Author + information
- Received April 18, 1994
- Revision received August 12, 1994
- Accepted August 25, 1994
- Published online February 1, 1995.
- Eliseo Guallar, MD†∗,
- Charles H. Hennekens, MD†,‡,
- Frank M. Sacks, MD‡,§,
- Walter C. Willett, MD†,‡,§ and
- Meir J. Stampfer, MD∗∗,†,‡
- ↵∗∗Address for correspondence: Dr. Meir J. Stampfer, Channing Laboratory, 180 Longwood Avenue, Boston, Massachusetts 02115.
Objectives. This study evaluated whether increased intake of fish oils (eicosapentaenoic and docosahexaenoic acids) might reduce the risk of coronary heart disease.
Background.Observational and clinical studies have suggested that increased intake of fish oils, as reflected in plasma levels of fish oils, may reduce the risk of myocardial infarction.
Methods.A nested case-control study was conducted among the 14,916 participants in the Physicians' Health Study with a sample of plasma before randomization. Each participant with myocardial infarction occurring during the first 5 years of follow-up was matched by smoking status and age with a randomly chosen control participant who had not developed coronary heart disease.
Results.Mean levels of fish oils (with 95% confidence interval [CI] for paired differences and p values) in case and control participants, expressed as present of total fatty acids, were, for eicosapentaenoic acid, 0.26 versus 0.25 (95% CI - 0.03 to 0.05, p = 0.70) in cholesterol esters and 0.56 versus 0.54 (95% CI -0.04 to 0.09, p = 0.44) in phospholipids, and for docosahexaenoic acid, 0.23 versus 0.24 (95% CI -0.07 to 0.04, p = 0.64) in cholesterol esters and 2.22 versus 2.14 (95% CI -0.10 to 0.27, p = 0.36) in phospholipids. Results adjusted for major cardiovascular risk factors showed a very similar lack of association between fish oil levels and the incidence of myocardial infarction.
Conclusions.These results indicate no beneficial effect of increased fish oil consumption on the incidence of a first myocardial infarction. However, the effect of very high levels of fish oils could not be evaluated.
↵∗ Present address: Escuela de Sanidad y Consumo, Ministerio de Sanidad y Consumo, Madrid, Spain.
☆ This study was supported by Research Grants CA 42182, CA 34944 and CA 40360 from the National Cancer Institute and HL 26490 and HL, 34595 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland and by an Established Investigator Award to Dr. Sacks from the American Heart Association, Dallas, Texas.
- Received April 18, 1994.
- Revision received August 12, 1994.
- Accepted August 25, 1994.