional drinkers [22, 27, 28] as
a drinker’s liver develops more enzymes for the
destruction of alcohol. However, ultimately this
can also damage the liver.[29]
3. Gender: Women are affected more by
alcohol than men partly as a result of body size
but also because they have lower levels of
enzyme activity for alcohol breakdown.[22, 30]
Thus, men may eliminate alcohol faster than
women when comparing breathalyser results.[31]
Those who drink excessively may suffer from
hangovers as alcohol is metabolised, with the
suggestion that hangovers may occur when the
body’s blood alcohol concentration (BAC)
returns to around zero (although empirical
evidence for this is not provided).[23] Symptoms
include: drowsiness, lack of concentration,
dizziness, nausea, anxiety and gastro-intestinal
complaints. In extreme cases, binge drinkers
may suffer hypoglycaemia (i.e. low blood
glucose).
The
precise
mechanisms
underpinning hangovers are still unknown.
However, dehydration, and reduced sleep
duration and quality may be involved, and
factors such as food consumption may alleviate
symptoms.[23, 24]
4. Age: Elderly people process alcohol more
slowly due to a reduction in the effectiveness of
the liver, and alcohol processing can slow
further when individuals are on certain
medications.[32]
5. Liver damage: The health of an individual’s
liver affects alcohol processing as alcoholinduced liver damage can disrupt normal
metabolism.[33]
6. Food consumption: Food in the stomach
reduces the rate at which alcohol passes
through the stomach to the small intestine
where absorption is fastest (Section 3.4.5).[22]
7. Type of alcohol: Drinks aerated with
carbon dioxide (champagne or those with soda)
are absorbed into the blood more quickly.[22] The
rate of absorption also increases with alcoholic
strength from 10% to 20% ABV (alcohol by
volume).[34] Up to 10% ABV, alcohol products
may be insufficient to stimulate quick
absorption. After 20% ABV, the rate of
absorption declines due to increased secretion
of stomach mucus in response to toxicity.[34]
5
2.2
Table 1). Exact calorific content will vary with
alcoholic strength and between brands, but with
no requirement for alcohol producers to place
calorie information on their products (see
Section 5.2.2), accurate assessment by
consumers is impossible. This may explain why
levels of awareness of the calorie content of
drinks are relatively low: in a survey of 1,954
drinkers in England, two fifths (42%) of women
did not know that the calorie contents of a glass
of white wine could equate to a bag of crisps
and two fifths (40%) of males were unaware that
a pint of lager can have a similar number of
calories to a sausage roll.[36]
Alcohol and nutrition
Historically, drinks such as beer were viewed as
highly nutritious but changes in large scale
manufacturing
(for
example,
longer
fermentation) have reduced nutritional content;
although no specific details are available as to
the extent of this.[4] Typically, many of today’s
alcoholic drinks are highly calorific but provide
relatively little other nutritional value (Table 1). A
gram of alcohol provides 7.1 kilocalories (kcal),
nearly as much as a gram of fat (9.1 kcal) and
considerably more than protein or carbohydrate
(4.1 kcal/gram).[35] Regular and binge drinkers
can accumulate considerable quantities of
calories from alcohol.
2.2.1 Alcohol is good for you?
A female adult consuming two large glasses
(250mls) of white wine (6.2 units) consumes 375
kcal or 18.8% of her daily energy requirement,
whilst a male drinking three pints of lager (8.4
units) could have consumed a fifth (19.8%) of
his daily energy requirement (494 kcal; Box 1;
Table 1:
Despite relatively low nutritional value (Table 1),
some alcohol products have been associated
with good health. In the earlier part of the
twentieth century, a particular stoutv (Guinness)
was advertised as being “good for you”.vi
Pregnant women, nursing mothers, blood
Approximate nutritional and alcohol content of selected drinks*
Low alcohol
Lager (568ml
lager (568ml /
/ one pint)
one pint)
568
568
165
57
689
238
23
68
86
9
Spirits: gin
and vodka
(25 ml)
15
56
232
0
0
Fresh orange
Coca Cola
juice (250ml)
(250ml)
***
225
250
95
98
397
408
5
20
24
26
Red wine
(250ml)
White wine
(250ml)
Weight (g)
Energy (kcal)
Energy (KJ)
Sodium (mg)
Carbohydrate (g)
225
170
711
25
0
240
188
785
53
9
Protein (g)
Fat (g)
Vitamin B1 /
Thiamine (mg)
Vitamin B3 /
Niacin (mg)
0.6
0
0.3
0
4
0
11
0
0
0
3
0
0
0
0
0
0
0
0
0
0
0.2
0
0
0.2
0.2
1.9
2.8
0
0.5
0
0
0
0
0.1
0.2
0
0.1
0
0
N/A
N/A
N/A
N/A
N/A
N/A
Vitamin B6 /
Pyridoxine (mg)
Number of units
Energy (kcal)
per unit
3.3 (for wine 3.1 (for wine
0.9 (for spirits
2.8 (for lager 1.1 (for lager
at 13.2%
at 12.3%
at 37.5%
at 5% ABV**) at 2% ABV**)
ABV**)
ABV**)
ABV)
51.5
60.5
58.8
51.6
61.7
Diet cola
(250ml)
250
3
10
13
0
* Individual drinks were weighed in order to calculate nutritional contents through Microdiet Plus.
** Alcohol by volume (ABV) is the percentage of alcohol content in a beverage, by volume. Average strength for wine was calculated in Table 2. Average strengths for lager
and spirits were calculated by Drinkaware.com.
*** Orange juice also contains other vitamins such as vitamin C; however this table has been limited to specific types of vitamin B for brevity.
Source: Microdiet Plus for Windows (2001); Drinkaware.com.
v
vi
Stouts are dark beers made using roasted malt.
See http://www2.guinness.com/en-gb/Pages/Adsdetails.aspx?adid=26 for examples of historical Guinness adverts.
6
donors and post-operative patients were
advised to drink it because of its supposed high
iron content.[37] In fact, it would take six pints of
stout to obtain the recommended daily
allowance for males.vii Other foods, such as
kidney beans, are much higher in iron.
• Quantity consumed: Any such cardioprotective effects are established at drinking
quantities below a unit a day and do not
appear to increase significantly at higher
levels of consumption.[41, 44]
• Other conditions: For many drinkers,
cardiovascular health gains will be cancelled
out because of the negative impacts of
alcohol consumption, even at lower levels,
on the risk of conditions such as
cancers (see Section 4).[45]
Red wine has also been hypothesised as having
beneficial effects. Compounds found in red wine
such as polyphenols (e.g. Resveratrol) have
been ascribed cardiovascular health benefits.[39]
However, the levels of resveratrol that would
need to be routinely consumed in order to affect
cardiovascular health would be vast.[40]
• Dietary factors: See Section 3.1.
2.3
It is hard to see how drinking, or even swimming
in, red wine can provide sufficient resveratrol to
reach protective levels.
There are strong associations between
increased alcohol consumption and elevated
body weight, particularly in men. Research in
Spain (n=15,630) showed a linear relationship
between Body Mass Index (BMI)viii and alcohol
for males, whereby increasing alcohol
consumption was associated with obesity
(p<0.001; the criteria for obesity were not
specified).[41] In fact, alcohol consumption can
contribute to weight gain directly through its
involvement in overall energy intake (see Section
2.2). The links between alcohol and weight are
highlighted below:
Corder: The wine diet (2007; p.37 [40])
More recently, procyanidins (which are also
found in foods including chocolate, and fruits
such as cranberries and apples) have been
suggested as being the protective substance.[40]
However, recent research in Spain indicates that
red wine has no cardio-protective abilities above
those of any other alcoholic drink.[41] In fact, the
much celebrated relationship between alcohol
consumption and lower cardiovascular disease
is also complicated by a variety of factors which
suggest the benefits have been exaggerated if
not erroneous:
• Levels of alcohol consumption: High
levels and more intense patterns of drinking
are associated with indicators of obesity.[4951]ix
For example, in a study of 23 pairs of
identical twins (who were discordant for
obesity), the obese twin was more likely to
report overconsuming items such as alcohol
compared with their lean twin (95.7%
compared with 17.4% respectively;
p<0.05).[50] However, some studies suggest
moderate alcohol consumption can be
associated with weight maintenance or even
• Lifetime consumption: Individuals who are
ill from conditions such as cardiovascular
disease may give up alcohol but be classified
as non-drinkers, thus creating the
impression that abstinence carries a higher
risk
to
health
than
drinking
in
[41-43]
moderation.
When such individuals
are accounted for appropriately, cardiac
protection associated with moderate alcohol
consumption diminishes.
vii
viii
ix
Alcohol and weight
Reports on the iron content of stout vary widely (from 0.11mg per pint to 1.1) and Microdiet does not provide estimates for iron contents. However, if we take the most
generous report found, one pint of stout would contain 1.1mg of iron.[37] The estimated average daily iron requirement for an adult male in the UK is 6.7mg.[38] For women
(18-50 years), the average daily requirement is 11.4 mg, and 6.7mg for older women.
BMI can be used to calculate likelihood of an individual being underweight or overweight. Weight in kilograms is divided by height in metres squared. Having a BMI of
less than 20 is seen as being underweight, and a BMI of over 30 is seen as obese.[46,47] However, BMI does not account for muscularity and is not appropriate for
some ethnic groups, young people or pregnant women.[48] See http://www.nutrition.org.uk/home.asp?siteId=43&sectionId=408&parentSection=321.
Heavy drinkers are here defined as those consuming at least 21 units per week, and alcohol consumption levels are compared with central adiposity indicators (such as
BMI).[49] More intense drinking patterns are where individuals do not necessarily drink everyday, but drink in much larger quantities when drinking does occur,[51] (such
as binge drinkers). Dorn et al. compared alcohol consumption with abdominal height - the height of an individual’s abdomen when they are lying down.[51]
7
weight loss.[51,52] For example, daily
consumption of less than one drinkx per
drinking day was inversely associated with
obesity in New York (USA; n=2,343),
particularly for women and wine consumers
(who were more likely to be women).[51]
However, confounding factors may be
present. Firstly, grape juice can have similar
effects.[53]xi Secondly, non-drinkers may be
more likely to report higher intake of sucrose,
chocolate and candy (or sweets), the latter
two being particularly the case for
women.[52]xii Thus, lower levels of snacking
amongst moderate drinkers may reduce
their risk of weight gain when compared with
non-drinkers.
a calorie limit.[16] This has been labelled
drunkorexia.[60] Further, those concerned
about their weight may choose only to drink
when they intend to become drunk, as doing
otherwise could waste allotted calories.[16]
“Alcohol has calories. If you plan on drinking,
plan accordingly, even if that means skipping a
meal (or two).”
Joel: Losing weight: tips and tricks (2006).[57]
• Alcohol consumption and eating
disorders: Misuse of alcohol can be
associated with eating disorders: a US
survey of over 9,200 adults showed that a
quarter of those suffering from anorexia
nervosa and a third of bulimia sufferers
reported alcohol abuse or dependence.[61]xiii
• Type of alcoholic drink: Beer consumption
has typically been associated with weight
gain more than, for instance, wine [54] and
has
often
been
associated
with
gynecomastia (abnormal development of
male mammary glands). Higher levels of
gynecomastia have been found in chronic
alcoholics (a study in India compared 200
alcoholics with matched controls).[55]
However, not all studies agree that beer in
particular is linked with either obesity or
gynecomastia.[56] Instead, simply more
intense or higher levels of alcohol
consumption may contribute to risks.[51]
“A female friend of mine would skip meals
before going out and partying, she was really
anorexic but she used to drink a lot.”
Samantha, young female, USA.[16]
• Alcohol consumption and fatigue:
Increased levels of intoxication are
associated with feelings of lethargy, at least
in young people.[62] This may affect
motivations for physical activity and, if this
occurs regularly, can impact on weight
maintenance.
2.4
• Substitution: Those dependent on alcohol
may substitute alcohol for food, meaning
that heavy drinking can be further
complicated by malnutrition.[58] Other groups
at risk of substitution include those suffering
economic deprivation (for example, in South
Africa[59]) and those on calorie controlled
diets. Here, women in particular may
substitute alcohol-derived energy for food in
order to consume alcohol and remain within
x
xi
xii
xiii
The impact of increased
strength of drinks
In Ancient Rome and Greece, it was considered
“barbaric” to consume undiluted wine.[4] Yet,
today this is the norm in the UK and the strength
of many alcoholic drinks has increased in recent
years, particularly wine [63] due, in part, to the
use of riper fruits.[64,65] Typically, wines are
approximately 12.8%ABV with higher levels of
alcohol in red wine and in wines produced
outside Europe (Table 2).[11] However, table wine
Participants were provided with examples of containers typically used for alcohol and asked to identify potential beverage size for usual drinks.[51] Ethanol grams were
then calculated by using the factors: wine 0.121, wine coolers 0.040, beer 0.045 and liquor (or spirits) 0.409.
