Are the opportunities to prevent alcohol related liver deaths in the UK in primary or secondary care? A retrospective clinical review and prospective interview study

Background  

Deaths from liver cirrhosis have increased at least 8 fold since the 1970's in the UK and further increases are anticipated, whereas in the rest of Europe liver deaths are decreasing. In the UK, we urgently need strategies to detect those who misuse alcohol and are at risk of developing alcoholic liver disease before they get to that point. One potential strategy is to screen admissions to hospital with alcohol related conditions for evidence of alcohol misuse.     

Treatment of advanced alcoholic liver disease

The poor prognosis of severe acute alcoholic hepatitis has stimulated interest in specific forms of treatment aimed at reducing the short term mortality as well as preventing progression to cirrhosis. Several controlled trials of steroid therapy have suggested an improvement in short-term survival, but the benefit seems to apply to highly selected cases only. Treatment with propylthiouracil and insulin and glucagon infusions has also shown promising results in controlled studies but there is still no general agreement on their value. Despite recent interest in the use of colchicine to prevent progression of cirrhosis in chronic liver disease of other aetiologies, its role in alcoholic liver disease is not yet clear. In end-stage alcoholic cirrhosis, excellent results are now being achieved with liver transplantation, although this is limited to patients who are not alcohol dependent and in whom there is no alcohol-induced extrahepatic disease.     

Coffee intake and mortality from liver cirrhosis

PURPOSE: The aim of the study was to evaluate the association between coffee consumption and mortality from liver cirrhosis. METHODS: We conducted a mortality follow-up of 51,306 adults who underwent screening for cardiovascular disease from 1977 to 1983. During the subsequent 17 years, the total number of deaths from all causes in the studied cohort was 4207. Fifty-three had the diagnosis of cirrhosis mentioned on the death certificate; of these, 36 had alcoholic cirrhosis. RESULTS: The relative risk of liver cirrhosis mentioned on the death certificate associated with an increase of two cups of coffee, adjusted for sex, age, alcohol use and other major cardiovascular risk factors was 0.6 (95% confidence interval, 0.5-0.8). For alcoholic cirrhosis the results were identical. When studying cirrhosis as the underlying cause of death, the inverse relationship becomes somewhat stronger. CONCLUSIONS: The present study confirms the existence of an inverse association between coffee consumption and liver cirrhosis.     

Oxygen gradients in alcohol-induced liver injury

Alcoholism is a major health problem and one of its primarymanifestations is alcoholic liver disease. The mechanisms responsiblefor the various forms of alcoholic liver disease - fatty liver,alcoholic hepatitis and cirrhosis - are at present poorly understood.Knowledge of these mechanisms is needed in order to providea sound framework for the therapy and prevention of liver diseasedue to alcohol and for the identification of those individualsmost susceptible to develop liver disease from alcohol abuse.     

Alcohol and dietary intake in the development of chronic pancreatitis and liver disease in alcoholism

Alcohol and dietary intake were determined in alcoholic patients with chronic pancreatitis and alcoholic liver disease. Patients with chronic pancreatitis, alcoholic hepatitis, and cirrhosis ingested approximately 50% of their calories as alcohol, and all had low mean intakes of protein, carbohydrate, and fat as compared with control subjects. Patients with severe alcoholic hepatitis had the lowest intake of nonalcohol calories and protein. Women with chronic pancreatitis had ingested alcohol for a shorter period of time than men whereas women with alcoholic hepatitis and cirrhosis had ingested less alcohol per kilogram body weight per day as compared with men. This study does not support the hypothesis that consumption of a high-protein and high-fat diet is a factor in the development of chronic pancreatitis in the alcoholic patient. The increased susceptibility of women as compared with men to alcoholic liver disease is established.     

