News Release

The Reason The French Have Low Levels Of Heart Disease

Peer-Reviewed Publication

BMJ

(Why heart disease mortality is low in France: the time lag explanation)

(Commentary: Alcohol and other dietary factors may be important)

(Commentary: Intrauterine nutrition may be important)

(Commentary: Heterogeneity of populations should be taken into account)

Low levels of ischaemic heart disease in France is not down to drinking red wine, suggest researchers in this week's BMJ. In their paper Dr Malcolm Law and Professor Nicholas Wald from the Wolfson Institute of Preventive Medicine in London present a new hypothesis to explain why the French population has experienced such a low incidence of heart disease and provide supporting evidence. The crux of their hypothesis is that animal fat consumption and serum cholesterol are relatively new phenomena in France and that there is a time-lag in the effect they have on health.

Animal fat consumption and serum cholesterol concentration have only been similar in French and British populations for the last 15 years, say the authors. For decades up to 1970 France had lower animal fat consumption and serum cholesterol and only between 1970 and 1980 did French levels increase to those in Britain.

Law and Wald explain that French mortality from ischaemic heart disease is nevertheless still only about a quarter of that in Britain because of a "time lag" effect. They estimate that the time lag between an increase in fat consumption and its effect on heart disease is somewhere between 25 to 35 years and explain that the time lag is similar to that which is seen in relation to lung cancer risk and smoking.

The authors examine previous explanations of the "French paradox" including the under certification of heart disease deaths by French doctors (which they say could account for about 20 per cent of the difference in mortality rates); smoking; alcohol intake (especially red wine); the consumption of garlic and onions and the moderately warmer climate in France. They conclude that apart from smoking in women, these factors explain little of the difference and that the most important explanation lies in the time-lag hypothesis.

Law and Wald emphasise that the consumption of animal fat leads to a slow increase in the risk of mortality from heart disease, but, as with smoking and lung cancer, these risks decrease rapidly on cessation.

Also see accompanying commentaries to this paper.

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Contact:

Dr Malcolm Law, Reader, Wolfson Institute of Preventive Medicine, St Bartholomew's and The Royal London School of Medicine and Dentistry, London or Professor Nicholas Wald M.R.Law@mds.qmw.ac.uk

Professor Meir Stampfer, Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston meir.stampfer@channing.harvard.edu

Professor David Barker, Director, MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton david.barker@mrc.soton.ac.uk

Professor Johan Mackenbach, Department of Public Health, Erasmus University Rotterdam, Netherlands mackenbach@mgz.fgg.eur.nl



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