The effects of a diet where 10% of energy was derived from grape juice was compared against a diet where 10% of energy was derived from white wine.[53]
Researchers studied questionnaires from 89,538 female, married, registered nurses involved in the Nurses’ Health Study in 1976 and 48,493 males aged 40-75 years
involved in the Health Professionals Follow-up Study in 1986.[52]
Diagnoses were categorised through the World Health Organization Composite International Diagnostic Interview (CIDI), which generates diagnoses according to the ICD10 (International Classification of Diseases) and the DSM-IV (Diagnostic and Statistical Manual of Mental Disorders.[61]
8
can be as strong as 15%ABV whilst high
strength lagers are available at 9%ABV
(equivalent to lower strength wines). Quantities
of alcohol consumed have also increased
through a move towards larger measures. For
example, wine glasses of 175ml or 250ml are
served rather than 125ml.[66]xiv Because of such
changes, national calculations of unit
consumption have been adjusted to provide a
Table 2:
more accurate understanding of quantities
consumed.[68] However, little information is
available on how calorific content has altered
with higher alcohol consumption. Certainly, little
or no efforts have been made to communicate
any changes to the public and most available
information does not provide details of calorific
or other content (e.g. sugar) other than the
alcoholic strength of the drink.
Strength of wine by region of origin and type of wine*
Red wine
Outside
Europe
Total
Overall (red and white wine)
Mean %ABV
Mean number of
units per 75 cl
bottle
Mean %ABV
Mean number of
units per 75 cl
bottle
Mean %ABV
Mean number of
units per 75 cl
bottle
(95%CI)
(95%CI)
(95%CI)
(95%CI)
(95%CI)
(95%CI)
12.8
9.6
11.8
8.8
12.3
9.2
(12.7-13.0)
(9.5-9.7)
(11.4-12.2)
(8.5-9.1)
(12.0-12.5)
(9.0-9.4)
13.5
10.1
12.8
9.6
13.2
9.9
(13.3-13.7)
(10.0-10.3)
(12.6-13.0)
(9.5-9.8)
(13.0-13.3)
(9.8-10.0)
13.2
9.9
12.3
9.2
12.8
9.6
(13.0-13.3)
(9.8-10.0)
(12.1-12.5)
(9.1-9.4)
(12.6-12.9)
(9.5-9.7)
Region
Europe
White wine
* A survey of 271 different types of red and white wine (75cl bottles) was conducted in October 2008, through Tesco’s online shopping facility. This table presents their
mean %ABV and 95% confidence intervals (95%CI). The differences in ABV between both regions of origin and type of wine (red or white) were statistically significant
(p<0.001). However, it should be noted that the UK guide to European Union wine regulations states that the percentage ABV provided can be within 0.8% of the actual
strength and so the accuracy of the details provided it is not known.xv
2.5
Patterns of combined
consumption
USA (n=165,057) has shown that higher levels
of consumption are associated with elevated
BMI. Here, those who consumed an average of
one drinkxvi per drinking day had a mean BMI of
25.8 (95% confidence interval (95%CI): 25.725.9) compared with those who drank four or
more who had a mean BMI of 26.8 (95%CI:
26.7-27.0).[70]
Consuming food before drinking alcohol can
slow the absorption of alcohol into the
bloodstream and subsequent levels of
intoxication (see Box 2). Conversely, alcohol
consumption (at 24g or three units) has been
linked to higher levels of food consumption, with
hunger potentially being increased up to six
hours after drinking compared with baseline
(although study sizes are small).[69] Low levels of
alcohol consumption (for instance, 8g or one
unit) do not appear to promote increased food
intake,[69] supporting findings that moderate
drinking (as part of an overall healthy lifestyle)
may not necessarily result in weight gain.
However, a cross-sectional national study in the
2.5.1 Combined consumption in
childhood
Childhood obesity may contribute towards early
alcohol use. In a study of two nationally
representative samples of girls in the USA,[71]xvii
higher relative weight was associated with
increased likelihood of having reached
menarche earlier while early pubertal maturation
xiv
There has been a move away from the 125ml glasses in favour of the larger glass sizes and purchasing by the bottle (reported in: [67]).
See http://www.food.gov.uk/multimedia/pdfs/euwineregs.pdf.
xvi
The term “drink” was not explicitly defined by the paper.[70] Participants were asked the number of drinks they had consumed in a given time period.
xvii
Data were extracted from cycles II and III of the National Health Examination Survey (NHES; 1963-70) and the Third National Health and Nutrition Examination Survey
(NHANES III; 1988-1994).[71] Data from the NHES cycles related to girls aged 10 years old and above at last birthday and from girls aged 12-15 at last birthday
respectively were used. For NHANES III, data from individuals aged 10-15 years were used. Combined, full data existed for 4,598 individuals.
xv
9
predicted alcohol use disorders (in 1,420 males
and females aged 9-13 years, Western North
California[72]). Recent studies in the UK have also
shown links between childhood obesity, early
puberty and subsequent early alcohol
consumption and drunkenness.[73]
Importantly, as studies have better controlled
for the differences between drinkers and
non-drinkers, the protective effects of
moderate alcohol consumption have
diminished.[44]
3.2
Historically, alcohol (especially in the form of
wine) was seen as the only safe and storable
drink[5] with consumption reducing an
individual's chances of contracting gastrointestinal infections that are associated with
unclean water. Even today, alcohol consumption
can be associated with a small reduction in the
risk of food poisoning.[79-81] For instance in
Spain, 51 people were infected by an acute
salmonella outbreak at an event.[79] Compared
with non-drinkers, those who drank up to 40g
(up to five units) at the event were 23% less
likely to have been affected and those who had
consumed more than this were 43% less likely.
In a similar incident, beverages with an alcoholic
content up to 10%ABV appeared to offer the
most protection compared with non-alcoholic
drinks and those over 10%ABV.[82] There is a
lack of understanding as to how this occurs;
although removal of poison through a diuretic
effect [83] and facilitating the eradication of the
organism in the gastro-intestinal tract have both
been postulated as likely mechanisms.[81]
Critically, alcohol provides no guarantee of
protection and high doses can be fatal through,
for example, alcohol poisoning.[84] Furthermore,
if an individual contracts food poisoning, alcohol
should be avoided to prevent further
dehydration.xviii
3 Combined consumption
– the positive health
effects?
3.1
Cardiovascular disease
In France, the incidence of cardiovascular
disease has historically been considerably lower
than elsewhere even though their diet is not
lower in saturated fat or cholesterol.[74] Whilst the
cause is uncertain, one protective factor
mooted is higher consumption of red wine.[75]
Regardless, the much celebrated relationship
between alcohol consumption and lower
cardiovascular disease is complicated by a
variety of factors, (see Section 2.2.1), including
dietary factors:
• Consumption with a meal: Any effects of
red wine (or alcohol) may rely on whether
alcohol is consumed with a meal: in New
York (USA), Stranges et al. showed that
participants mostly consuming alcohol
without food were at a significantly higher
risk of hypertension than lifetime abstainers
or those who mostly drank alcohol with food
(n=2,609).[76]
• Diet: Wine drinkers tend to eat healthier
diets, exercise more and occupy relatively
affluent socio-economic groups compared
with non-drinkers and other drinkers.[77, 78]
Research in New York (USA; n=3,756, aged
35-79 years) showed that wine drinkers may
consume higher quantities of fruit and
vegetables
than
other
drinkers.[78]
xviii
xix
Food poisoning
3.3
Diabetes
A meta-analysisxix of 15 prospective cohort
studies has highlighted that alcohol may offer
protective effects against type 2 diabetes.[85]
Here, risk of type 2 diabetes was found to be
lowest amongst those who drank 12-24g (1.5-
Please see http://www.nhsdirect.nhs.uk/articles/article.aspx?articleId=411&sectionId=11 for more information.
A meta-analysis is a statistical technique which combines the results from a number of independent studies. This then provides an overall understanding of the impact
of a given factor, such as the effect of alcohol on diabetes.
10
hypoglycaemia.[92] However, a systematic review
concluded that there was no compelling
evidence to suggest that such sugars could
prevent or treat a hangover.[93]xx Further, regular
application can contribute to weight gain.
3.0 units) per day compared with non-drinkers.
For those consuming more than 48g per day
(more than 6.0 units), risk was equivalent to
non-drinkers. However, as with heart disease, it
is likely that other factors such as lifestyle and
diet are involved (see Section 3.1).
3.4
3.4.3 Dietary supplements
Foods protective against the
effects of alcohol misuse
Alcohol consumption can lead to an imbalance
of minerals and vitamins.[29] Thus, academic
reviews of early research suggest that chronic
alcohol consumption can be associated with a
reduced intake of vitamin B1 (or thiamine).[94,95]
Critically, vitamin B1 may play a key role in
maintaining cognitive functioning [96,97] and in
extreme cases a lack of this vitamin has been
linked with the development of WernickeKorsakoff syndrome in heavy drinkers (Box 3).
3.4.1 Coffee
Whilst coffee cannot provide sobriety, it has long
been seen as an antidote to alcohol and, to
some extent, can be used to restore controlled
behaviour.[4,86,87] Further, coffee may offer some
protection against liver cirrhosis,[88-90] that other
caffeinated drinks such as tea do not.[88,90] In a
US longitudinal study of 125,580 people (197885), the risk of developing alcoholic liver
cirrhosis fell with increased coffee consumption:
those drinking four or more cups of coffee per
day were 80% less likely to develop alcoholic
liver cirrhosis than non-coffee drinkers.[90] There
was no such relationship for non-alcoholic liver
cirrhosis. However, some participants who
claimed lifelong abstinence (or very low levels of
drinking) did in fact develop the condition.
Importantly, abstinence from alcohol or low
levels of consumption are far more effective at
preventing liver disease than coffee.[90] Further, a
systematic review concluded that increased
regular caffeine consumption may be linked with
high blood pressure for those already prone to
hypertension,[91] a condition also linked with
alcohol consumption (see Section 4.2).
Box 3: Wernicke-Korsakoff syndrome
Heavy drinkers are at risk of developing
Wernicke-Korsakoff syndrome, where short
term memory loss is experienced due to a lack
of vitamin B1.[99,100] The severity of the extent of
memory loss can result in institutionalisation as
sufferers cannot process any new information.
Heavy drinkers are at risk because of poor
eating habits, frequent vomiting (reducing
vitamin intake), and inflammation to the
stomach lining (obstructing vitamin absorption).
Although the condition tends to be seen in older
men, women are also susceptible. Treatment is
through abstinence and a healthy diet.
In Australia in 1987, the National Health and
Medical
Research
Council
(NHMRC)
recommended adding vitamin B1 to beer and
flagon wine to tackle this.[100] However, this was
rejected as it conflicts with sensible drinking
health messages,[101] especially as those at risk
are likely to be heavy drinkers already and such
a tactic might provide an incentive to continue
consumption. The population level effects of
alcohol on memory are poorly studied but in a
study of 15-16 year old drinkers (North West of
England; n=9,833), 45% reported having
3.4.2 Sugary diets
Excessive alcohol consumption can result in a
fall in blood sugar levels and lead to fatigue,
weakness, shakiness, mood disturbances and
in extreme cases, hypoglycaemia.[24] Folk
remedies to help sober up and treat hangovers
include cola for rehydration and to boost sugar
levels. Glucose can also help to prevent
xx
A systematic review identified 15 trials examining eight agents: fructose, glucose, propranolol, tropisetron, tolfenamic acid, and the dietary supplements Borago officinalis
(borage), Cynara scolymus (artichoke) and Opuntia ficus-indica (prickly pear).[93] None were shown to be effective in preventing or treating a hangover.
11
drunkenness.[22,105] Carbohydrates, especially,
are thought to slow the rate of absorption,[22]
making individuals feel less drunk[106] and
potentially reducing peaks in blood alcohol
levels. However, all alcohol absorbed still has to
be processed by the liver, regardless of how
quickly absorption occurs. Further, a controlled
experiment investigating the impact of different
diets found no significant effect of
carbohydrates compared with a high-fat or
protein diet.[31]xxiii Researchers also compared
the effects of eating a meal one hour before
consuming alcohol with fasting for 12 hours
before alcohol consumption. This showed
alcohol elimination rates to be between 25%
and 45% higher when participants had eaten
beforehand compared with fasting. Alcohol
elimination rates were significantly higher for
males. Whether combining food with drink
reduces or even increases risks such as liver
disease remains unclear but some evidence
suggests that the risk of hypertension may be
lessened when drinking alcohol with food
(compared with drinking it alone; see Section
3.1). Moreover, individuals may use knowledge
of how food consumption can reduce
inebriation by purposefully avoiding food to aide
intoxication.[15,16]
forgotten things after drinking with a greater
prevalence in those drinking more and more
often.[102]
Some dietary supplements claim to reduce the
unwanted side effects of alcohol including low
energy levels.[103] Producers suggest that their
ingredients, for example succinic and fumaric
acids, help to metabolise alcohol and reduce
toxic by-products. Another supplement claims
to reduce alcohol levels identified through a
breathalyser by more than 50% in 40 minutes
by accelerating alcohol metabolism.xxi However,
large-scale, independent and empirical studies
on their effectiveness have yet to be
undertakenxxii and any long term consequences
of routinely utilising such products to accelerate
alcohol metabolism are unknown.
