BMJ 2002;325:191-194 ( 27 July )

Papers

Alcohol consumption and mortality: modelling risks for men and women at different ages

Ian R White, medical statisticianDan R Altmann, medical statisticianKiran Nanchahal, medical statistician

Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London WC1E 7HT

Correspondence to: I R White, Medical Research Council Biostatistics Unit, Institute of Public Health, Cambridge CB2 2SR ian.white{at}mrc-bsu.cam.ac.uk


    Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References

Objective: To estimate the relation between alcohol consumption and risk of death, the level of alcohol consumption at which risk is least, and how these vary with age and sex.
Design: Analysis using published systematic reviews and population data.
Setting: England and Wales in 1997.
Main outcome measures: Death from any of the following causes: cancer of lip, oral cavity, pharynx, oesophagus, colon, rectum, liver, larynx, and breast, essential hypertension, coronary heart disease, stroke, cirrhosis, non-cirrhotic chronic liver disease, chronic pancreatitis, and injuries.
Results: A direct dose-response relation exists between alcohol consumption and risk of death in women aged 16-54 and in men aged 16-34. At older ages the relation is U shaped. The level at which the risk is lowest increases with age, reaching 3 units a week in women aged over 65 and 8 units a week in men aged over 65. The level at which the risk is increased by 5% above this minimum is 8 units a week in women aged 16-24 and 5 units a week in men aged 16-24, increasing to 20 and 34 units a week in women and men aged over 65, respectively.
Conclusions: Substantially increased risks of all cause mortality can occur even in people drinking lower than recommended limits, and especially among younger people.

What is already known on this topic
Non-drinkers and heavy drinkers have higher all cause mortality rates than light drinkers---the U shaped curve

The precise shape and location of the U are likely to depend on age and sex, but this has not been quantified

What this study adds
The level of alcohol consumption that carries the lowest mortality ranges from 0 in men and women aged under 35 to 3 units a week in women aged over 65 and 8 units a week in men aged over 65

The level of alcohol consumption that carries a 5% increase in mortality increases with age from 8 to 20 units a week in women and from 5 to 34 units a week in men

Our calculations were for England and Wales in 1997: nadirs are likely to be lower in the future and in countries with less ischaemic heart disease




    Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References

Alcohol consumption increases the risk of various cancers, hypertension, liver disease, unintentional injuries, and violence. 1 2 Definitions of light and moderate alcohol consumption vary, but these levels of consumption are generally found to decrease the risk of ischaemic heart disease.2-6 For all cause mortality the relation is typically U shaped, with non-drinkers and heavier drinkers having higher risks than light and moderate drinkers. 2 7-9 The royal colleges of physicians, psychiatrists, and general practitioners have therefore advised men and women to drink less than 21 and 14 units a week, respectively, whereas the UK government has recommended no more than 4 and 3 units a day, respectively; 1 unit is 8-10 g of alcohol. 10 11 However, the levels giving the lowest or a low risk are likely to vary with age as well as sex and have not been systematically quantified.12 We used statistical models relating alcohol consumption to the risk of death from single causes to estimate the all cause risk for men and women of different ages in England and Wales.


    Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References

Relative risks
Three reviews have quantitatively related alcohol consumption to comprehensive lists of causes of death. 1 13 14 The most appropriate review for our study was by Corrao and others because it included more recent studies, assessed study quality, and estimated risk as a function of alcohol consumption. 14 15

Corrao and others described each cause specific risk by way of a linear, quadratic, or cubic function of alcohol consumption, or, for ischaemic heart disease, a model involving linear and square root terms. Where appropriate they excluded studies of lower quality. They reported results separately when significant differences were found between Mediterranean and non-Mediterranean countries, case-control and cohort studies, incident disease and death, or men and women: we used the results for non-Mediterranean countries, cohort studies, and deaths. Otherwise we used the pooled results. We expressed alcohol consumption in units a week, taking 1 unit as 9 g of alcohol.16 The risk functions for each cause of death by alcohol consumption are given on bmj.com.

