A paper describing a dramatic change during the 20th century in England and Wales in the association between social class and mortality from liver cirrhosis features in Alcohol and Alcoholism. While deaths from cirrhosis were more common among higher social classes in the early part of the century, the pattern changed so that deaths from cirrhosis were much more common among the lower social classes by the end of the century. Data on male cirrhosis mortality by social class were obtained from the Registrar General’s Decennial Supplements for the years 1921–1991.
The authors of this paper state that more recent research suggests that alcohol drinking may not be the reason for this change over time, as surveys in the UK have shown that lower-social-class individuals do not drink more than those at higher social classes. .
Background: There has been an increase in mortality rates from hepatic cirrhosis in the UK in recent decades.1 On the other hand, as reported by Bosetti et al,2 mortality from cirrhosis has shown favorable trends in most countries of the world, following a reduction in alcohol consumption and hepatitis B and C virus infection. The authors state that steady upward trend in cirrhosis observed over more recent calendar periods in the UK and central and eastern European countries are probably due to an increase in alcohol consumption.2
Epidemiologic analyses have shown that “alcohol-related diseases,” especially cirrhosis of the liver, are much more common among individuals with less education, lower income, and other components of what has been defined as lower “social class.” This has been attributed to a number of causes, including poorer diet, more obesity, and fewer of the other aspects of a healthy lifestyle, as well as less access to health care. The main explanation usually given, however, relates to alcohol drinking pattern: people classified as being of lower social class tend to report less-frequent but larger amounts of alcohol per occasion (a binge-drinking pattern). Also, many studies show poorer health effects associated with the consumption of spirits and beer, especially when consumed infrequently and in large amounts, than with the consumption of wine. This is a pattern that may be more common among lower social-class individuals.3,4
Multiple risk factors for hepatic cirrhosis: While alcohol is generally considered the most important risk factor for hepatic cirrhosis, there are a number of other factors. One Forum member stated: “The general impression is that approximately one half of the cases of cirrhosis are related to alcohol consumption; the second important cause is “fatty liver” associated with abdominal obesity, followed by autoimmune diseases, virus hepatitis, and metabolic diseases.” Another factor may be the ingestion of medications, such as paracetamol or acetaminophen, which break down to more toxic metabolites. Heavy use of acetaminophen has been shown to relate to cirrhosis in a large study in the United States.5
Obesity is being increasingly appreciated as an important factor in the risk of cirrhosis, especially when combined with alcohol consumption. In the Million Women Study,6 the combination of obesity and alcohol consumption of 150g or more each week was associated with a marked increased risk of cirrhosis (about fivefold) compared with that seen in obese women who drank less than 70g of alcohol a week. Hart and colleagues7 showed that being overweight or obese and drinking 15 units of alcohol or more each week had a synergistic effect, which amplified the insult to the liver and greatly increased the risk of liver-related morbidity and mortality. In the Scottish Health Survey for 2003, compared with a 1.7% risk of cirrhosis for middle-weight participants, the risk for men who were both obese and reported drinking more than 15 units of alcohol a week was 9.4%.8
The consumption of wine with meals may be associated with lower risk of cirrhosis. In the Third National Health and Nutrition Examination Survey in the US, non-alcoholic fatty liver disease (NAFLD) was observed in 14.3% of non-drinkers and 8.6% of modest wine drinkers with an adjusted odds ratio of 0.51 (95% CI 0.33-0.79).9 In the Dionysos Study drinking alcohol outside meal times and drinking multiple different alcoholic beverages both increased the risk of developing alcohol-induced liver damage.10 Among participants of the Copenhagen City Heart Study and the Glostrup Population Studies heavy drinkers who consumed more than 50% of their alcohol intake as wine, the relative risk of developing alcoholic cirrhosis was 8.2 (95% CI 1.8-20.8) compared to individuals drinking less than 1 drink per week. In contrast heavy drinkers who drank no wine had a relative risk of 21.1 (95% CI 12.4-36.1) for developing alcoholic cirrhosis.11
In a study of heavy drinkers and/or those with cirrhosis by Naveau et al,12 after dividing France along a Bordeaux-Strasbourg axis, there was more histologically proven or probable cirrhosis in the North (46%) than in the South (36%). At the same time, daily drinking was greater in the South (150 g +/- 6 g) than in the North (129 g +/- 4 g). When age, sex, daily consumption of alcohol over the past 5 years, presence of hepatitis B surface antigen and antibodies to hepatitis C virus and total duration of alcohol abuse were considered together in a stepwise logistic regression analysis, geographic location changed the prediction of cirrhosis: the odds ratio for cirrhosis in patients living to the north of the Bordeaux-Strasbourg axis, rather than to the south, was 1.9 (95% CI 1.1-3.2), suggesting the role of nutritional factors.12 However, the pattern of drinking or the choice of beverage may also have played a role.