3.4.4 Foetal alcohol syndrome
Consumption of alcohol during pregnancy may
cause a range of physical, behavioural, and
cognitive abnormalities in the unborn child
known as foetal alcohol spectrum disorders
(FASD; see Section 4.7). Food consumed by the
mother may reduce alcohol’s toxicity to the
foetus and conversely, malnutrition (at least in
animals) may increase risk because of impaired
alcohol metabolism.[104] However, the safest way
is to avoid alcohol consumption during
pregnancy.
4
3.4.5 Intoxication
“Me and my friend have a rule that if we go out,
eating is cheating. If you eat it is going to soak
up all the alcohol.”
Harms related to both
food and alcohol
A number of diseases such as cancer and
cardiovascular disease are associated with both
alcohol consumption and unhealthy eating.[45,48]
However, the relationships are complex and it
can be difficult to ascribe particular cases to
individual health behaviours.[107] In addition,
excessive alcohol consumption can complicate
conditions further because of its association
Female, 18 - 20 years old.[15]
Eating food before or with alcohol reduces the
rate of alcohol absorption into the bloodstream
and potentially reduces the immediate risk of
xxi
Sixty-four participants were involved in a placebo-controlled, randomized clinical trial. Pepp contains digestive and metabolic enzymes, organic acids, vitamins and
nutrients. These aim to break down and reduce the effects of alcohol. See www.pepp-up.com.
xxii
To our knowledge no peer-reviewed published studies are available on their evaluation.
xxiii
In study one (n=20), the same subjects experienced two settings: firstly, alcohol elimination rates were studied after a 12-hour fast and secondly the rates were
studied one hour after consuming a breakfast of 530 calories.[31] In the second study (n=8), four settings were compared: after a 12-hour fast; and one hour after a
high-fat, high-protein or high-carbohydrate meal (each consisting of 530 calories). Breathalysers were used to monitor alcohol elimination rates.
12
with poor self care.[108] Regardless, highlighting
the links between alcohol, unhealthy eating and
harm is important in developing effective
interventions.
4.1
approximately 1-2 mmHg (millimetres of
mercury) for each 10g of alcohol (1.3 units)
routinely consumed per day for those who drink
over 30g per day (3.8 units),[115] and 1 mmHg for
every 1.7kg increase in body weight for men or
1.25kg for women.[116]xxv. Even for children, US
research shows that obese children (12-16 year
olds with a BMI in the 95th percentile) are three
times more at risk of hypertension than nonobese children (33% compared with 11%;
n=2,460).[117] In England, a quarter of
hypertension cases admitted to hospital in
males and a tenth in females are estimated to
be alcohol-related.[45] Research has also
investigated the links with heart failure. In the
USA, longitudinal research (n=5,881) has shown
that obese individuals (BMI of 30 or more) are
at double the risk of heart failure than non obese
and that a rise in BMI by one increment
increases the risk of heart failure by 5% for men
and 7% for women.[118] For alcohol it is
estimated that 0.4% of cases of heart failure for
males and 0.2% for females are associated with
alcohol consumption.[45] Thus, overall,
hypertension and cardiovascular risks are
highest in higher consumers of food and of
alcohol.
Cancer
Approximately a third of the population in
England and Wales develop cancer in their
lifetime and it causes a quarter of all deaths.[109]
Few studies report on the combined effect of
alcohol and obesity for cancer, other than as a
confounding variable[110] or within the same
study but as isolated issues.[111] However,
certain types of cancer are related to both
alcohol use and obesity including: breast, colon,
liver, oesophageal and stomach.[45,110] A 16-year
longitudinal study in the USA (n=900,053)
identified that fatalities from cancer in the
morbidly obese (BMI of over 40) were 52%
higher in males and 62% higher in females
compared with those within the normal range
(BMI=18.5-24.9).[110] For alcohol, the Million
Women Study in the UK suggested that for
every drink (10g) additionally consumed per day,
the incidence of cancer for women (under 75
years) in developed countries increased by 11
per 1,000 for breast cancer, one per 1,000 for
oral cavity and pharynx cancers, and 0.7 per
1,000 for oesophageal, larynx and liver
cancers.[112]xxiv Thus, the World Report on
Cancer expressly states that to avoid cancer,
there are no safe levels of alcohol
consumption.[113]
4.2
4.3
Incidents of choking can be brought on by
eating too fast or through alcohol consumption.
In an investigation of 133 choking mortalities in
San Diego (USA) from 1994 to 2004, 14% of
individuals had consumed alcohol prior to
choking.[119] In 2005/06 in England, there were
364 person-specific hospital admissions due to
inhalation of gastric contents that were related
to alcohol.[45] Individuals suffering from alcohol
poisoning (caused by excessive consumption)
may experience a suppression of normal
reflexes, unconsciousness, and nausea or
vomiting.[62] In such circumstances, vomit may
not be effectively eradicated from the body,
Hypertension and
Cardiovascular disease
Conditions such as hypertension (or high blood
pressure) and cardiovascular disease (including
strokes, transient ischaemic attacks, angina and
peripheral vascular disease) cause millions of
premature deaths worldwide every year.[114] The
links with alcohol and unhealthy eating patterns
are evident. Blood pressure can rise by
xxiv
xxv
Choking
Allen et al. routinely followed 1,280,296 middle-aged women in the UK.[112]
Doll et al.’s study was based on a sample population of 3,116 people aged between 35 and 64 years old who were not taking medication for hypertension.[116]
Participants were recruited from both the Seychelles and Switzerland.
13
leading to suffocation.[120] In England in 2008,
alcohol poisoning resulted in 149 deaths.[121]
Young people may be particularly at risk.[62]
4.4
4.6
Mental health issues affect one in four families
worldwide.[131] Conditions such as depression
are related to excessive alcohol consumption,
obesity, and eating disorders.[132-135] For
example, in a sample of female inpatients
(n=2,436) being treated for eating disorders in
New Mexico (USA; 1995-2000), 97% showed
one or more comorbid diagnoses such as
unipolar depression, anxiety disorders and
substance use disorders (including alcohol).[133]
Relationships are also apparent between
suicidal behaviour and eating disorders, obesity
or alcohol consumption.[134,136,137] For example,
an American study (n=40,829) showed that
obese women (with a BMI of over 30) were
more likely to report major depression (odds
ratio (OR): 1.37; 95% CI: 1.09-1.73) and suicide
ideation (OR: 1.20; 95% CI: 0.96-1.50) in the
past year compared with those of average
weight (BMI of 20.78-29.99).[134] Equally in 427
suicides in 1999 in Estonia, 10% of cases
showed evidence of alcohol abuse and 51% of
dependence (compared with 7% and 14% of
control individuals selected at random from
general practitioner records; p<0.001 and
p<0.001 respectively).[136]
Dental health
Dental health affects health and wellbeing
through its impacts on speech, self-esteem,
and the ability to chew and swallow food.[122]
Unhealthy alcohol and food consumption can
both affect dental health. Heavy drinkers are
more likely to experience gingival bleeding than
those who consume less.[123]xxvi This can lead to
periodontal disease. A study in Cleveland (USA)
of 13,665 adults highlighted that those who are
obese (BMI of 30 or more) are 1.8 times more at
risk of periodontal disease.[124] In addition, dental
erosion may be associated with frequent
vomiting (defined here as being at least
weekly).[125] Thus, bulimics and binge drinkers
(who may vomit frequently) may be at higher
risk. Of course, many non-alcoholic drinks are
also related to poor dental health, especially
those with a high sugar content.[125]
4.5
Liver conditions and other
digestive disorders
Rates of liver cirrhosis increased in Britain by
69% for males and 44% for females between
1987/1991 and 1997/2001, compared with
declines in most other Western European
countries.[126] Obesity and excessive alcohol
consumption are strongly linked to fatty liver
disease and liver cirrhosis.[45,127-129] For example,
a meta-analysis highlighted how consumption
of 25g (3.1 units) of alcohol daily tripled the risk
of liver cirrhosis compared with non-drinkers.[128]
Alcohol consumption and obesity are also linked
with other digestive disorders including
pancreatitis
and
digestive
tract
[45,110,128,130]
cancers.
xxvi
Mental health
4.6
Nightlife harms
Patterns of food and alcohol consumption in
nightlife may present a number of harms:
• Large numbers of people drinking in town
and city centres can create competition
between drunk individuals over late night
resources (such as takeaways) and may lead
to violence.[138,139]
• US research highlighted that energy drinks
containing caffeine and sugar can increase
perceptions of stamina over a night out.[140]
In fact, those who mix alcohol and energy
drinks may be twice as likely to experience
harms including accidents than those who
do not.[141]
In a study in Erie County, New York (USA; n=1,371 aged 25 years to 74),[123] those reported to be consuming five or more drinks per day were 1.65 times more likely
to experience higher gingival bleeding (95% CI: 1.22-2.23) compared with those consuming less. One drink was defined as 12 ounces of beer, four ounces of wine or
one ounce of hard liquor (spirits).
14
more than two alcoholic drinks.[36]
Consumption of kebabs combined with
average alcohol consumption on a night out
equate to a calorie intake of 2,177 kcal for
males, 87.1% of their recommended daily
intake, and 1,731 kcal for females, 86.5% of
their recommended daily intake (Table 3).
Individuals consuming an unhealthy
breakfast to ease their hangover (such as a
fry-up or bacon sandwich, which 28% of
drinkers reported doing in the above survey)
further elevate their calorific intake. This
contributes to risks of becoming overweight
especially if such behaviour is routine.
Further, as such food may be salty,xxvii they
may increase thirst and so raise alcohol
consumption.
• Individuals who may want to remain within a
calorie controlled diet while drinking[16] or
simply look thinner when going out may
choose not to eat that day (see also Section
2.3).
“I am dead skinny when I am drunk, I would
wear the skimpiest little bikini and I would look
fab in it.”
Female (21-24 yrs).[15]
• Body image concerns can motivate alcohol
consumption as individuals may drink to feel
more comfortable with their size.[15]
• Nightlife users may become hungry because
of alcohol's appetite stimulant effects,
craving fatty and high carbohydrate food
with strong tastes. In a recent survey of
English drinkers (n= 1,954), 29% reported
that they ordered crisps, nuts or pork
scratchings (although frequency is not
provided) and 19% regularly consume a
pizza, burger, chips or kebab when drinking
4.7
Reproductive health
• Reproductive health: Both alcohol and
obesity may be linked with cancers affecting
the reproductive organs,[45,110] and infertility
Table 3: Number of alcohol units and calories consumed on a typical night out in
Liverpool by nightlife users aged 18-35 years (n=424)* and examples of food consumed**
Males
Females
Mean number of units
(95%CI)
Mean number of
kilocalories
(95%CI)
Mean number of units
(95%CI)
Mean number of
kilocalories
(95%CI)
Alcohol consumed when
pre-loading
4.0
(3.3-4.6)
232.5
(195.4-269.6)
4.4
(3.7-5.1)
243.5
(202.3-284.7)
Alcohol consumed on a
night out
19.2
(17.9-20.5)
1,141.2
(1,066.5-1,215.8)
11.5
(10.5-12.4)
677.2
(625.1-729.2)
N/A
1,000
N/A
1,000
Total
23.2
(21.7-25.6)
2,176.5
15.9
(14.7-17.0)
1,730.5
Recommended daily
intake (or maximum
recommended for
alcohol)
Maximum:
3-4 units
Recommended: 2,500
kcal
Maximum
2-3 units:
Recommended: 2,000
kcal
Doner kebab (not
including salad or
sauces)
* Data from a previous survey[143] were re-analysed using the unit and calorie estimates from Table 2. Calorie intake from mixers is not included.
** Mean number of kilocalories for kebabs was provided by a sample of 494 doner kebabs from across the UK.[142]
Source: Alcohol data;[143] kebab calorie data;[142] Microdiet Plus for Windows (2001); Drinkaware.com.
xxvii A UK sample of 494 doner kebabs (without sauce or salad) on average contained 98% of recommended daily salt allowance.[142]
15
issues.[144,145]
This
includes
erectile
dysfunction
and/or
impotence,[146-148]
although here evidence is mixed.[147-149]
related behaviour) also has links with poor sleep,
with 45% of nearly 2,000 drinkers in a YouGov
poll reporting experiencing tiredness the day
after drinking.[162] Conversely, alcohol has also
been used as an aid to sleep.[163,164] However, a
review of earlier academic studies suggests that
individuals can become tolerant to its sedative
effects,[165] which may lead to increased alcohol
consumption to achieve the same effect.