Alcoholic cirrhosis of the liver in the Scandinavian countries 1961-1974

The increase in mortality from alcohol induced cirrhosis of the liver in Sweden, Norway, Finland and Denmark from 1961 to 1974 is compared. Mortality from alcoholic cirrhosis of the liver increased in Finland and Denmark tenfold and fivefold respectively from 1961 to 1974. The increase has been particularly marked since 1968. In Sweden a threefold increase and in Norway a doubling of mortality in males was ascribed to alcohol induced liver cirrhosis. Mortality from non-alcoholic cirrhosis of the liver remained practically unchanged during the period. Increases in mortality from liver cirrhosis due to alcohol abuse run parallel with increases in alcohol consumption; the countries with the highest mortality have the highest consumption. The distribution of consumption of beer, wine and spirit is compared in the four countries: consumption of spirits predominates in Sweden, in Finland spirits and beer, in Denmark beer and wine and in Norway spirits and beer. Doubling of alcohol consumption in a country is followed by a fourfold increase in the number of addicts, and fourfold increase in alcohol induced diseases.     

Alcohol, smoking, coffee, and cirrhosis.

Since most heavy drinkers do not develop alcoholic cirrhosis, other causes or predisposing factors are probable. The authors studied traits of 128,934 adults who underwent health examinations at the Oakland and San Francisco, California, facilities of the Kaiser Permanente Medical Care Program from January 1978 to December 1985 in relation to subsequent hospitalization or death from cirrhosis of the liver. In analyses adjusted for nine covariates, past and current alcohol drinking were strongly related to cirrhosis risk, but usual choice of alcoholic beverage had no independent relation. Cigarette smoking was independently related to risk of alcoholic cirrhosis, with cigarette smokers of a pack or more per day at trebled risk compared with lifelong nonsmokers. Coffee drinking, but not tea drinking, was inversely related to alcoholic cirrhosis risk, with persons who drank four or more cups per day at one-fifth the risk of noncoffee drinkers. This inverse relation between coffee consumption and risk of alcoholic cirrhosis was consistent in many subsets, including persons free of gastrointestinal disease and those with 5 or more years before hospitalization or death. Cigarette smoking and coffee consumption were not consistently related to risk of hospitalization or death for nonalcoholic cirrhosis. These data could mean that cigarette smoking promotes alcoholic cirrhosis and that coffee drinking might be protective.     

Cytotoxic T-lymphocyte antigen-4 A49G polymorphism is associated with susceptibility to and severity of alcoholic liver disease in Italian patients

AIMS: To determine whether the functional A49G polymorphism of cytotoxic T-lymphocyte antigen-4 (CTLA-4), a T-cell surface molecule that modulates T-lymphocyte activation and influences the risk of developing alcohol-induced autoantibodies, plays a role in susceptibility to alcoholic liver disease (ALD) and influences disease severity in Italian alcohol abusers. METHODS: One hundred and eighty-three patients with chronic ALD (61 cirrhosis), 115 end-stage HCV cirrhosis, 102 non-alcoholic fatty liver disease (NAFLD), 93 healthy subjects and 43 heavy drinkers without liver disease were studied. CTLA-4 gene polymorphism was analysed by restriction analysis. RESULTS: The frequency of the CTLA-4 polymorphism was higher in patients with ALD than in patients with HCV chronic hepatitis and NAFLD, healthy subjects (P < 0.0001), and heavy drinkers without liver disease (P = 0.02). In patients with ALD, homozygosity for the CTLA-4 polymorphic allele (G/G genotype) was more represented in subjects with cirrhosis (P = 0.047), and independently associated with the risk of cirrhosis (OR 3.5; P = 0.03). CONCLUSIONS: The CTLA-4 polymorphic G allele, probably by interfering with the immune response, may confer susceptibility to ALD and, in homozygous state, to alcoholic cirrhosis.     