Comments on the present study
In the present study, subjects were classified by occupation into the following classes:
II Managerial and technical
III Skilled occupations
IV Partly skilled occupations
V Unskilled occupations.
The authors report that while the early classifications were based on “social class,” there was little effect when later classifications were based on occupational level.
A Forum member states: “This is an interesting and intriguing paper when it comes to reversal of mortality from cirrhosis. The authors describe a strong association between social class and mortality from cirrhosis early in the 20th century and late in the 20th century, but the direction of the associations changed dramatically over time. Hepatic cirrhosis was primarily a cause of death of individuals of higher social class at the beginning of the 20th century, but by the end of the century it was much more common among lower-social-class individuals. As the authors state: ‘The change in the mortality gradient is stark: in 1921, social classes I and II had a cirrhosis mortality at least twice that of social classes IV and V, but by 1991, this ratio had reversed with the higher social classes having only half the mortality.”
“It is noteworthy that for social class I, there was an increase in mortality from cirrhosis between 1921 and 1951, followed by a decline from 1961 to 1991. In contrast, class V showed a somewhat steady increase in SMR for secular trend. The data do not support under-reporting of alcohol in class I as a major explanation of the reversal unless there was a worsening of under-reporting from 1921 to 1991. As to secular trend in dietary pattern, it is noticeable that the decline in SMR in class I mirrors mortality decline in the US population after 1968 (highest levels) when the “rich-diet” phenomenon (i.e. lard, butter, & dietary cholesterol) tended to be replaced among better educated people with a healthier diet (margarine, poultry, fish), as well as a reduction in smoking.”
The authors of this paper state that more recent research suggests that alcohol drinking may not be the reason for this change over time, in that more recent surveys in the UK have shown that lower-social-class individuals do not drink more than those at higher social classes.13,14 However, as shown by many studies, the pattern of drinking may be more important than the average amount of alcohol consumed. It is suggested that drinking patterns in social classes I and II may have changed during the 20th century from weekend beer and whisky drinking towards a Mediterranean-type diet that included wine with food. In addition, people in lower social classes are generally more likely to drink in binges.
One reviewer stated that “The main cause of change over time in the relation of social class with mortality from cirrhosis is probably an improvement of dietary behavior and lifestyle in the high social classes, and often still unhealthy diet and lifestyle in the lower classes. People in the lower classes are more often obese, are more likely to have metabolic syndrome, and thus more often a fatty liver. In the present paper, it is possible that an increase in the prevalence of obesity during the years 1921 – 1991, less among the professional and managerial classes than among lower social classes, could have played a role.”
Additional factors to consider have been raised by other questions: Did various forms of hepatitis, hepatoxins, or iron-loading diseases vary by class and over time? Did the amount of alcohol or the pattern of drinking change over time? A possibility is that the upper classes drank much more in the early part of the 20th century than more recently (which has been suggested by accounts of some dinners at that time).
One further risk factor to consider for the changes in cirrhosis mortality may be coffee intake, as coffee consumption has been shown to have an inverse association with cirrhosis.15,16 Coffee may have become more popular among the higher social classes during the 20th century.