Moreover, higher levels of consumption
including those associated with alcoholism are
linked with poor sleep quality.[164,166]
• Risks to an unborn baby: Unhealthy
consumption of both alcohol and food are
linked with miscarriage and low birth
weight.[150-152] For example, consumption of
some cheeses during pregnancy can lead to
listeriosis and even miscarriage,[153]xxviii whilst
approximately one in five spontaneous
abortions are thought to be caused by
alcohol consumption.[45] In fact, prenatal
alcohol consumption has been linked with a
wide range of possible consequences for the
unborn
child
such
as
FASD.[154]
Understanding of the precise effects of
prenatal alcohol consumption on the unborn
baby is limited and in some cases
contradictory;[155,156] as collecting evidence
is fraught with methodological limitations.[155]
4.8
4.9
• Deprivation: Populations living in more
deprived areas may be at elevated risk from
harms relating to, for example, both harmful
drinking (such as alcohol-related mortality)
and obesity.[48,167,168]
• Age: Ageing bodies are more susceptible to
weight gain[169] and the effects of
alcohol.[170]
Sleep disorders
Lack of sleep can be extremely disruptive, with
fatigue elevating the risk of accidents[157] and
conditions such as coronary heart disease
(through increased arterial calcification[158]). Lack
of sleep may be associated with increased
appetite, which contributes towards the
potential for obesity.[159] A cross-sectional study
of 11-16 year olds in South East Texas (USA)
suggested that for every hour of lost sleep, the
likelihood of obesity increased by 80%
(n=383).[160]xxix Further, a study amongst adults
in Valencia (Spain; n=1,772), suggested a similar
link with individuals reporting at least nine hours
of sleep per day having a lower risk of obesity
(BMI of 30 or more) than those sleeping for six
or less hours (OR: 0.43; 95% CI: 0.27-0.67).[161]
Whilst both studies acknowledge that this does
not mean that lack of sleep is a causative factor
for obesity, it does highlight a significant
relationship. Alcohol consumption (and/or
xxviii
xxix
xxx
Examples of other ecological
and demographic links
• Education: A study in Copenhagen
(Denmark; n=30,632) highlighted how those
receiving less than eight years of education
were significantly more likely to drink heavily,
have low levels of physical activity and be
obese.[171]xxx
• Adverse
childhood
experiences:
Research in California (US) has shown that
adverse childhood experiences (such as
child abuse, parental substance abuse) are
strongly related to initiation of alcohol use
before 14 years,[1] alcohol abuse as an
adult[172] and adult obesity.[173] So, for
example, adults (n=13,777; aged 19-92
years) who reported being often hit or injured
as children (2.5% of sample) were 1.4 times
more likely to have a BMI of 30 or more
compared with those who reported no
physical abuse (95% CI:1.2-1.6).[173]
Kongo et al. looked at the effects of the Portuguese São Jorge cheese, a cheese made from raw cow’s milk. In this study, two of the raw milk samples (n=105) analysed
tested positive for the pathogen.[153]
Obesity was defined as having a BMI above the 85th percentile for sex and age according to the Centers for Disease Control and Prevention (CDC) growth charts, as
well as having 25% body fat for boys and 35% for girls.[160] For the whole sample, the mean undisturbed sleep time was 7.68 hours (range 5.7-9.1 hours).
The relationship between years in education and drinking heavily (that is consuming more than 42 drinks per week) was only significant for males.[171] Obesity was
defined as having a BMI of more than 28.
16
• Smoking: Smoking has strong associations
with both alcohol and weight issues.
Individuals who drink often report an
increased desire to smoke after consuming
alcohol, especially in nightlife.[174] The
smoking ban may have helped to curb this,
but research carried out in Victoria (Australia)
suggests that 75% of smokers frequenting
nightlife did not intend to quit following the
ban implemented there (n=409).[174] Whilst
alcohol has been linked with increased food
consumption, smoking can curb appetites
and individuals who are attempting to stop
smoking often find that their weight
increases at least initially (for reviews on this,
see: [175,176]).
consumption as a whole. A combined approach
would be more efficient as settings
recommended for intervening are often the
same: in schools, in health services (such as
general practice), at the point of purchase, in
communities, families, and the workplace.[2, 177]
5.1 Providing alternative options
• Activities for young people: Providing
physical activities can encourage weight loss
and protect against risky drinking amongst
young people.[178-180] Not only does
physical
exercise
increase
energy
expenditure but may also raise self-esteem,
as in the case of a residential weight loss
programme (involving exercise).[181]xxxi This is
important because low self-esteem
associated with obesity in children may lead
to an increased likelihood of drinking
alcohol.[182] For alcohol, a survey of
teenagers in the North West of England (n=
10,271; aged 15-16) found that drinkers
who were members of a sports or youth
team were less likely to drink frequentlyxxxii
compared with those who were not.[180]
However, activities must be affordable,
attractive and accessible to all youths.
5 Interventions for
promoting healthy food
and alcohol
consumption
Achieving behavioural change at an individual,
community and population level is challenging,
especially in relation to food and alcohol where
the behaviours may be enjoyable and rooted in
local culture. Despite this, behaviour change is
essential if harms are to be reduced. This
section briefly outlines a number of interventions
that could be used to tackle unhealthy
xxxi
xxxii
• Activities for adults: Many of the studies
surrounding activity provision focus on
children; however, such an approach may
also be relevant for adults. In UK town and
city centres, nightlife is dominated by
activities that involve alcohol and, to a lesser
extent, eating with few activities available
that do not involve consumption. Alternative
activities (such as the theatre, dancing
studios and so on) could be offered to
encourage diversion from consumption and
to encourage other groups into town and
cities at night.
Gateley et al compared 185 overweight children (mean age of 13.9 years) who were enrolled in a six-week residential course for weight loss between 1999 and 2002
with 94 children of similar ages not attending the course.[181]
Drink frequently was defined as drinking alcohol at least twice a week.[180]
17
• Food in nightlife: Tapas were introduced in
Spain to prevent alcohol consumption on an
empty stomach and to reduce the risk of
drunkenness (see Section 1).xxxiii Small plates
of food are still served in many bars. In
Blackburn, providing toast in nightlife
environments has been reported to have
contributed to reductions in the number of
violent incidents; although no formal
assessment has been undertaken.[183]
Alternative possible foods include: non-salty
products (salty foods may encourage further
consumption due to thirst); carbohydrates,
which may slow the absorption of alcohol
into the bloodstream;[22] and fruit,[184]
which
is
healthy
and
can
aid
[185]
rehydration.
provide food, some licensees allow people
to eat takeaway meals with bought drinks.[18]
However, this may encourage unhealthy
consumption of processed foods where
healthy takeaways are not always accessible
or chosen.
In supermarkets, environmental strategies could
be utilised to distinguish food and alcohol
consumption. For example, supermarkets used
to have a dedicated separate section for
alcohol, which could be closed off outside
licensing hours. Today, however, alcohol is sold
alongside all other food and drink products with
few warnings of its effects and bright coloured
posters and discounts to encourage sales.
There have been renewed calls to separate
alcohol from other food products in
supermarkets through, for example, alcohol only
checkouts where alcohol can only be sold by
specially trained staff. It is hoped that this would
reduce quantities purchased and prevent
underage sales.[189] Those measures taken to
combine alcohol and food are often offers
aimed at selling more alcohol and food. Such
measures may encourage individuals to exceed
recommended maximum guidelines (e.g. £10
for a meal for two and a bottle of wine (see Box
4).
• Alternative environmental strategies:
Encouraging venues to supply tables and
chairs can create a more relaxed
environment and may even encourage
slower drinking.xxxiv Such measures make the
provision of food more economically
attractive as the space and furniture required
is already present. Further, mixed use
venues may be more profitable over a longer
period because they attract different
clientele.[188] Although not all venues can
xxxiii
xxxiv
Please see http://www.arrakis.es/~jols/tapas/index2.html for more information.
Crowded, uncomfortable, and poorly managed nightlife settings contribute to elevated aggression,[186] increasing the potential for disorder. Venues that encourage
vertical drinking (through a lack of seating) have been associated with increased disorder.[187] Licensing conditions can be used here to specify
environmental measures because they have the potential to promote a reduction in crime and disorder (one of the aims of the Licensing Act 2003).
18
Box 4: Marketing strategies
combining alcohol and food
Alcohol Concern recently raised awareness of a
marketing strategy being employed by Marks
and Spencers, where consumers can purchase
a meal for two people and a bottle of wine for
£10.[190] Concern was raised because a bottle
shared between two would equate to the
individuals each consuming more than their
recommended daily intake (a bottle of wine is
approximately 10 units, using the calculations in
Table 1). Further, the offer implied that
consumption at such levels with a meal is a
sensible consumption pattern.
carbohydrate limit may be subject to
substitution with members cutting back on
food to save points for alcohol, increasing
risk for slimmers (see Section 2.3). Guidance
for one diet states: “Because there are no
prohibited foods, both [alcohol and caffeine]
are fine, but you'll have to give up food to
make room for the wine.”xxxvi
• Providing alternative drinks: A number of
lower strength alcoholic drinks (e.g. lower
strength beers or Sovio Zinfandel - an
equivalent to wine with 5.5%ABV) have been
launched, which may also have lower overall
calorific content (see Table 1). Their use
could help to decrease risk relating to both
alcohol and obesity. However, such
products typically struggle in the UK and do
not reap the benefits of lower taxes and
more favourable pricing seen in countries
such as the USA and Australia.[63, 191]
5.2
• Diets which suggest reducing carbohydrate
intake may inadvertently increase the appeal
of stronger drinks (spirits and wine) as they
contain fewer carbohydrates than, for
instance, lager (see Table 1).
Providing advice
For alcohol, abstinence and moderation
programmes encourage reduced alcohol intake
but often have relatively little discussion on the
role of food.[192,193] Yet, the North West Big Drink
Debate (n=30,857) highlighted that three fifths
(59%) of harmful drinkersxxxvii were concerned
about the impacts of their consumption on their
weight,[194] and national advice on healthy
weight maintenance recommends reducing
alcohol intake because of its calorific
contents.[195] Importantly, such programmes
represent an opportunity through which the
impacts of alcohol misuse and obesity can be
tackled together.
5.2.1 Consumption moderation
programmes
A key part of weight management programmes
(such as Weightwatchers and Slimmers’ World)
and weight loss diets is advice on food
moderation, but they can also cover alcohol
moderation.xxxv However, work is needed to
ensure messages for alcohol and food
consumption are not contradictory, as for
example:
• Weight loss diets stipulating that slimmers
must stay within an overall points or
xxxv
GoodHousekeeping compared 14 different diets. The majority of these advocated alcohol moderation. Where this was defined, moderation was much lower than the
recommended maximum weekly limits For more information, see http://www.goodhousekeeping.com/health/diet-comparison-results/?diet1=0&diet2=14.
xxxvi
For more information, see http://www.goodhousekeeping.com/health/diet-comparison-results/?diet1=0&diet2=14.
xxxvii
Harmful drinkers are defined as those who drink over 35 units per week for females and those who drink over 50 units per week for males.[194]
19
by-products such as gelatine, and whilst
these are removed, the final product is not
guaranteed to be vegetarian.[202,203]
Traces of alcohol may be used to enhance
flavour in products such as crisps, although
the amounts likely to be present in the final
product are tiny.[204] This may be of
importance to non-drinkers.
5.2.2 Labelling
The European Union (EU) plans to impose
standard nutritional information on food labelling
to counter obesity. Pre-packaged food will
display, for example, quantities of sugar, salt and
fat (including saturated).[197] Mixed drinks
(alcopops) and drinks of less than 1.2% ABV are
included in these regulations but other alcoholic
products (wine, lager and spirits) will be exempt.
In the UK, food must be labelled highlighting, for
example, its ingredients to enable informed
decisions (Box 5; Figure 1).[198] Alcohol is not
included because it is believed that people are
not interested in receiving this information for
alcohol.[199,200] However, whilst the European
study that informed the EU consultation on
labelling [199] showed that participants were not
interested in ingredients labelling for beer or
wine, it was based on a small number of people
across a large geographical area[200] and so
cannot be said to be representative of all
drinkers.
Given the rising levels of obesity and the high
calorific value of alcohol, it is difficult to
understand why alcohol products do not have
to display proper nutritional labelling.
Box 5: The Food Standards Agency on
labelling
“Consumers should be able to be confident with
their choice of foods and be able to buy
according to their particular requirements, be it
for diet and health, personal taste and
preferences, or cost.... People who cannot eat
certain foods because they are intolerant or
allergic to them may suffer severe or life
threatening reactions. It makes it much more
difficult to avoid these foods if they have
incorrect or inaccurate labels.”[196]
Comprehensive labels should be provided for
alcoholic products, ideally containing:
• Nutritional information: This should
include ingredients, number of calories and
other nutritional properties (such as vitamins
and minerals) in line with other food
substances.
• Strength of alcoholic drink and number
of units: A mandatory code should be
adopted which requires retailers to
provide unit content and health guidelines
on each bottle or container in the offlicensed trade. Suggestions for the licensed
trade include ensuring such information is
available on at least a representative sample
of products.[201]
• Manufacturing processes: Filtration
processes for lager and wine can use animal
20
Figure 1: Labels currently in use
Non-alcohol product (fruit juice)
Mixed alcohol product (sangria)
Alcohol product
Labels for alcoholic products display very little nutritional information compared with a mixed alcohol product and food product.