Alcohol consumption
Alcohol consumption was reported by respondents aged 16 and over in the 1996-7 general household survey.17 We computed the proportions of men and women in England and Wales drinking 0 units of alcohol a week, drinking occasionally (taken as 0.25 units a week), drinking from 1 up to 100 in increments of 1 unit a week, and drinking more than 100 units a week, for age bands 16-24, 25-34, 35-44, and so on up to over 85.

Mortality
We obtained data on mortality for England and Wales in 1997 from the Office for National Statistics.18



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Fig 1.   Risk of all cause mortality (relative to non-drinkers) by level of alcohol consumption in women and men

Pooling causes
We estimated absolute risk functions from the relative risk functions for each sex, age band, and cause by using the observed number of deaths and the distribution of alcohol consumption (see bmj.com). We summed the absolute cause specific risks to get all cause mortality for each sex and age band. The nadir is the level of alcohol consumption at which all cause risk is lowest.16




    Results
Top
Abstract
Introduction
Methods
Results
Discussion
References

Alcohol risk relations
Figure 1 shows the relation between all cause mortality and alcohol consumption, by age and sex. The absolute risks vary widely (table), so we show all risks relative to non-drinkers. For women there is a positive relation up to age 35-44, but the U shape appears from age 45-54. For men aged below 35 the curve is steeper than it is for women, but the U shape appears at age 35-44, and the reduction in mortality in the lightest drinkers is larger and is sustained up to higher levels of consumption than for women. Drinking at the royal colleges' recommended limit increases risk by 9% in women aged 16-24 and by 23% in men aged 16-24. For government limits these figures are 15% and 32%, respectively.


                              
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Nadirs and 5% bounds (units a week) with 95% confidence intervals showing uncertainty owing to relative risk functions and percentage annual risk

Estimated nadirs
Figure 2 and the table show the estimated nadirs. The nadir increases from 0 at ages 16-34 to around 3 units a week in women and around 8 units a week in men aged over 65. The 95% confidence intervals around the estimated nadirs are narrow, but they account only for uncertainty in the relative risks.19



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Fig 2.   Level of alcohol consumption at which mortality is least (nadir) and level at which risk is raised by 5% above this minimum risk in women and men (95% confidence intervals show uncertainty due to relative risk functions only)

The 5% bounds are the levels of alcohol consumption at which risk is no more than 5% greater than the risk at the nadir. For women the 5% bound increases from 8 units a week at ages 16-24 to around 20 units a week over age 85. For men it increases from only 5 units a week at ages 16-24 (reflecting the steeper slope of the risk curve in young men compared with young women) to 30-35 units a week over age 65.

Sensitivity analyses
An alternative risk function for ischaemic heart disease lowers the nadirs, for example from 8 to 5 units a week in men aged over 65. An alternative way of splitting deaths from stroke lowers the nadir for men aged over 75. Assuming ischaemic stroke to be unrelated to alcohol consumption slightly increases the nadirs, whereas assuming breast cancer to be unrelated to alcohol consumption has no appreciable effect.




    Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References

If our results are not subject to bias or confounding (see bmj.com) and if the effects of alcohol consumption act over no more than 5-10 years, then the average person can decrease his or her risk of mortality by drinking at a level nearer the nadir.

Possible evidence based guidelines for sensible drinking can be derived from figure 2 and the table if no more than a 5% increase in risk of mortality is considered acceptable. Women would be advised to limit their drinking to 1 unit a day up to age 44, 2 units a day up to age 74, and 3 units a day over age 75. Non-drinking men aged 55-84 have a risk slightly more than 5% above the minimum risk, but we would not encourage these men to drink, because this might increase the overall public health burden of heavier drinking. Men would be advised to limit their drinking to 1 unit a day up to age 34, 2 units a day up to age 44, 3 units a day up to age 54, 4 units a day up to age 84, and 5 units a day over age 85. These levels are similar to current limits at older ages but considerably lower at younger ages.