Reference: Changes in the relation of social class to mortality from cirrhosis. Crombie IK, Precious E. Changes in the social class gradient of cirrhosis mortality in England and Wales across the 20th century. Alcohol and Alcoholism 2011;46:80–82.
For the full review, visit http://www.bu.edu/alcohol-forum/critique-028-changes-in-the-relation-of-social-class-to-mortality-from-cirrhosis-9-january-2011/
References from Forum review
Leon DA, Mccambridge J. Liver cirrhosis mortality rates in Britain from 1950 to 2002: an analysis of routine data. Lancet 2006;367:52–56.
Bosetti C, Levi F, Lucchini F, Zatonski WA, Negri E, La Vecchia C. Worldwide mortality from cirrhosis: An update to 2002. J Hepatol 2007;46:827–839.
Gronbaek M. Alcohol and cardiovascular disease—more than one paradox to consider. Type of alcoholic beverage and cardiovascular disease—does it matter? J Cardiovasc Risk 2003;10:5-10.
Ruidavets J-B, Ducimetiere P, Evans A. et al. Patterns of alcohol consumption and ischaemic heartdisease in culturally divergent countries: the Prospective Epidemiological Study of Myocardial Infarction (PRIME). BMJ 2010;341:c6077; doi:10.1136/bmj.c6077.
Larson AM, Polson J. Fontana RJ. Davern TJ, Lalani E, Hynan LS, Reisch JS, Schiødt FJ, Ostapowicz G. Shakil AO, Lee WM. and the Acute Liver Failure Study Group, Acetaminophen-Induced Acute Liver Failure: Results of a United States Multicenter, Prospective Study
Liu B, et al. Body mass index and risk of liver cirrhosis in middle aged women in UK: prospective study. BMJ 2010;340:c912.
Hart CL, et al. Effect of body mass index and alcohol consumption on liver disease: analysis of data from two prospective cohort studies. BMJ 2010;340:c1240.
Bromley C, et al. The Scottish Health Survey 2003. Scottish Government. www.scotland.gov.uk/Publications/2005/11/25145024/50251.
Dunn W, et al. Modest wine drinking and decreased prevalence of suspected non-alcoholic fatty liver disease. Hepatology 2008;47:1947-1954.
Bellantani S, et al. Drinking habits as cofactors of risk for alcohol induced liver damage. Gut 1997;41:845-850.
Grønbæk M, et al. Intake of beer, wine and spirits and risk of heavy drinking and alcoholic cirrhosis. Biol Res 2004;37:195-200.
Naveau S, et al. Patients with alcoholic liver disease hospitalized in hepatogastroenterology. A French national multicenter investigation. Gastroenterologie Clinique et Biologique 2001;25:131-136.
Foster K, Wilmot A, Dobbs J. General Household Survey 1988. London: HMSO, 1990.
Smyth M, Browne F. General Household Survey 1990. London: HMSO, 1992.
Tverdag A, et al. Coffee intake and mortality from liver cirrhosis. Ann Epidemiol 2003;13:419-423.
Corrao G, et al. Coffee, caffeine, and the risk of liver cirrhosis. Ann Epidemiol 2001;11:458-465.
Contributions to this critique by the International Scientific Forum on Alcohol Research were made by the following members:
Pierre-Louis Teissedre, PhD, Faculty of Oenology – ISVV, University Victor Segalen Bordeaux 2, Bordeaux, France
Arne Svilaas, MD, PhD, general practice and lipidology, Oslo University Hospital, Oslo, Norway
Erik Skovenborg, MD, Scandinavian Medical Alcohol Board, Practitioner, Aarhus, Denmark
Harvey Finkel, MD, Hematology/Oncology, Boston University Medical Center, Boston, MA, USA
R. Curtis Ellison, MD, Section of Preventive Medicine & Epidemiology, Boston University School of Medicine, Boston, MA, USA
Luc Djoussé, MD, DSc, Dept. of Medicine, Division of Aging, Brigham & Women’s Hospital and Harvard Medical School, Boston, MA, USA
Roger Corder, PhD, MRPharmS, William Harvey Research Institute, Queen Mary University of London, UK