Note that the mixed alcohol product has ingredients but does not state the ingredients within wine.
5.2.3 Leaflets
5.3 Community-based lifestyle
improvement programmes
Leaflets are often used as a way of conveying
health promotion messages on a wide variety of
different issues including alcohol, smoking and
obesity. They provide details on the dangers of
risky behaviour, how such behaviours can be
changed and support available. Information
resources tackling both food and alcohol are
rare. However, leaflets published by the Scottish
Nutrition and Diet Resources Initiative (SNDRí)
on vitamin B1 deficiency (see Section 3.4.3)
provide information on the relationship between
alcohol and diet, and how a balanced diet is
essential to counteract the negative
consequences of substitution (where individuals
substitute food for alcohol; see Section 2.3).xxxviii
No evaluation details were provided.
xxxviii
Community-based services are available for
those who want to stop smoking, reduce
alcohol consumption, and lose weight. For
example, Connect 4 Life in Tameside and
Glossop is a local targeted programme piloted
to reduce health inequalities associated with
alcohol, smoking, obesity and sedentary
lifestyles amongst 50-64 year olds in areas at
risk of chronic health problems (n=172).[205] The
pilot trialled initiatives including health risk
assessments, health coaching and phone
support.
Along
with
general
health
improvements, participants reported a reduction
in alcohol intake and an increase in fruit and
Copies of these leaflets are available at http://www.caledonian.ac.uk/sndri/index.html and are titled Moving On and Making Changes.
21
vegetable consumption after six months. Its
evaluation estimates that if 10,000 people were
engaged in the programme for ten years, it
would prevent 99 premature deaths.[206]
However, robust data on factors such as alcohol
consumption and nutrition are so far not
available.[205]
5.4
Pricing strategies for food and alcohol are often
viewed in isolation from each other with
supermarkets reported as having lowered the
cost of alcohol but raised the cost of food [212]
and little being published on how the price of
one affects purchasing behaviour towards the
other. In South Africa, high food costs in
deprived areas helped to increase the
purchasing of alcohol instead of food.[59]
Promoting healthy
consumption
5.4.2 Marketing campaigns
5.4.1 Price
Some health promotion campaigns are bringing
together alcohol and food, aiming to raise
awareness of the calorific contents of alcohol
and its links with weight gain. Pssst! in Liverpool
has followed such a strategy, but its evaluation
has not examined whether knowledge of calorie
contents affected alcohol consumption (Box 6).
Nevertheless, lessons could be learned from the
alcohol industry in marketing combined
consumption: for example, in order to combat
the perceived loss in trade from the smoking
ban, lower consumer spending and the small
alcohol tax rises, licensed venues are
increasingly investing in food sales.[213,214]
Initiatives include: discounts on combined
purchasing (Box 4; Figure 2);[190] opening for
breakfast (enabled by the increased flexibility of
hours since the Licensing Act 2003, although
most early morning customers order coffee
rather than alcohol);[215] providing snacks (the
smoking ban may have increased snacking in
licensed premises[216]); budget carveries and allyou-can-eat offers in pubs;[213] pubs without
kitchens encouraging customers to order and
eat their takeaways in the pub;xxxix and
suggesting particular types of wine and/or beer
to accompany specific meals.
Price affects purchasing behaviour.[207,208]
Modelled data estimate that a 10% price
increase in alcohol could reduce the number of
alcohol-specific deaths by 29% for males and
37% for females in the UK.[209] However, the
timescale for this is not provided. Greater price
rises have larger effects: a minimum price of 30p
per unit could reduce total crimes by around
3,800 per annum in England whereas 40p could
reduce the total number by 16,000 per
annum.[207] For food, the situation may be more
complex because of the vast choice available,
and pricing strategies may be more successful
in closed environments such as schools or the
workplace.[210] Nevertheless, pricing strategies
relating to food and alcohol can be implemented
in a number of ways:[208,210]
• through taxation increases, a minimum price
or linked with the nature of the product (such
as the strength of the drink);
• through tax incentives for healthier products
such as lower strength drinks or fresh
produce - campaigners are currently calling
for licensed venues to lower the costs of soft
drinks (often sold at a similar price to
alcoholic drinks) in order to discourage
excessive consumption;[211]
• using funds raised from increased prices to
promote health; and
• banning promotions, which encourage
unhealthy consumption.
xxxix
See http://www.viewlondon.co.uk/pubsandbars/the-lion-review-13538.html for more details.
22
Box 6: Pssst!
The Pssst! campaign was launched in Liverpool
in November 2007 and aimed to change
students’ drinking behaviour. Positive messages
were provided on enjoying alcohol responsibly
using a ‘Chill Out’ cabin sited in one of
Liverpool’s key drinking areas, radio coverage
and Bluetooth texts. The award-winning brand
has been highlighted as an example of good
practice.[217] However, whilst the campaign
incorporated combined messages surrounding
alcohol consumption and obesity, this aspect
and its effects on consumption were not
assessed under the evaluation.[218-220]
Figure 2: Combined discounts on food and alcohol
6 Discussion
there is little available research on the effects of
combined consumption, and evaluations of
combined lifestyle interventions aimed at
improving health and reducing health
inequalities are limited. Other countries such as
those in the Mediterranean have maintained
strong links between food and alcohol
consumption in local cultures. However, in the
UK, such links appear to be missing whilst
This report has highlighted the intertwined
nature of alcohol and food in relation to
consumption and their short and long-term
physical and sociological effects. Alcohol affects
how we eat food and the food we choose to
eat, and unhealthy consumption of alcohol and
food contributes significantly to the numbers of
people at risk from cardiovascular disease,
cancer and liver disease in the UK. However,
23
harms continue to rise. In 2007, almost one in
four adults in England were obese and trends
suggest levels will continue to increase
steeply.[221] Further, there was a 69% increase in
alcohol-related admissions to hospital from
2002/03 to 2007/08. If this continues, by 2012,
there will be over a million alcohol-related
hospital admissions in England.[222] As such,
reducing levels of obesity and alcohol-related
harm are key priorities for the Government.[2, 177]
Further, in order to tackle health inequalities, the
Government has outlined the need to challenge
the structural boundaries in policy organisation
and service delivery (silo working) to promote a
cross-cutting approach, ‘building in joined up
action nationally and locally, vertically and
horizontally’.[223] To date, there is little evidence
of this in relation to food and alcohol policy.
in reducing mortality and morbidity. Traditionally
in the Mediterranean, children were introduced
to alcohol gradually at the dinner table within a
family setting.[13] Such parenting techniques
have been suggested as a method to protect
individuals from developing risky drinking
patterns. Today, children in the UK are more
likely to have drunk a glass of wine, beer or
spirits before the age of 13 years than their
Mediterranean counterparts but critically are
also more likely to have been drunk by 15-16
years (for the latter, 66% in the UK compared
with 49% for Europe overall).[225]xi This suggests
that early exposure to alcohol alone does not
discourage dangerous drinking and, in fact,
small-scale US studies show that parental
provision may increase risk if drinking is
undertaken without establishing the parameters
of acceptable behaviour.[226-228] However, in
children that drink, parental provision
accompanied by setting an example of
moderate consumption with food and
discussion of limits of responsible drinking may
help develop healthier attitudes towards
alcohol.[180,228,229] In children that do not drink
there are no established benefits of introducing
them to alcohol.[230]
Many people are likely to have multiple
behavioural health risks linked to obesity,
smoking and alcohol behaviours,[224] which
together are likely to reinforce and accelerate
each other’s contributions to morbidity. The
Department of Health has stated that it will
commission a broader research programme to
understand good and bad multiple health
behaviours, cluster effects, the impacts of
behaviour change, and how to intervene
effectively to help people make positive changes
and reduce risky behaviours.[223] Until such
research becomes available, it would seem
logical that initiatives which aim to
simultaneously tackle clusters of health
behaviours (such as alcohol, smoking, poor diet
and obesity) are likely to have a stronger impact
than those that address single behaviours.[224]
Many current social marketing campaigns fail to
realise this potential.
In order to reduce levels of obesity and alcoholrelated harm, it may be necessary to adopt a
more traditional Mediterranean-style diet and
lifestyle in the UK, focusing on the consumption
of alcohol as an accompaniment to other foods
rather than a mechanism to achieve inebriation.
In the UK, such a transition may be facilitated
through the wide provision of low alcohol beers
and lower alcoholic strength wine; more familyorientated pubs and restaurants with better
facilities for children and young people; and
food/alcohol outlets offering a healthier range of
products, both seasonal and locally sourced.
The beginning of this report outlined the
perceived benefits of a Mediterranean-style diet
xi
Here, alcohol consumption refers to having consumed at least one glass of beer, wine or spirits.[225]
24
Encouraging such styles of consumption could
be particularly important in young people who
may be more likely to binge drink,[231] but may
also be least likely to consume alcohol with
food.[194] The UK is not alone in needing to
promote more responsible diet and drinking
behaviours as increases in obesity and evidence
for binge drinking are now being reported in
Mediterranean countries including Spain.[232,233]
Academic reviews suggest this may be as a
result
of
food
globalisation,
cultural
contamination caused in part by increased
travelling and improved economic conditions.[6,
7. Tierney J. (2006). 'We want to be more European': The 2003
Licensing Act and Britain's Night-Time Economy. Social Policy and
Society, 5(04):453-60.
234]
13. Anderson B. (1968). How French children learn to drink. Human
Organization, 5:20-2.
Whilst the outcomes of research to evaluate
effective interventions for clusters of risky health
behaviours such as unhealthy eating, drinking
and smoking are awaited, we need to ensure
that all current Government policies relating to
alcohol and food are consistent in their
approach. In addition, public health policy
aimed at reducing obesity and alcohol-related
harm must consider unhealthy consumption,
lifestyle issues and wellbeing as a whole, where
possible, implementing combined interventions
within local communities in order to maximise
the potential to influence risky behaviours. In this
way, people may start once again to make the
connections
between
alcohol,
food
consumption, and healthy lifestyles.
14. Hupkens CLH, Knibbe RA, and Drop MJ. (1993). Alcohol
consumption in the European Community: uniformity and diversity in
drinking patterns. Addiction, 88(10):1391-404.
7 References
23. Verster JC. (2008). The alcohol hangover: a puzzling phenomenon.
Alcohol and Alcoholism:163.
8. Trichopoulou A, Costacou T, Bamia C, et al. (2003). Adherence to
a Mediterranean diet and survival in a Greek population. New England
Journal of Medicine, 348(26):2599-608.
9. Estruch R, Martinez-Gonzalez MA, Corella D, et al. (2006). Effects
of a Mediterranean-style diet on cardiovascular risk factors. Annals of
Internal Medicine, 145(1):1-11.
10. Knoops KTB, de Groot LCPGM, Kromhout D, et al. (2004).
Mediterranean diet, lifestyle factors, and 10-Year mortality in elderly
European men and women: the HALE project. Journal of the American
Medical Association, 292(12):1433-9.
11. Colville R. (2006). Wine industry finds strength isn't everything.
Telegraph. 22 May 2006.
12. Boehmer A. (2006). Style in new world wines: is a new style
emerging? Online article: http://newworldwine.suite101.com/
articlecfm/style_in_new_world_wines [accessed 10 December 2009].
15. Engineer R, Phillips A, Thompson J, et al. (2003). Drunk and
disorderly: a qualitative study of binge drinking among 18-24 year olds.
Home Office Research Study 262. Home Office, London.
16. Peralta RL. (2002). Alcohol use and the fear of weight gain in
college: reconciling two social norms. Gender Issues, 20:0-42.
17. Consensus for Action on Salt and Health. (2009). UK favourite pub
chains lagging behind in salt reduction. Consensus for Action on Salt
and Health. Press release. 3 June 2009 Available from:
http://www.actiononsalt.org.uk/publications/newsletters/newsletter_su
mmer_2009.doc [accessed 2 November 2009].
18. Philby C. (2008). Raising the bar: why Britain's pubs are getting
creative. Independent. 16 August 2008.
19. Department of Health. (2007). Cancer reform strategy. Department
of Health, London.
20. Department of Health. (2000). Coronary heart disease: national
service framework for coronary heart disease - modern standards and
service models. Department of Health, London.
21. Department of Health. (2007). National stroke strategy. Department
of Health, London.
22. Paton A. (2005). Alcohol in the body. British Medical Journal,
330(7482):85-7.
24. Swift R and Davidson D. (1998). Alcohol hangover. Alcohol Health
and Research World, 22(1):54.
25. Gibney M, Elia M, Ljunggvist O, et al. (2005). Clinical nutrition.
Blackwell Publishing, London.
1. Dube SR, Miller JW, Brown DW, et al. (2006). Adverse childhood
experiences and the association with ever using alcohol and initiating
alcohol use during adolescence. Journal of Adolescent Health,
38(4):444.e1-.e10.
26. Craig R and Mindell J, eds. (2008). Health Survey for England
2006: latest trends. National Centre for Social Research and University
College Medical School, London.
