Dietary fat & risk of coronary heart disease in men: cohort follow up study in the United States.

January 1, 1996 Human Health and Nutrition Data 0 Comments

Dietary fat & risk of coronary heart disease in men: cohort follow up study in the United States.

Year: 1996
Authors: A Ascherio, E B Rimm, E Giovannucci, D Spiegelman, M Stampfer, W Willett.
Publication Name: British Medical Journal.
Publication Details: Volume 313; Number 7049; Page 84.


Diets high in saturated fat (SFA) and cholesterol, and low in polyunsaturated fat (PUFA), result in an increased risk of coronary heart disease (CHD). Results from prospective epidemiological investigations and randomized trials have been inconsistent. The objective of this study was to examine the association between dietary fat and cholesterol and risk of myocardial infarction (MI) in a large cohort of men in the United States. Data from the Health Professional Follow-up Study, which commenced in 1986, was used to investigate the association between dietary fat and MI. 43757 eligible men, aged 40 – 75 years of age, completed a 131-item food frequency questionnaire at baseline in 1988, 1990, and 1992. Information regarding medical history, risk factors for heart disease, and dietary changes during the past 10-years was also provided. Greater than 94% of the participants returned follow-up questionnaires in each two-year follow-up cycle. End points assessed were fatal coronary disease (including sudden death) and non-fatal MI occurring between completion of the baseline questionnaire in 1986 and completion of the final questionnaire in 1992. During the 6-year follow-up, 734 coronary events were documented, which included 505 non-fatal MI’s and 229 deaths. After controlling for age and several coronary risk factors, a significant positive association was observed between SFA intake and risk of coronary disease. Positive associations between cholesterol intake and risk of CHD were also observed, but were attenuated after adjustment for fibre intake. A positive association between intake of trans fatty acids and risk of CHD was also observed. Finally, an inverse association between ALA and MI was also observed, but became significant only after adjustment for non-dietary risk factors, and became strengthened after adjustment for total fat intake. In conclusion, the observed inverse association between intake of ALA and risk of CHD is consistent with previous findings, further supporting the hypothesis of the specific preventative effect of this fatty acid. Further studies will reveal whether the favorable effects of ALA on CHD are attributed to its conversion to the longer n-3 EPA and DHA, or whether ALA exerts beneficial effects on its own.

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