Letters

Dietary fats and prevention of cardiovascular disease

BMJ 2001; 323 doi: https://doi.org/10.1136/bmj.323.7319.1000 (Published 27 October 2001) Cite this as: BMJ 2001;323:1000

Conclusion may have been underplayed

  1. Jim Mann, professor in human nutrition and medicine (jim.mann@stonebow.otago.ac.nz),
  2. Murray Skeaff, senior lecturer in human nutrition,
  3. Stewart Truswell, professor of human nutrition
  1. Department of Human Nutrition, University of Otago, Dunedin, New Zealand
  2. Human Nutrition Unit, University of Sydney, Sydney, New South Wales 2006, Australia
  3. Department of Nutrition, Harvard School of Public Health, Boston, MA 02115, USA
  4. Manchester Dental and Education Centre (MANDEC), University Dental Hospital of Manchester, Manchester M15 6FH
  5. School of Health, University of Teesside TS1 3BA
  6. Public Health Nutrition, Institute of Human Nutrition, Southampton General Hospital, Southampton SO16 6YD
  7. Department of Clinical Biochemistry, Princess Royal Hospital NHS Trust, Apley Castle, Telford TF6 6TF
  8. Department of Social Medicine, University of Bristol, Bristol BS8 2PR
  9. Cardiovascular Research, University of Edinburgh, Edinburgh EH8 9XF
  10. Department of Social Medicine, University of Bristol, Bristol BS8 2PR

    EDITOR—The paper by Hooper et al may fulfil the Cochrane review criteria for a meta-analysis of clinical trials, but it does not provide a systematic review of the issues relating to dietary fat intake and the prevention of cardiovascular disease.1

    It is important to consider the overall appropriateness of each trial before its inclusion in a meta-analysis. Several of the trials included are small or of short duration. It is difficult to imagine how the risk of coronary heart disease that has accrued over a prolonged period may be reversed by dietary modification in less than two years. The diet and infarction trial (fat modification arm) contributed the greatest number of cardiovascular end points, yet there are at least two reasons why this trial was unlikely to show a beneficial effect. Limited dietary instruction was given, so there was little change in cholesterol concentrations. Since modification of fat quality produces a predictable average change in cholesterol, there was clearly limited compliance with dietary advice. Furthermore, the study was too short (two years) to have the expected reduction in clinical events and mortality.

    The Veterans' Administration study, which contributed the second largest number of deaths, fulfilled the criteria for a good randomised, controlled, double blind clinical trial. But the experimental diet entailed a ratio of polyunsaturated to saturated fatty acids of 1.5, far greater than would today be considered desirable. Such a diet would be expected to reduce cholesterol and coronary heart disease morbidity and mortality—as indeed it did, but perhaps not total mortality, as was also the case. Is it appropriate to compare such an intervention with that used in the Oslo study, in which saturated fats were replaced by whole grain cereals, vegetables, fruit, and some unsaturated fatty acids and in which study cardiovascular events and total mortality …

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