Hemochromatosis and alcoholic liver disease

The close association of excessive alcohol consumption and clinical expression of hemochromatosis has been of widespread interest for many years. In most populations of northern European extraction, more than 90% of patients with overt hemochromatosis are homozygous for the C282Y mutation in the HFE gene. Nevertheless, the strong association of heavy alcohol intake with the clinical expression of hemochromatosis remains. We (individually or in association with colleagues from our laboratories) have performed three relevant studies in which this association was explored. In the first, performed in 1975 before the cloning of the HFE gene, the frequency of clinical symptoms and signs was compared in patients with classical hemochromatosis who consumed 100 g or more of alcohol per day versus in nondrinkers or moderate drinkers who consumed less than 100 g of alcohol per day. The results showed no difference between the two groups except for features of complications of alcoholism in the first group, especially jaundice, peripheral neuritis, and hepatic failure. Twenty-five percent of those with heavy alcohol consumption showed histologic features of alcoholic liver disease (including cirrhosis) together with heavy iron overload. It was concluded that these patients had the genetic disease complicated by alcoholic liver disease. In the second study (2002), 206 subjects with classical HFE-associated hemochromatosis in whom liver biopsy had been performed were evaluated to quantify the contribution of excess alcohol consumption to the development of cirrhosis in hemochromatosis. Cirrhosis was approximately nine times more likely to develop in subjects with hemochromatosis who consumed more than 60 g of alcohol per day than in those who drank less than this amount. In the third study (2002), 371 C282Y-homozygous relatives of patients with HFE-associated hemochromatosis were assessed. Eleven subjects had cirrhosis on liver biopsy and four of these drank 60 g or more of alcohol per day. The reason why heavy alcohol consumption accentuates the clinical expression of hemochromatosis is unclear. Increased dietary iron or increased iron absorption is unlikely. The most likely explanation would seem to be the added co-factor effect of iron and alcohol, both of which cause oxidative stress, hepatic stellate cell activation, and hepatic fibrogenesis. In addition, the cumulative effects of other forms of liver injury may result when iron and alcohol are present concurrently. Clearly, the addition of dietary iron in subjects homozygous for hemochromatosis would be unwise.     

Wine consumption is not associated with a decreased risk of alcoholic cirrhosis in heavy drinkers

- AIMS: While it was thought that all alcoholic beverages share a similar liver toxicity when drunk at a high level, recent epidemiological surveys have suggested that wine drinking might decrease the risk of alcoholic cirrhosis in heavy drinkers. Therefore, we performed a study aiming to analyse the type and the intake levels of alcoholic beverages in heavy drinkers according to the severity of the liver disease. METHODS: This is a case-control study enrolling 42 cirrhotic and 60 non-cirrhotic patients. Liver status was assessed using clinical, biological, histological and ultrasonographic procedures. Alcohol consumption was recorded using the Lifetime Drinking History method. RESULTS: We did not find any significant differences in total alcohol consumption between cases and controls and, moreover, in our series, the relative percentage of pure alcohol drunk in wine was significantly higher in cirrhotic, than in non-cirrhotic, patients. CONCLUSIONS: Our results confirm that the absence of a link between the type of alcoholic beverage and the occurrence of cirrhosis is still valid.     

Liver disease in alcohol abusers: clinical perspective.

Alcoholic liver disease remains one of the most common causes of chronic liver disease in the world. The severity of liver damage related to alcohol varies among different individuals and even within any given individual at different times. Certain symptoms, signs, and abnormal findings on laboratory tests help clinicians distinguish among the various stages of alcohol-induced liver damage and, thus, have some prognostic significance. However, because all stages of this disease can persist for decades without causing overt evidence of serious liver damage, liver biopsy is the only test that can reliably distinguish among the various stages of alcohol-induced liver damage in many patients. The therapy of alcohol-induced liver disease varies according to the severity of histologic liver damage and clinically overt portal hypertension and hepatic dysfunction. Abstinence from alcohol consumption improves the clinical outcome of all stages of alcoholic liver disease. However, only two agents have proved to lessen early mortality in patients who require hospitalization for acutely decompensated alcoholic liver disease. It is not known whether either of these agents or other treatments prevent the development of alcohol-induced cirrhosis or improve the survival of patients who have already developed cirrhosis.     