2. Department of Health, Home Office, Department for Education and
Skills, et al. (2007). Safe. Sensible. Social. The next steps in the National
Alcohol Strategy. Department of Health, London.
27. Kater RMH, Carulli N, and Iber FL. (1969). Differences in the rate of
ethanol metabolism in recently drinking alcoholic and nondrinking
subjects. American Journal of Clinical Nutrition, 22(12):1608-17.
3. Johnson H. (1991). The story of wine. Mandarin Paperbacks,
London.
4. Standage T. (2007). A history of the world in six glasses. Atlantic
Books, London.
28. Portans I, White J, and Staiger P. (1989). Acute tolerance to
alcohol: changes in subjective effects among drinkers.
Psychopharmacology, 97(3):365-9.
5. Johnson H and Robinson J. (2007). The world atlas of wine: sixth
edition. Mitchell Beazley, London.
29. Lieber CS. (1994). Susceptibility to alcohol-related liver injury.
Alcohol and Alcoholism Supplement, 2:315-26.
6. Rubba P, Mancini F, Gentile M, et al. (2007). The Mediterranean
diet in italy: an update, in More on Mediterranean diets. World Review
of Nutrition and Dietetics. 97:85-113, A Simopoulos and F Visioli,
Editors.
30. Baraona E, Abittan CS, Dohmen K, et al. (2001). Gender
differences in pharmacokinetics of alcohol. Alcoholism: Clinical and
Experimental Research, 25(4):502-7.
25
31. Ramchandani VA, Kwo PY, and Li TK. (2001). Effect of food and
food composition on alcohol elimination rates in healthy men and
women. Journal of Clinical Pharmacology, 41(12):1345-50.
51. Dorn JM, Hovey K, Muti P, et al. (2003). Alcohol drinking patterns
differentially affect central adiposity as measured by abdominal height in
women and men. Journal of Nutrition, 133(8):2655-62.
32. Reid MC and Anderson PA. (1997). Geriatric substance use
disorders. Medical Clinics of North America, 81(4):999-1016.
52. Colditz GA, Giovannucci E, Rimm EB, et al. (1991). Alcohol intake
in relation to diet and obesity in women and men. American Journal of
Clinical Nutrition, 54(1):49-55.
33. Gordis E. (1998). Alcohol and the liver: research update. No 42.
National Institute on Alcohol Abuse and Alcoholism. Online document.
Available from: http://pubs.niaaa.nih.gov/publications/aa42.htm
[accessed 10 October 2008].
53. Flechtner-Mors M, Biesalski HK, Jenkinson CP, et al. (2004). Effects
of moderate consumption of white wine on weight loss in overweight
and obese subjects. International Journal of Obesity & Related
Metabolic Disorders, 28(11):1420-6.
34. Stark M and Norfolk G. (2005). Substance misuse, in Clinical
forensic medicine: a physician's guide, M Stark, Editor. Humana Press,
New Jersey.
54. Vadstrup ES, Petersen L, Sorensen TIA, et al. (2003). Waist
circumference in relation to history of amount and type of alcohol: results
from the Copenhagen City Heart Study. International Journal of Obesity
& Related Metabolic Disorders, 27(2):238-46.
35. Liu S, Serdula MK, Williamson DF, et al. (1994). A prospective study
of alcohol intake and change in body weight among US adults.
American Journal of Epidemiology, 140(10):912-20.
55. Rao G. (2004). Cutaneous changes in chronic alcoholics. Indian
Journal of Dermatology, Venereology and Leprology, 70(2):79-81.
36. Department of Health. (2009). Drinkers pile on the pounds: new
stats reveal England's calorific alcohol intake. Department of Health.
Press
release.
17
April
2009
Available
from:
http://www.dh.gov.uk/en/News/Recentstories/DH_098315 [accessed
2 November 2009].
56. Braunstein G. (2008). Environmental gynecomastia. Endocrine
Practice, 14(4):409-11.
57. Joel. (2006). Losing weight: tips and tricks. Online article. Available
from: http://dethroner.com/2006/10/16/losing-weight-tips-and-tricks/
[accessed 20 April 2009].
37. Saner E. (2006). What’s your poison? Guardian. 12 December
2006.
58. Lieber CS. (2003). Relationships between nutrition, alcohol use,
and liver disease. Alcohol Research and Health, 27:220-31.
38. Expert Group on Vitamins and Minerals (2002). Review of iron revised version. Food Standards Agency, London.
39. Szmitko PE and Verma S. (2005). Red wine and your heart.
Circulation, 111(2):e10-1.
59. Kruger A, Lemke S, Phometsi M, et al. (2006). Poverty and
household food security of black South African farm workers: the legacy
of social inequalities. Public Health Nutrition, 9(07):830-6.
40. Corder R. (2007). The wine diet: a complete nutrition and lifestyle
plan. Sphere, London.
60. Smith R. (2008). 'Drunkorexia slimmers skip meals for alcohol'.
Telegraph. 19 March 2008.
41. Arriola L, Martinez-Camblor P, Larranaga N, et al. (2009). Alcohol
intake and the risk of coronary heart disease in the Spanish EPIC cohort
study. Heart:hrt.2009.173419.
61. Hudson JI, Hiripi E, Pope Jr HG, et al. (2007). The prevalence and
correlates of eating disorders in the National Comorbidity Survey
replication. Biological Psychiatry, 61(3):348-58.
42. Fillmore KM, Kerr WC, Stockwell T, et al. (2006). Moderate alcohol
use and reduced mortality risk: systematic error in prospective studies.
Addiction Research and Theory, 14(2):101-32.
62. Zeigler DW, Wang CC, Yoast RA, et al. (2005). The neurocognitive
effects of alcohol on adolescents and college students. Preventive
Medicine, 40(1):23-32.
43. Fillmore KM, Stockwell T, Chikritzhs T, et al. (2007). Moderate
alcohol use and reduced mortality risk: systematic error in prospective
studies and new hypotheses. Annals of Epidemiology, 17(5):S16-S23.
63. Morleo M, Phillips-Howard P, Cook P, et al. (2008). Fact sheet 7:
reducing alcohol content in drinks. Centre for Public Health, Liverpool
John Moores University, Liverpool.
44. Di Castelnuovo A, Costanzo S, Bagnardi V, et al. (2006). Alcohol
dosing and total mortality in men and women: an updated meta-analysis
of 34 prospective studies. Archives of Internal Medicine, 166(22):243745.
64. International Center for Alcohol Policies. (2007). Lower alcohol
beverages. ICAP reports 19. International Center for Alcohol Policies,
Washington DC.
65. Pavia W and Foster P. (2007). The wine whose weakness is its
strength. The Times. 30 July 2007.
45. Jones L, Bellis M, Dedman D, et al. (2008). Alcohol-attributable
fractions for England: alcohol-attributable mortality and hospital
admissions. North West Public Health Observatory, Centre for Public
Health Research Directorate, Liverpool John Moores University,
Liverpool.
66. Milne J and Gardner J. (2008). Pubs supersize wine glasses to get
people to drink more. The Times. 23 April 2008.
67. Wilmore J. (2008). Nearly a third of venues still offer 125ml
measure. The Publican. 14 April 2008.
46. World Health Organization. (no date). Obesity and overweight.
World Health Organization, Geneva.
68. Office for National Statistics. (2008). Drinking adults' behaviour and
knowledge in 2007, ONS Omnibus Survey Report. No. 34. Office for
National Statistics, Newport.
47. Hart CL, Hole DJ, Lawlor DA, et al. (2007). How many cases of
type 2 diabetes mellitus are due to being overweight in middle age?
Evidence from the Midspan prospective cohort studies using mention of
diabetes mellitus on hospital discharge or death records. Diabetic
Medicine, 24(1):73-80.
69. Caton SJ, Ball M, Ahern A, et al. (2004). Dose-dependent effects
of alcohol on appetite and food intake. Physiology and Behavior,
81(1):51-8.
70. Breslow RA and Smothers BA. (2005). Drinking patterns and Body
Mass Index in never smokers: National Health Interview Survey, 19972001. American Journal of Epidemiology, 161(4):368-76.
48. Jones A, Harrison R, Carlin H, et al. (2008). Healthy weight in the
North West population. North West Public Health Observatory,
Liverpool.
71. Anderson SE, Dallal GE, and Must A. (2003). Relative weight and
race influence average age at menarche: results from two nationally
representative surveys of US girls studied 25 years apart. Pediatrics,
111(4):844-50.
49. Wannamethee SG, Shaper AG, and Whincup PH. (2005). Alcohol
and adiposity: effects of quantity and type of drink and time relation with
meals. International Journal of Obesity and Related Metabolic Disorders,
29(12):1436-44.
72. Costello EJ, Sung M, Worthman C, et al. (2007). Pubertal
maturation and the development of alcohol use and abuse. Drug and
Alcohol Dependence, 88(Supplement 1):S50-S9.
50. Rissanen A, Hakala P, Lissner L, et al. (2002). Acquired preference
especially for dietary fat and obesity: a study of weight-discordant
monozygotic twin pairs. International Journal of Obesity and Related
Metabolic Disorders, 26:973.
26
73. Downing J and Bellis MA. (In press). Early pubertal onset and its
relationship with sexual risk taking, substance use and anti-social
behaviour: a preliminary cross-sectional study. BMC Public Health.
94. Martin PR, Singleton CK, and Hiller-Sturmhofel S. (2003). The role
of thiamine deficiency in alcoholic brain disease. Alcohol Research and
Health, 27(2):134-42.
74. Artaud-Wild SM, Connor SL, Sexton G, et al. (1993). Differences in
coronary mortality can be explained by differences in cholesterol and
saturated fat intakes in 40 countries but not in France and Finland. A
paradox. Circulation, 88(6):2771-9.
95. Todd KG, Hazell AS, and Butterworth RF. (1999). Alcohol-thiamine
interactions: an update on the pathogenesis of Wernicke
encephalopathy. Addiction Biology, 4(3):261-72.
96. Benton D, Griffiths R, and Haller J. (1997). Thiamine
supplementation
mood
and
cognitive
functioning.
Psychopharmacology, 129(1):66.
75. Renaud S and de Lorgeril M. (1992). Wine, alcohol, platelets, and
the French paradox for coronary heart disease. Lancet,
339(8808):1523-6.
97. Easton CJ and Bauer LO. (1997). Beneficial effects of thiamine on
recognition memory and P300 in abstinent-cocaine dependent patients.
Psychiatry Research, 70(3):165-74.
76. Stranges S, Wu T, Dorn JM, et al. (2004). Relationship of alcohol
drinking pattern to risk of hypertension: a population-based study.
Hypertension, 44(6):813-9.
98. Butterworth RF, Gaudreau C, Vincelette J, et al. (1991). Thiamine
deficiency and Wernicke's encephalopathy in AIDS. Metabolic Brain
Disease, 6(4):207-12.
77. Barefoot JC, Gronbaek M, Feaganes JR, et al. (2002). Alcoholic
beverage preference, diet, and health habits in the UNC Alumni Heart
Study. American Journal of Clinical Nutrition, 76(2):466-72.
99. Alzheimer Scotland. (2004). Alcohol-related brain damage Wernicke's encephalopathy and Korsakoff's psychosis. Information
Sheet. Action on Dementia. IS 31 April 2004. Alzheimer Scotland,
Edinburgh.
78. McCann SE, Sempos C, Freudenheim JL, et al. (2003). Alcoholic
beverage preference and characteristics of drinkers and nondrinkers in
western New York (United States). Nutrition, Metabolism and
Cardiovascular Diseases, 13(1):2-11.
100. Drew L and Truswell A. (1998). Wernicke's encephalopathy and
thiamine fortification of food: time for a new direction. Medical Journal
of Australia, 168(534-535):534.
79. Bellido-Blasco JB, Arnedo-Pena A, Cordero-Cutillas E, et al.
(2002). The protective effect of alcoholic beverages on the occurrence
of a salmonella food-borne outbreak. Epidemiology, 13(2):228-30.
101. Meikle J. (2002). A pint of best and be generous with the B1,
please landlord. Guardian. 18 November 2002.
80. Gessner BD and Middaugh JP. (1995). Paralytic shellfish poisoning
in Alaska: a 20-year retrospective analysis. American Journal of
Epidemiology, 141(8):766-70.
102. Bellis M, Phillips-Howard P, Hughes K, et al. (2009). Teenage
drinking, alcohol availability and pricing: a cross-sectional study of risk
and protective factors for alcohol-related harms in school children. BMC
Public Health, 9(1):380.
81. Murray LJ, Lane AJ, Harvey IM, et al. (2002). Inverse relationship
between alcohol consumption and active Helicobacter pylori infection:
the Bristol Helicobacter project. American Journal of Gastroenterology,
97(11):2750-5.
103. Krull K. (2007). RU-21 ingredients. RU21. Online article. Available
from: http://ru21.com/ingredients.htm [accessed 2 November 2009].