Alternatively, the 9-32% increase in risk for younger people at the current limits of sensible drinking might be considered acceptable because it implies a smaller absolute increase than the same percentage at older ages, even allowing for additional years of life lost through deaths at a younger age. Public health must also take account of morbidity and social harm, which are harder to measure than mortality but much more adversely affected by alcohol consumption.20 Finally, as most deaths attributable to alcohol at younger ages are due to injuries, a greater focus could be placed on avoiding risky patterns of drinking rather than on reducing average alcohol consumption. 21 22

    Acknowledgments

We thank Gianni Corrao and Vincenzo Bagnardi for helpful discussions and for analysing their data further for us and Annie Britton for helpful discussions.

Contributors: See bmj.com

    Footnotes

Funding: Alcohol Education and Research Council (grant No R17/97).

Competing interests: None declared.

The full version of this article appears on bmj.com


    References
Top
Abstract
Introduction
Methods
Results
Discussion
References

1. English DR, Holman CDJ, Milne E, Winter MG, Hulse GK, Codde JP, et al. The quantification of drug caused morbidity and mortality in Australia 1995. Canberra: Commonwealth Department of Human Services and Health, 1995.
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8. Poikolainen K. Alcohol and mortality: a review. J Clin Epidemiol 1995; 48: 455-465[CrossRef][Web of Science][Medline].
9. Rehm J, Bondy S. Alcohol and all-cause mortality: an overview. In: Novartis Foundation Symposium, ed. Alcohol and cardiovascular diseases. Chichester: Wiley, 1998.
10. Royal Colleges of Physicians, Psychiatrists, and General Practitioners. Alcohol and the heart in perspective: sensible limits reaffirmed. London: Royal Colleges, 1995.
11. Inter-Departmental Working Group. Sensible drinking. London: Department of Health, 1995.
12. Holman CDJ, Armstrong BK. The quantification of alcohol-caused morbidity and mortality in Australia: the authors respond. Med J Aust 1992; 157: 560-561[Web of Science][Medline].
13. Holman CDJ, Armstrong BK, Arias LN, Martin CA, Hatton WM, Hayward LD, et al. The quantification of drug caused morbidity and mortality in Australia (appendix 1). Canberra: Commonwealth Department of Community Services and Health, 1988.
14. Corrao G, Bagnardi V, Zambon A, Arico S. Exploring the dose-response relationship between alcohol consumption and the risk of several alcohol-related conditions: a meta-analysis. Addiction 1999; 94: 1551-1573[CrossRef][Web of Science][Medline].
15. Corrao G, Rubbiata L, Bagnardi V, Zambon A, Poikolainen K. Alcohol and coronary heart disease: a meta-analysis. Addiction 2000; 95: 1505-1523[CrossRef][Web of Science][Medline].
16. White IR. The level of alcohol consumption at which all-cause mortality is least. J Clin Epidemiol 1999; 52: 967-975[CrossRef][Web of Science][Medline].
17. Office for National Statistics, Social Survey Division. General household survey , 1996-1997 (computer file SN 3804), 2nd edn. Colchester, Essex: Data Archive [distributor], 5 Oct 1998.
18. Office for National Statistics. Twentieth century mortality: 95 years of mortality data in England and Wales by age, sex, year and underlying cause. [CD ROM and 1997 Update disk]. London: ONS, 1997.
19. White IR, Nanchahal K. The number of deaths and person-years of life lost attributable to alcohol consumption in England and Wales in 1995. London: London School of Hygiene and Tropical Medicine, 1997. [Technical report.]
20. Murray JL, Lopez AD, eds. The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries and risk factors in 1990 and projected to 2020. Cambridge, MS: Harvard University Press, 1996.
21. White IR, Altmann DR, Nanchahal K. `Optimal' levels of alcohol consumption for men and women at different ages, and the all-cause mortality attributable to drinking. London: London School of Hygiene and Tropical Medicine, 2000. [Technical report.]
22. Britton A, McPherson K. Mortality in England and Wales attributable to current alcohol consumption. J Epidemiol Community Health 2001; 55: 383-388[Abstract/Free Full Text].

(Accepted 12 February 2002)


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