Alcohol misuse in older people: heavy consumption and protean presentations

BACKGROUND: Alcohol misuse, especially binge drinking in young people, and alcoholic liver disease are major public health concerns. However, alcohol misuse in older people is underestimated and often goes undetected. OBJECTIVE: To document alcohol consumption and clinical presentation of alcohol misuse in hospital inpatients aged >or=60 years. METHODS: 208 inpatients aged >or=60 years, referred to the alcohol liaison nurse between 1998 and 2003 at the Royal Bolton Hospital, Bolton, UK, were assessed for sex, alcohol intake, primary and secondary reasons for admission, and other concurrent health problems and death. RESULTS: 90% of men drank >21 units weekly and 93% of women drank >14 units weekly. Median weekly alcohol intake was 78.5 units for men and 47 units for women. Acute intoxication, falls, circulatory problems and alcoholic liver disease were the main primary reasons for admission. Neglect or malnutrition, alcoholic liver disease and hypertension were the main secondary reasons and concurrent health problems. 30% of patients died between 1998 and 2003. CONCLUSION: In inpatients aged >or=60 years who were referred to the alcohol liaison nurse in a district general hospital, heavy alcohol consumption, often to very high levels, was characteristic in both men and women and was associated with a wide variety of primary and secondary clinical presentations, including death.     

Alcohol consumption as a major risk factor for the rise in liver cancer mortality rates in Japanese men

BACKGROUND: Age-adjusted liver cancer mortality rates have been increasing for both men and women in Japan since 1970; however, increases in mortality rates in men are much greater than those in women. Hepatitis C virus infections and heavy alcohol consumption are considered to be the major risk factors of liver cancer deaths in Japanese. The purpose of this study is (1) to examine the pattern of liver cancer mortality by gender and birth year to compare those with the pattern of other alcohol-related mortality and (2) to estimate the attributable risk per cent of heavy alcohol consumption for liver cancer deaths in Japanese men. METHODS: Age-specific liver cancer mortality rates by gender were compared with those of cirrhosis mortality rates. Then male-to-female mortality rate ratios were calculated by birth cohort and compared with cirrhosis mortality rate ratios and oesophageal cancer mortality rate ratios. The attributable risk per cent of alcohol consumption for liver cancer death was calculated, using female liver cancer mortality rates as standard rates. RESULTS: Examination of both gender and birth cohort mortality rates revealed that male-to-female liver cancer mortality rate ratios by birth cohort correspond well with those rate ratios for liver cirrhosis and oesophageal cancer mortality. The attributable risk per cent of alcohol consumption for liver cancer deaths in Japanese men was 70%. CONCLUSION: Alcohol consumption is more important than hepatitis C virus infections as a major cause of liver cancer deaths in Japanese men.     

Biochemical Mechanisms of the Alcohol-Induced Liver Injury

1. The biochemical mechanisms of the alcohol-induced liver injuryare reviewed. 2. Acute alcohol intake causes redox changes inpyridine nucleotides, a fatty liver and an exacerbation of hepaticporphyrias. 3. The redox changes are caused by alcohol metabolism,and it is hoped that substances other than fructose, which areknown to accelerate alcohol metabolism, will be tested clinicallyin acute alcoholic intoxication. 4. The acute fatty liver isproduced by an increased hepatic uptake of plasma free fattyacids secondary to enhanced hepatic blood flow, an activationof phosphatidate phosphohydrolase and a possible hypermobilizationof adipose-tissue fat. 5. The alcohol exacerbation of hepaticporphyrias may be due to the further removal of the regulatoryhaem pool controlling haem biosynthesis. 6. Chronic alcoholintake causes redox changes similar to those mentioned above,a fatty liver and hepatitis, cirrhosis and necrosis. 7. Theredox change in the NADP couple is caused by that in the NADcouple. 8. The chronic fatty liver is produced mainly by anincreased esterification of fatty acids. Dietary fat plays animportant role, and factors such as increased hepatic uptakeof plasma free fatty acids and activation of phosphohydrolasemay also be involved. 9. We know very little about the biochemicalpathology of the alcoholic hepatitis and cirrhosis. 10. In experimentalanimals, chronic alcohol consumption causes hepatic-cell necrosisif the liver is either exposed to a high concentration of alcoholor if made anoxic by exposing the animals to low oxygen atmospheresor by bleeding. 11. There is evidence that acetaldehyde maybe involved in some of the hepatotoxic effects of alcohol. 12.Alcohol also causes lipid peroxidation and the possibility thatdestruction of membrane phospholipid is involved in the hepatotoxicityof alcohol cannot be ruled out.     