82. Desenclos J-CA, Klontz KC, Wilder MH, et al. (1992). The
protective effect of alcohol on the occurrence of epidemic oyster-borne
hepatitis A. Epidemiology, 3(4):371-4.
104. Shankar K, Ronis MJJ, and Badger TM. (2007). Effects of
pregnancy and nutritional status on alcohol metabolism. Alcohol
Research and Health, 30(1):55-9.
83. Hines HB, Naseem SM, and Wannemacher Jr RW. (1993). [3H]Saxitoxinol metabolism and elimination in the rat. Toxicon, 31(7):905-8.
105. Gentry RT. (2000). Effect of food on the pharmacokinetics of
alcohol absorption. Alcoholism: Clinical and Experimental Research,
24(4):403-4.
84. Jones A. (1999). The drunkest drinking driver in Sweden: blood
alcohol concentration 0.545% w/v. Journal of Studies on Alcohol and
Drugs, 60(3):400-6.
106. Finnigan F, Hammersley R, and Millar K. (1998). Effects of meal
composition on blood alcohol level, psychomotor performance and
subjective state after ingestion of alcohol. Appetite, 31(3):361-75.
85. Koppes LLJ, Dekker JM, Hendriks HFJ, et al. (2005). Moderate
alcohol consumption lowers the risk of type 2 diabetes. Diabetes Care,
28(3):719-25.
107. Peters TJ and Cook CCH. (2002). Obesity as a cause of "falsepositive" alcohol misuse laboratory investigations. Addiction Biology,
7(4):443-6.
86. Grattan-Miscio KE and Vogel-Sprott M. (2005). Alcohol, intentional
control, and inappropriate behavior: regulation by caffeine or an
incentive. Experimental and Clinical Psychopharmacology, 13(1):48-55.
108. Ahmed AT, Karter AJ, and Liu J. (2006). Alcohol consumption is
inversely associated with adherence to diabetes self-care behaviours.
Diabetic Medicine, 23:795-802.
87. Liguori A and Robinson JH. (2001). Caffeine antagonism of alcoholinduced driving impairment. Drug and Alcohol Dependence, 63(2):1239.
109. Office for National Statistic. (2006). Health Statistics Quarterly. No.
29. Office for National Statistics, Newport.
88. Corrao G, Zambon A, Bagnardi V, et al. (2001). Coffee, caffeine,
and the risk of liver cirrhosis. Annals of epidemiology, 11(7):458-65.
110. Calle EE, Rodriguez C, Walker-Thurmond K, et al. (2003).
Overweight, obesity, and mortality from cancer in a prospectively studied
cohort of US adults. New England Journal of Medicine, 348(17):162538.
89. Gallus S, Tavani A, Negri E, et al. (2002). Does coffee protect
against liver cirrhosis? annals of epidemiology, 12(3):202-5.
90. Klatsky AL, Morton C, Udaltsova N, et al. (2006). Coffee, cirrhosis,
and transaminase enzymes. Archives of Internal Medicine,
166(11):1190-5.
111. Cancer Epidemiology Biomarkers and Prevention, Vaughan TL,
Davis S, Kristal A, et al. (1995). Obesity, alcohol, and tobacco as risk
factors for cancers of the esophagus and gastric cardia:
adenocarcinoma versus squamous cell carcinoma. Cancer
Epidemiology Biomarkers and Prevention, 4(2):85-92.
91. Nurminen ML and Niittynen L. (1999). Coffee, caffeine and blood
pressure: a critical review. European Journal of Clinical Nutrition,
53(11):831-9.
112. Allen N, Beral V, Casabonne D, et al. (2009). Moderate alcohol
intake and cancer incidence in women. Journal of the National Cancer
Institute, 101(5):296-305.
92. Choleau C, Dokladal P, Klein J-C, et al. (2002). Prevention of
hypoglycemia using risk assessment with a continuous glucose
monitoring system. Diabetes, 51(11):3263-73.
113. Stewart B and Kleihaus P. (2002). World cancer report. IARC Press,
Lyon.
93. Pittler MH, Verster JC, and Ernst E. (2005). Interventions for
preventing or treating alcohol hangover: systematic review of
randomised controlled trials. British Medical Journal, 331(7531):15158.
114. Lawes CMM, Hoorn SV, and Rodgers A. (2008). Global burden of
blood-pressure-related disease, 2001. Lancet, 371(9623):1513-8.
27
115. Keil U, Liese A, Filipiak B, et al. (1998). Alcohol, blood pressure and
hypertension. Novartis Foundation symposium, 216:125-44.
137. Pompili M, Mancinelli I, Girardi P, et al. (2004). Suicide in anorexia
nervosa: a meta-analysis. International Journal of Eating Disorders,
36(1):99-103.
116. Doll S, Paccaud F, Bovet P, et al. (2002). Body Mass Index,
abdominal adiposity and blood pressure: consistency of their
association across developing and developed countries. International
Journal of Obesity and Related Metabolic Disorders, 26:48.
138. Hughes K and Bellis M. (2003). Safer nightlife in the North West of
England. Centre for Public Health, Liverpool John Moores University,
Liverpool.
117. Sorof JM, Poffenbarger T, Franco K, et al. (2002). Isolated systolic
hypertension, obesity, and hyperkinetic hemodynamic states in children.
Journal of Pediatrics, 140(6):660-6.
139. Office of the Deputy Prime Minister. (2004). Good practice in
managing the evening and night-time economy: a literature review from
an environmental perspective. The Stationery Office, London.
118. Kenchaiah S, Evans JC, Levy D, et al. (2002). Obesity and the risk
of heart failure. New England Journal of Medicine, 347(5):305-13.
140. Malinauskas B, Aeby V, Overton R, et al. (2007). A survey of energy
drink consumption patterns among college students. Nutrition Journal,
6(1):35.
119. Dolkas L, Stanley C, Smith A, M, et al. (2007). Deaths Associated
with Choking in San Diego County. Journal of Forensic Sciences,
52(1):176-9.
141. O'Brien MC, McCoy TP, Rhodes SD, et al. (2008). Caffeinated
cocktails: energy drink consumption, high-risk drinking, and alcoholrelated consequences among college students. Academic Emergency
Medicine, 15(5):453-60.
120. Jones AW and Holmgren P. (2003). Urine/blood ratios of ethanol in
deaths attributed to acute alcohol poisoning and chronic alcoholism.
Forensic Science International, 135(3):206-12.
142. Local Authority Coordinators of Regulatory Services. (2009).
What's in your doner? Local Authority Coordinators of Regulatory
Services. Press release. 27 January 2009 Available from:
http://www.lacors.gov.uk/lacors/PressReleaseDetails.aspx?id=21017
[accessed 3 November 2009].
121. NHS Information Centre. (2008). Statistics on alcohol: 2008. NHS
Information Centre, London.
122. Medical News Today. (2008). Why is dental health so important?
How are dental caries formed? What is tooth erosion? Medical News
Today.
30
May
2004
Available
from:
http://www.medicalnewstoday.com/articles/8881.php
[accessed
October 2008].
143. Anderson Z, Hughes K, and Bellis M. (2007). Exploration of young
people's experience and perceptions of violence in Liverpool's nightlife.
Centre for Public Health, Liverpool John Moores University, Liverpool.
123. Tezal M, Grossi SG, Ho AW, et al. (2001). The effect of alcohol
consumption on periodontal disease. Journal of Periodontology,
72(2):183-9.
144. Eggert J, Theobald H, and Engfeldt P. (2004). Effects of alcohol
consumption on female fertility during an 18-year period. Fertility and
Sterility, 81(2):379-83.
124. Al-Zahrani MS, Bissada NF, and Borawski EA. (2003). Obesity and
periodontal disease in young, middle-aged, and older adults. Journal of
Periodontology, 74(5):610-5.
145. Lake JK, Power C, and Cole TJ. (1997). Women's reproductive
health: the role of body mass index in early and adult life. International
Journal of Obesity & Related Metabolic Disorders, 21:432.
125. Jarvinen VK, Rytomaa II, and Heinonen OP. (1991). Risk factors in
dental erosion. Journal of Dental Research, 70(6):942-7.
146. Blanker MH, Bohnen AM, Groeneveld FP, et al. (2001). Correlates
for erectile and ejaculatory dysfunction in older Dutch men: a
community-based study. Journal of the American Geriatrics Society,
49(4):436-42.
126. Leon DA and McCambridge J. (2006). Liver cirrhosis mortality rates
in Britain from 1950 to 2002: an analysis of routine data. Lancet,
367(9504):52-6.
147. Derby CA, Mohr BA, Goldstein I, et al. (2000). Modifiable risk
factors and erectile dysfunction: can lifestyle changes modify risk?
Urology, 56(2):302-6.
127. Bedogni G, Bellentani S, Miglioli L, et al. (2006). The Fatty Liver
Index: a simple and accurate predictor of hepatic steatosis in the general
population. BMC Gastroenterology, 6(1):33.
148. Okulate G, Olayinka O, and Dogunro AS. (2003). Erectile
dysfunction: prevalence and relationship to depression, alcohol abuse
and panic disorder. General Hospital Psychiatry, 25(3):209-13.
128. Corrao G, Bagnardi V, Zambon A, et al. (2004). A meta-analysis of
alcohol consumption and the risk of 15 diseases. Preventive Medicine,
38(5):613-9.
149. Mak R, Backer GD, Kornitzer M, et al. (2002). Prevalence and
correlates of erectile dysfunction in a population-based study in Belgium.
European Urology, 41(2):132-8.
129. Ratziu V, Giral P, Charlotte F, et al. (2000). Liver fibrosis in
overweight patients. Gastroenterology, 118(6):1117-23.
150. Jacobson JL, Jacobson SW, Sokol RJ, et al. (1998). Relation of
maternal age and pattern of pregnancy drinking to functionally significant
cognitive deficit in infancy. Alcoholism: Clinical and Experimental
Research, 22(2):345-51.
130. Martinez J, Sanchez-Paya J, Palazon J, et al. (2004). Is obesity a
risk factor in acute pancreatitis? A meta-analysis. Pancreatology,
4(1):42-8.
131. World Health Organization. (2001). World Health Report 2001.
Mental health: new understanding, new hope. World Health
Organization, Geneva.
151. Lashen H, Fear K, and Sturdee DW. (2004). Obesity is associated
with increased risk of first trimester and recurrent miscarriage: matched
case-control study. Human Reproduction, 19(7):1644-6.
132. Anton SD and Miller PM. (2005). Do negative emotions predict
alcohol consumption, saturated fat intake, and physical activity in older
adults? Behavior Modification, 29(4):677-88.
152. Micali N, Simonoff E, and Treasure J. (2007). Risk of major adverse
perinatal outcomes in women with eating disorders. British Journal of
Psychiatry, 190(3):255-9.
133. Blinder BJ, Cumella EJ, and Sanathara VA. (2006). Psychiatric
comorbidities of female inpatients with eating disorders. Psychosomatic
Medicine, 68(3):454-62.
153. Kongo JM, Malcata FX, Ho AJ, et al. (2006). Detection and
characterization of listeria monocytogenes in Sao Jorge (Portugal)
cheese production. Journal of Dairy Science, 89(11):4456-61.
134. Carpenter KM, Hasin DS, Allison DB, et al. (2000). Relationships
between obesity and DSM-IV major depressive disorder, suicide
ideation, and suicide attempts: results from a general population study.
American Journal of Public Health, 90(2):251-7.
154. British Medical Association. (2007). Fetal alcohol spectrum
disorders: a guide for healthcare professionals. British Medical
Association, London.
155. Henderson J, Kesmodel U, and Gray R. (2007). Systematic review
of the fetal effects of prenatal binge-drinking. Journal of Epidemiology
and Community Health, 61(12):1069-73.
135. Gilman SE and Abraham HD. (2001). A longitudinal study of the
order of onset of alcohol dependence and major depression. Drug and
Alcohol Dependence, 63(3):277-86.
136. Kolves K, Varnik A, Tooding L-M, et al. (2006). The role of alcohol
in suicide: a case-control psychological autopsy study. Psychological
Medicine, 36(07):923-30.
28
156. Mukherjee RAS, Hollins S, and Turk J. (2006). Fetal alcohol
spectrum disorder: an overview. Journal of the Royal Society of
Medicine, 99(6):298-302.
177. Department of Health. (2008). Healthy weight, healthy lives: a
cross-government strategy for England. Department of Health, London.
178. Yancey A. (2006). Tackling childhood obesity: requires a shift in
social norms, not just an exercise programme. British Medical Journal,
333(7577):1031-2.
157. Latimer Hill E, Cumming RG, Lewis R, et al. (2007). Sleep
disturbances and falls in older people. Journals of Gerontology Series A:
Biological Sciences and Medical Sciences, 62(1):62-6.
179. LeMura LM and Maziekas MT. (2002). Factors that alter body fat,
body mass, and fat-free mass in pediatric obesity. Medicine and Science
in Sports and Exercise, 34(3):487-96.
158. King CR, Knutson KL, Rathouz PJ, et al. (2008). Short sleep
duration and incident coronary artery calcification. Journal of the
American Medical Association, 300(24):2859-66.
