Objective To estimate the impact of achieving alternative average population alcohol consumption levels on chronic disease mortality in England.
Design A macro-simulation model was built to simultaneously estimate the number of deaths from coronary heart disease, stroke, hypertensive disease, diabetes, liver cirrhosis, epilepsy and five cancers that would be averted or delayed annually as a result of changes in alcohol consumption among English adults. Counterfactual scenarios assessed the impact on alcohol-related mortalities of changing (1) the median alcohol consumption of drinkers and (2) the percentage of non-drinkers.
Data sources Risk relationships were drawn from published meta-analyses. Age- and sex-specific distributions of alcohol consumption (grams per day) for the English population in 2006 were drawn from the General Household Survey 2006, and age-, sex- and cause-specific mortality data for 2006 were provided by the Office for National Statistics.
Results The optimum median consumption level for drinkers in the model was 5 g/day (about half a unit), which would avert or delay 4579 (2544 to 6590) deaths per year. Approximately equal numbers of deaths from cancers and liver disease would be delayed or averted (∼2800 for each), while there was a small increase in cardiovascular mortality. The model showed no benefit in terms of reduced mortality when the proportion of non-drinkers in the population was increased.
Conclusions Current government recommendations for alcohol consumption are well above the level likely to minimise chronic disease. Public health targets should aim for a reduction in population alcohol consumption in order to reduce chronic disease mortality.
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Review history and Supplementary material
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To cite: Nichols M, Scarborough P, Allender S, et al. What is the optimal level of population alcohol consumption for chronic disease prevention in England? Modelling the impact of changes in average consumption levels. BMJ Open 2012;2:e000957. doi:10.1136/bmjopen-2012-000957
Contributors PS conceived the study and developed the methods, with support from MN, SA and MR. MN conducted literature searches to inform the model and PS and MN built the model and conducted analysis. All authors contributed to interpretation of the results. MN prepared the initial draft and led the preparation of the manuscript. All authors were involved in drafting and reviewing the manuscript. MN and PS act as guarantors for the manuscript.
Funding PS, SA and MR are supported by the British Heart Foundation (grant numbers PPC/Jul05/5b and PPC/JAN05/6biii). MN and SA were partially supported by the Australian Government Department of Health and Ageing.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement The PRIME-Alcohol model is available for use upon request from PS ( ).
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