Relationships between blood lead concentration and aminolevulinic acid dehydratase in alcoholics and workers industrially exposed to lead

Blood lead concentration (Pb-B), aminolevulinic acid dehydratase (ALAD), and gamma-GT were measured in 265 workers industrially exposed to lead and in 184 patients with liver disease resulting from alcohol consumption. The first group was divided according to alcohol use, i.e., nondrinkers, moderate drinkers, and heavy drinkers. The second group was divided according to the following criteria: hepatopatic without cirrhosis, hepatopatic with compensated cirrhosis, and hepatopatic with decompensated cirrhosis. Heavy drinkers who were industrially exposed had the highest Pb-B (40.4 +/- 14.6 micrograms/dl) and the lowest ALAD (22.2 +/- 9.1 U/L). The correlations between Pb-B and ALAD show no significant change with the increase of Pb-B. In the alcoholic group, 76 patients with alcoholic liver disease without cirrhosis had the highest Pb-B (40.3-9.1 micrograms/dl) and ALAD the lowest (18.6 +/- 7.7 U/L). The negative correlation between Pb-B and log ALAD disappeared completely in individuals with Pb-B that exceeded 50 micrograms/dl, independent from the seriousness of illness.     

A case-control study on alcohol consumption and the risk of chronic liver disease.

We carried out a hospital based case-control study involving 655 patients with chronic liver disease encompassing chronic hepatitis, asymptomatic liver cirrhosis and symptomatic liver cirrhosis and 655 pair-matched control individuals in order to estimate the dose-response relationship between alcohol consumption and the occurrence of chronic liver disease. Alcohol intake was measured by a questionnaire and expressed as Daily Alcohol Intake (DAI) during the patient life. DAI estimates from patient interviews were in good agreement with those obtained by interviewing a sample of relatives. We found an exponential positive association between DAI and the risk of chronic hepatitis and cirrhosis. However, consuming less than 100g of alcohol every day did not increase the risk of developing chronic liver disease. For asymptomatic cirrhosis the risk was lower than for chronic hepatitis, especially at high DAI, probably because high consumption carried a high probability of liver decompensation. For symptomatic cirrhosis, the risk function showed a similar pattern as for chronic hepatitis. Chronic hepatitis patients were 6-7 years younger than cirrhotics. Our results suggest that the evolution towards cirrhosis once a chronic liver damage has occurred is probably time-dependent, but not or minimally dependent on alcohol intake.     

Nutritional assessment in various stages of liver cirrhosis

OBJECTIVES: The aims of this study were to determine the prevalence of protein-calorie malnutrition, characteristics, and clinical importance of nutrition disorders in patients with liver cirrhosis according to severity of disease. METHODS: Nutrition assessments such as subjective global assessment, anthropometric and biochemical measurements, immunocompentency, thiamin and riboflavin status in 60 patients with cirrhosis (33 male and 27 female) were recorded between June 1999 and December 1999 at an outpatient clinic at Ramathibodi Hospital, Bangkok, Thailand. The origin of liver disease was alcohol related in 50% of patients. Child-Pugh criteria were used to establish the severity of liver disease. RESULTS: In terms of energy malnutrition, 13.3% of patients had ideal body weights below 90% and 11.7% had body mass indexes below 18.5 kg/m(2). Protein malnutrition (low albumin) and immunoincompetence (abnormal response to skin tests) were found much more frequently (45% and 22%) than energy malnutrition. Patients with alcoholic cirrhosis had ascites (P < 0.05) and hepatic encephalopathy (P < 0.001) more frequently and less triceps skinfold thickness than those with non-alcoholic cirrhosis. Subjective global assessment and serum proteins correlated with the degree of liver-function impairment, but immunologic tests correlated inversely in cirrhosis patients. Mean values for creatinine-height index, hemoglobin, cholesterol, and complement C4 showed significant decreases in severe liver failure (Child-Pugh class C) only in patients with alcoholic cirrhosis (P < 0.05). Malnutrition was correlated with the clinical severity of liver disease. CONCLUSIONS: The study showed that protein-energy malnutrition is a common complication of liver cirrhosis. Nutritional disorders appeared to be related to the degree of liver injury and the etiology of nutritional disorders. Nutritional disorders were more severe with alcoholic cirrhosis than with non-alcoholic cirrhosis.     