180. Bellis MA, Hughes K, Morleo M, et al. (2007). Predictors of risky
alcohol consumption in schoolchildren and their implications for
preventing alcohol-related harm. Substance Abuse, Treatment,
Prevention and Policy, 2(1):15.
159. Taheri S, Ling L, Austin D, et al. (2004). Short sleep duration is
associated with reduced leptin, elevated ghrelin, and increased Body
Mass Index. Public Library of Science Medicine, 1:210-7.
160. Gupta NK, Mueller WH, Chan W, et al. (2002). Is obesity associated
with poor sleep quality in adolescents? American Journal of Human
Biology, 14(6):762-8.
181. Gately PJ, Cooke CB, Barth JH, et al. (2005). Children's residential
weight-loss programs can work: a prospective cohort study of shortterm outcomes for overweight and obese children. Pediatrics,
116(1):73-7.
161. Vioque J, Torres A, and Quiles J. (2000). Time spent watching
television, sleep duration and obesity in adults living in Valencia, Spain.
International Journal of Obesity & Related Metabolic Disorders, 24:1683.
182. Strauss RS. (2000). Childhood obesity and self-esteem. Pediatrics,
105(1):e15.
162. National Health Service. (2009). Don't lose your snooze, cut back
on the booze. Press release. 19 August 2009 Available from:
http://units.nhs.uk/downloads/Alcohol_and_sleep.pdf [accessed 19
August 2009].
183. Morning Advertiser. (2007). Hot buttered toast = peace. Morning
Advertiser. 24 April 2007.
184. Lindsay J. (2005). Drinking in Melbourne pubs and clubs: a study
of alcohol consumption contexts. School of Political and Social Inquiry,
Monash University, Clayton.
163. Johnson E, Roehrs T, Roth T, et al. (1998). Epidemiology of alcohol
and medication as aids to sleep in early adulthood. Sleep, 21(2):178-86.
185. Arnold M. (2004). Ecstatic equality, happy health and raver rights.
in Club Health Conference, Melbourne.
164. Vitiello MV. (1997). Sleep, alcohol and alcohol abuse. Addiction
Biology, 2(2):151.
186. Graham K, Bernards S, Osgood DW, et al. (2006). Bad nights or
bad bars? Multi-level analysis of environmental predictors of aggression
in late-night large-capacity bars and clubs. Addiction, 101(11):1569-80.
165. Roehrs T and Roth T. (2001). Sleep, sleepiness and alcohol use.
National Institute on Alcohol Abuse and Alcoholism.
166. Foster JH and Peters TJ. (1999). Impaired sleep in alcohol misusers
and dependent alcoholics and the impact upon outcome. Alcoholism:
Clinical and Experimental Research, 23(6):1044-51.
187. Chatterton P. (2002). Governing nightlife: profit, fun and (dis)order
in the contemporary city. Entertainment Law, 1:23-49.
188. Hollands R and Chatterton P. (2002). Changing time for an old
industrual city: hard times, hedonism and corporate power in
Newcastle's nightlife. City, 6(3):291-315.
167. Deacon L, Hughes S, Tocque K, et al. (2007). Indications of public
health in the English regions 8: alcohol. Association of Public Health
Observatories, York.
189. Simpson A. (2008). Supermarket shoppers could be forced
through alcohol-only checkout. Telegraph. 22 October 2008.
168. Kinra S, Nelder RP, and Lewendon GJ. (2000). Deprivation and
childhood obesity: a cross sectional study of 20 973 children in
Plymouth, United Kingdom. Journal of Epidemiology and Community
Health, 54(6):456-60.
190. Devlin K. (2009). £10 'dinner and wine for two' offers fuelling rise
in middle-class drinking. Telegraph. 31 October 2009.
191. Huddleston N. (2008). Enlightened times. Morning Advertiser. 24
April 2008.
169. Information Centre for Health and Social Care. (2006). Health
Survey for England 2005 [online]. Information Centre for Health and
Social Care. Available from: http://www.ic.nhs.uk/pubs/hseupdate05
[accessed 1 February 2008].
192. Department of Health and National Treatment Agency for
Substance Misuse. (2006). Models of Care for Alcohol Misuse.
Department of Health, London.
170. Morleo M, Phillips-Howard P, Cook P, et al. (2008). Fact sheet 1:
tolerance and perceptions of drinking. Centre for Public Health,
Liverpool John Moores University, Liverpool.
193. Gossop M. (2006). Treating drug misuse problems: evidence of
effectiveness. National Treatment Agency for Substance Misuse,
London.
171. Schnohr C, Hojbjerre L, Riegels M, et al. (2004). Does educational
level influence the effects of smoking, alcohol, physical activity, and
obesity on mortality? A prospective population study. Scandinavian
Journal of Public Health, 32(4):250-6.
194. Cook P, Tocque K, Morleo M, et al. (2008). Opinions on the impact
of alcohol on individuals and communities: early summary findings from
the North West Big Drink Debate. Centre for Public Health, Liverpool
John Moores University, Liverpool.
172. Dube SR, Anda RF, Felitti VJ, et al. (2002). Adverse childhood
experiences and personal alcohol abuse as an adult. Addictive
Behaviors, 27(5):713-25.
195. National Institute for Clinical and Health Excellence. (2006).
Understanding NICE guidance: information for the public. Preventing
obesity and staying a healthy weight. National Institute for Clinical and
Health Excellence, London.
173. Williamson DF, Thompson TJ, Anda RF, et al. (2002). Body weight
and obesity in adults and self-reported abuse in childhood. International
Journal of Obesity & Related Metabolic Disorders, 26(8):1075.
196. Food Standards Agency. (no date). Understanding labelling rules.
Food Standards Agency. Online article.
Available from:
www.food.gov.uk/foodlabelling/ull [accessed 20 April 2009].
174. Trotter L, Wakefield M, and Borland R. (2002). Socially cued
smoking in bars, nightclubs, and gaming venues: a case for introducing
smoke-free policies. Tobacco Control, 11(4):300-4.
197. Commission of the European Communities. (2008). Proposal for a
regulation of the European Parliament and of the Council on the
provision of food information to consumers. Commission of the
European Communities,. Online document.
Available from:
http://ec.europa.eu/food/food/labellingnutrition/foodlabelling/proposed_
legislation_en.htm [accessed 24 June 2009].
175. Li MD, Kane JK, and Konu O. (2003). Nicotine, body weight and
potential implications in the treatment of obesity. Current Topics in
Medicinal Chemistry, 3:899.
176. Cheskin LJ, Hess JM, Henningfield J, et al. (2005). Calorie
restriction
increases
cigarette
use
in
adult
smokers.
Psychopharmacology, 179(2):430-6.
198. Food Standards Agency (1996). Food Labelling Regulations. The
Stationery Office, Editor.
29
199. European Commission. (2006). Labelling: competitiveness,
consumer information and better regulation for the EU. A DG SANCO
consultative document. European Commission.
222. Centre for Public Health. (2007). New Local Authority Alcohol
Profiles for England reveal major differences in drinking behaviours and
impact on health. Centre for Public Health, Liverpool John Moores
University, Liverpool.
200. OPTEM. (2005). The European consumers' attitudes regarding
product labelling: qualitative study in 28 European countries. European
Commission.
223. Department of Health. (2009). Tackling health inequalities: 10 years
on. A review of the developments in tackling health inequalities in
England over the last 10 years. Department of Health, London.
201. Home Office. (2009). Safe. Sensible. Social. Selling alcohol
responsibly: a consultation on the new code of practice for alcohol
retailers. England and Wales. Home Office, London.
224. Department of Health. (2008). Ambitions for health. Department of
Health, London.
202. Good Food Channel. (no date). Vegetarian and vegan wine. Good
Food
Channel.
Online
article.
Available
from:
http://uktv.co.uk/food/item/aid/580883 [accessed 3 November 2009].
225. Hibell B, Guttormsson U, Ahlstrom S, et al. (2009). The 2007
ESPAD report: substance use among students in 35 European
countries. Swedish Council for Information on Alcohol and other Drugs.
203. Veggie Wines. (no date). What? There's animals in booze? Veggies
Wines. Online article. Available from: http://www.veggiewines.co.uk/
[accessed 2 November 2009].
226. Jackson C. (1997). Initial and experimental stages of tobacco and
alcohol use during late childhood: Relation to peer, parent, and personal
risk factors. Addictive Behaviors, 22(5):685-98.
204. Elliott V. (2008). Muslims shocked to learn that crisps contain
alcohol. The Times. 22 February 2008.
227. Jackson C, Henriksen L, Dickinson D, et al. (1997). The early use
of alcohol and tobacco: its relation to children's competence and
parents' behavior. American Journal of Public Health, 87(3):359-64.
205. Mills P. (2008). Connecting the dots: an economis evaluation of the
Connect 4 Life Health programme. Vielife.
228. Wood MD, Read JP, Mitchell RE, et al. (2004). Do parents still
matter? Parent and peer influences on alcohol involvement among
recent high school graduates. Psychology of Addictive Behaviors,
18(1):19-30.
206. Vielife. (2008). Connect 4 Life: assisting cost effective use of NHS
resources. Vielife.
207. Meier P, Booth A, O'Reilly D, et al. (2008). Independent review of
the effects of alcohol pricing and promotion: Part B. Modelling the
potential impact of pricing and promotion policies for alcohol in England:
results from the Sheffield Alcohol Policy Model Version 2008 (1-1).
Department of Economics, University of Sheffield, Sheffield.
229. Plant M and Miller P. (2001). Young people and alcohol: an
international insight. Alcohol and Alcoholism, 36(6):513-5.
230. Department for Children Schools and Families. (2009). Draft
guidance on the consumption of alcohol and young people from the
Chief Medical Officers of England, Wales and Northern Ireland.
Department for Children Schools and Families, London.
208. Phillips-Howard P, Morleo M, Cook P, et al. (2008). Fact sheet 3:
cheaply available alcohol, irresponsible promotions and deep
discounting. Centre for Public Health, Liverpool John Moores University,
Liverpool.
231. Morleo M, Elliott G, and Cook P. (2008). Investigating drinking
behaviours and alcohol knowledge amongst people resident in the
Linacre and Derby wards of Sefton: an evaluation of the 'It's Your
Choice' Intervention. Centre for Public Health, Liverpool John Moores
University, Liverpool.
209. Academy of Medical Sciences. (2004). Calling time: the nation's
drinking as a major health issue. Academy of Medical Sciences, London.
210. Caraher M and Cowburn G. (2005). Taxing food: implications for
public health nutrition. Public Health Nutrition, 8(08):1242-9.
232. Rodríguez Artalejo F, López García E, Gutiérrez-Fisac JL, et al.
(2002). Changes in the prevalence of overweight and obesity and their
risk factors in Spain, 1987-1997. Preventive Medicine, 34(1):72-81.
211. Alcohol Concern. (2008). Alcohol Concern urges pubs to up their
game against drink driving this season - charity recommends slashing
soft drink prices for designated drivers. Alcohol Concern. Press release.
Available from: http://www.alcoholconcern.org.uk/servlets/doc/1406
[accessed 5 November 2009].
233. Valencia-Martín JL, Galán I, and Rodríguez-Artalejo F. (2007). Binge
drinking in Madrid, Spain. Alcoholism: Clinical and Experimental
Research, 31(10):1723-30.
234. Gracia A and Albisu LM. (1999). Moving away from a typical
Meditteranean diet: the case of Spain. British Food Journal, 101(9):70114.
212. Smith C. (2008). New booze culture row: food up 20% but alcohol
prices plunge. Scotsman. 14 June 2008.
213. Muspratt C. (2008). Pubcos ride out the downturn. Morning
Advertiser. 8 May 2008.
214. Creasey S. (2008). Plan your snack attack. Morning Advertiser. 3
July 2008.
215. Quinn C. (2007). The breakfast club. Morning Advertiser. 1 March
2007.
216. Yates N. (2007). Snacks focus: fill the snack gap. Morning
Advertiser. 24 May 2007.
217. Boyce T, Robertson R, and Dixon A. (2008). Commissioning and
behaviour change: kicking bad habits final report. The King's Fund,
London.
218. Alchemy Research Associates. (2008). 'Pssst!' campaign
evaluation research. Quantitative: Stage #1 toplines. Liverpool Primary
Care Trust, Liverpool.
219. Alchemy Research Associates. (2008). 'Pssst!' campaign
evaluation research. Qualitative stage. Liverpool Primary Care Trust,
Liverpool.
220. Alchemy Research Associates. (2008). 'Pssst!' campaign
evaluation research. December 2007 - March 2008. Liverpool Primary
Care Trust, Liverpool.
221. Information Centre and Lifestyles Statistics (2009). Statistics on
obesity, physical activity and diet: England, February 2009. Health and
Social Care Information Centre, London.
30
Centre for Public Health
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Published January 2010
ISBN: 978-1-907441-14-1 (print version)
ISBN: 978-1-907441-15-8 (pdf version)