Risk of end-stage renal disease associated with alcohol consumption

Alcohol consumption has been linked to kidney disorders in selected patient groups, but whether it contributes to the burden of end-stage renal disease (ESRD) in the general population is unknown. The authors conducted a population-based case-control study to assess the relation between alcohol consumption and risk of ESRD. The study took place in Maryland, Virginia, West Virginia, and Washington, DC, in 1991. Participants were 716 patients who had started treatment for ESRD and 361 control subjects of similar age (20-64 years) selected by random digit dialing. The main risk factor of interest was self-reported consumption of alcoholic beverages (frequency of drinking days and number of drinks consumed per drinking day). In univariate analysis, consumption of alcohol exhibited a J-shaped association with risk of ESRD. The J shape disappeared after exclusion of persons who had ever consumed home-distilled whiskey ("moonshine") and adjustment for age, race, sex, income, history of hypertension, history of diabetes mellitus, use of acetaminophen, use of opiates, and cigarette smoking; however, the odds ratio for ESRD remained significantly increased (odds ratio = 4.0; 95% confidence interval: 1.2, 13.0) among persons who consumed an average of >2 alcoholic drinks per day. The corresponding population attributable risk was 9 percent. Thus, consumption of more than two alcoholic drinks per day, on average, was associated with an increased risk of kidney failure in the general population. A lower intake of alcohol did not appear to be harmful. Because these results are based on self-reports in a case-control study, they should be seen as preliminary.     

Alcohol consumption in the new millennium – weighing up the risks and benefits for our health

• 1 Introduction
• 2 An introduction to alcohol and alcoholic beverages
  • 2.1 How is alcohol produced
  • 2.2 The production of alcoholic beverages
  • 2.3 Calculation of alcohol content in beverages
  • 2.4 Other measures of alcohol
• 3 Guidelines for sensible drinking
  • 3.1 UK guidelines
  • 3.2 Guidelines for sensible drinking around the world
• 4 Alcohol consumption
  • 4.1 Current alcohol intakes in the UK
  • 4.2 Recent trends in alcohol intake in the UK
  • 4.3 Trends around the world
• 5 Absorption and metabolism of alcohol
  • 5.1 Absorption of alcohol
  • 5.2 Alcohol metabolism
• 6 Alcohol and nutrition
  • 6.1 Nutrient composition of alcoholic beverages
  • 6.2 The effect of alcohol on energy intake
  • 6.3 Nutritional implications of chronic excessive alcohol consumption
  • 6.4 Other components of alcoholic beverages
• 7 The burden of disease and mortality related to alcohol
• 8 Alcohol and disease risk
  • 8.1 Methodological problems of studies assessing associations between alcohol consumption and disease risk
  • 8.2 Alcohol and bodyweight
  • 8.3 Alcohol and coronary heart disease
  • 8.4 Alcohol and blood pressure
  • 8.5 Alcohol and stroke
  • 8.6 Alcohol and type 2 diabetes
  • 8.7 Alcohol and cancer
• 9 Alcohol and other conditions
  • 9.1 Adverse reactions to alcohol for some susceptible individuals
  • 9.2 Alcohol and peptic ulcers
  • 9.3 Alcohol during pregnancy
  • 9.4 Alcohol, bone mineral density and fracture risk
  • 9.5 Alcohol and renal dysfunction
• 10 Alcohol and social issues
  • 10.1 Short‐term psychological and psychomotor effects of alcohol intake
  • 10.2 Crime and public disorder as a result of drinking alcohol
  • 10.3 Alcohol‐related harms and other public health issues
  • 10.4 The economics of alcohol consumption
  • 10.5 Population‐based initiatives underway to reduce the incidence of binge drinking
• 11 Conclusions

Summary Alcohol is produced via the anaerobic fermentation of sugars by yeast and involves glucose molecules (C₆H₁₂O₆) being broken down to yield ethanol (C₂H₅OH), carbon dioxide (CO₂) and energy. The amount of alcohol contained in different alcoholic beverages varies considerably and is referred to as the ‘strength’ of the drink, which is expressed as the percentage of alcohol by volume (ABV). A standard unit of alcohol in the UK equates to 8 g or 10 ml of pure alcohol. Guidelines for sensible drinking set by the UK government are 3–4 units (24–32 g) a day or less for men, and 2–3 units (16–24 g) a day or less for women. Specific recommendations have been set for those planning pregnancy and pregnant women, who should drink no more than 1–2 units of alcohol once or twice a week and should avoid heavy drinking sessions. Guidelines for sensible drinking are similar in other countries. When taking into account the standard drink unit used to define guidelines, the most commonly recommended limit is 24 g/day for men and 20 g/day for women. Older people are more likely to drink in line with the sensible drinking guidelines, as they tend to consume alcohol over a period of time, as opposed to consuming large quantities on one or two days of the week, a practice that is more popular among younger people. Consuming double the sensible drinking guidelines in one day is classified as binge drinking (an alternative definition is drinking until intoxicated). It has become recognised that binge drinking is a common phenomenon in the UK, particularly among younger people. Other factors, such as income, ethnicity and region of residence, are also recognised to be predictive of the quantity of alcohol consumed; for example, higher‐income households are more likely to consume large quantities of alcohol and consume alcohol more frequently. The quantity of alcohol consumed is an important factor in determining how it affects health and well‐being. In terms of nutritional health, chronic excessive alcohol intake is well recognised to affect an individual’s nutrient status, because it reduces food intake and/or may interfere with the digestion, absorption, metabolism and utilisation of some nutrients. However, when consumed in moderation, alcohol is unlikely to interfere with the metabolism of nutrients or be associated with impaired vitamin function or depletion to an extent that may harm health, provided that dietary intakes are adequate. Alcoholic beverages contain alcohol, carbohydrate and only small amounts of some vitamins, trace elements and minerals. They are therefore unlikely to contribute significantly to micronutrient intake. Any association that exists between moderate alcohol consumption and the absorption and metabolism of nutrients from the diet is dependant on a number of factors, including: the nutrient in question; habitual intake of the nutrient and the nutritional status of the individual; and the quantity of alcohol consumed over a period of time. Overall, little information exists about the implications of binge drinking on nutrient status; but it may alter food intake, and excessive alcohol consumption can cause disturbances to the digestive system. While infrequent binge drinking is unlikely to have any long‐term nutritional implications (although it may affect nutrient status in the short‐term), regular binge drinking may have a more negative impact. Although alcoholic beverages tend to have few nutrients, they can be a significant source of energy, as alcohol provides 7 kcal per gram. Studies indicate that alcoholic beverages are usually additive to an individual’s normal energy intake and individuals are unlikely to compensate for energy from them during the day. The aperitif effect of alcohol may also encourage an increase in energy intake. It is therefore not surprising that alcohol intake has been associated with weight gain and an increase in body mass index (BMI) (with the exception of chronic excessive drinkers). However, there are a number of methodological problems that need to be considered when comparing the findings of studies investigating the association between alcohol intake and disease risk, including: potential misreporting of total intake; the use of an appropriate control group; and the need for comparable measurement units. Consumption of alcoholic beverages has also been associated with increasing the risk of ill‐health associated with pre‐existing conditions. For example, it may contribute to ulcer development or aggravate symptoms of existing ulcers. There is evidence that moderate alcohol consumption during pregnancy may affect the development of the fetus’s central nervous system, and may result in low birthweight. However, there is currently no consensus as to whether alcohol should be completely avoided during pregnancy. However, it is well recognised that excess alcohol consumption during pregnancy can put the fetus at risk of fetal alcohol syndrome. Quantity of alcohol consumed is particularly important when considering the association between alcohol and chronic diseases; for example, there is now strong evidence that light to moderate (1–3 drinks per day) consumption decreases the risk of a coronary heart disease (CHD) episode compared with abstainers (with particular benefits in men aged over 55 years and post‐menopausal women). However, heavy drinking is associated with an increased risk of CHD. Further information is required to determine the association between drinking patterns and heart health. However, there is a consensus of opinion that it is the alcohol per se that influences heart health, rather than a particular type of alcoholic beverage; and other factors that affect an individual’s choice of drink may be important in distorting the findings from studies that show otherwise. As with risk of CHD, light to moderate alcohol consumption is associated with a decreased risk (of 30–40%) of type 2 diabetes, when compared with teetotallers. Heavy drinking may be associated with an increased risk, resulting in a ‘J’ or ‘U’ shaped relationship between alcohol consumption and the incidence of type 2 diabetes. A ‘J’ shaped relationship has also been reported between alcohol consumption and blood pressure. It is widely accepted that heavy alcohol intake is a risk factor for high blood pressure, and evidence indicates that moderate intakes may exert a short‐term lowering effect, while abstainers/teetotallers are reported to have a higher blood pressure. The type of stroke is important when considering the association between stroke and alcohol, as any alcohol consumption is associated with an increased risk of haemorrhagic stroke, but low intakes (i.e. one drink per day) may have a protective effect on ischaemic stroke. Heavy drinking is associated with an increased risk of both types of stroke. Alcohol intake has also been associated with an increased risk of cancers at a number of sites. However, a consensus for a likely causal association has only been identified between alcohol and cancers of the upper‐aero digestive tract and liver. The mechanisms to explain the positive associations between alcohol and breast cancer, and alcohol and colorectal cancer, have yet to be identified. It is unclear whether some types of alcoholic beverage are more strongly associated with increased risk of cancer than others. Mechanisms identified to date suggest that it is the alcohol per se that exerts damage and, therefore, quantity of alcohol consumed is the most important variable. Studies looking at the relationship between alcohol and mortality suggest that 10–80 g (approximately 1–8 drinks) of alcohol each week is optimal to reap the health benefits, but increased risk is noted at higher intakes (thus indicating a ‘U’ shaped relationship between alcohol intake and mortality). Gender and age are important factors when considering the association between alcohol and mortality. For example, for younger people, the benefits of alcohol may be outweighed by the increased risk of other diseases (e.g. alcohol‐related cancers, liver cirrhosis) and increased risk of violence and accidents. Aggressive behaviour, increased risk taking and decreased responsiveness to social expectations, which may lead to personal ‘harm’, including accidents and violence, are usually the result of alcohol intoxication (i.e. through binge drinking). Excess alcohol consumption may also result in a ‘hangover’, which disrupts normal life through symptoms of fatigue and increased anxiety, and has economic consequences in the workplace through poor performance or absenteeism. The extent to which a hangover can affect an individual’s performance, including psychomotor, recognition and managerial skills, is still being debated. Binge drinking is also associated with an increased risk of sexually transmitted diseases and unplanned pregnancies. Although the cost of binge drinking in terms of long‐term health has yet to be established, the significant economic cost is well recognised. A number of population‐based initiatives are underway to try and change the ‘drinking culture’, and thus reduce the incidence of binge drinking. Initiatives include: advertising campaigns; changes to alcohol advertising regulations; and changes to pub licensing regulations.