Fear of margarine: The trans fat myth

By Steve Milloy
November 29, 1999, JunkScience.com
(Note: The many links in this article are no longer active but have been left in for historical purposes.)

The Food and Drug Administration recently proposed (FDA proposal home page | Federal Register notice) to amend its regulations on nutrition labeling to require the amount of trans fatty acids in foods be included in Nutrition Facts panels. But the science behind this move is suspect.

A recent editorial in the New England Journal of Medicine reviewed the epidemiolgic evidence linking trans fatty acids to heart disease. The editorial concludes “Metabolic and epidemiologic studies indicate and adverse effect of trans fatty acids on the risk of coronary heart disease.” Below (in italics) is what the editorial says about the epidemiology studies — the studies that should validate the theories developed from the metabolic studies. My comments are in bold. Decide for yourself whether trans fats are guilty as charged.

• In a case-control study of subjects in the Boston area, we found a strong and significant positive association between the intake of trans fatty acids, assessed with the use of dietary questionnaires, and the risk of acute myocardial infarction. The relative risk of acute myocardial infarction for the quintile with the highest intake of trans fatty acids as compared with the quintile with the lowest intake was 2.4 (P for trend less than 0.001); this association was entirely explained by the intake of these fats from hydrogenated vegetable oil.

  This small study (only 239 patients from the Boston area) did not consider non-dietary risk factors for heart disease other than age and sex. Astonishingly, smoking, exercise level, health history, family health history and alcohol consumption were not considered as confounding risk factors.

• Bolton-Smith et al. performed a cross-sectional analysis of the association between the intake of trans fatty acids and the presence of previously undiagnosed coronary heart disease among participants in the Scottish Heart Study. The intake of trans fatty acids was positively correlated with the ratio of LDL plus very-low-density lipoprotein cholesterol to HDL cholesterol. The odds ratios for coronary heart disease in the quintile with the highest intake as compared with the quintile with the lowest intake were elevated but not significantly so (1.26 in women and 1.08 in men).

  The results from this study were weak statistical associations that were not statistically significant — meaning the probability was unacceptably high the barely detectable associations could have occurred by chance. Even the study authors conclude,”The results, therefore, do not support a major effect of dietary trans fatty acid…”

• Studies in which the composition of fatty acids in tissue or plasma was used as a marker of trans-fatty-acid intake have yielded conflicting results. With one exception, however, these studies have been too small to detect an association reliably. The results of the only large study, which included 671 men with acute myocardial infarction from eight European countries, were inconclusive. The overall analyses revealed no association between the intake of trans fatty acids and the risk of myocardial infarction.

  No comment necessary.

• The relative risk of coronary heart disease associated with an absolute increase of 2 percent in the intake of trans fatty acids was 1.36 (95 percent confidence interval, 1.03 to 1.81) in the Health Professionals Follow-up Study…

  The result spotlighted is so misleading as to constitute scientific misconduct. The relative risk of 1.36 is a raw result, without any adjustment for other heart disease risk factors. When other risk factors are adjusted for — including age, body mass index, smoking habits, alcohol consumption, physical activity, history of hypertension or high blood cholesterol, family history of myocardial infarction before age 60, profession, and fibre intake — the weak relative risk is substantially reduced (by more than 50 percent) and becomes statistically insignificant.

• The relative risk of coronary heart disease associated with an absolute increase of 2 percent in the intake of trans fatty acids was … 1.14 (95 percent confidence interval, 0.96 to 1.35) in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study…

  The spotlighted result is a weak association that is not statistically significant. This study consisted of 21,930 male smokers. Can you really study dietary factors for heart disease in a population where the basic lifestyle (i.e., smoking and its attendant unhealthy tendencies) is a risk factor for heart disease?

• The relative risk of coronary heart disease associated with an absolute increase of 2 percent in the intake of trans fatty acids was… 1.93 (95 percent confidence interval, 1.43 to 2.61) in the Nurses’ Health Study.

  This is my favorite study of the bunch. Check out its results.

  • It reports no statistically significant association between total fat intake and risk of cornary heart disease.
  • It reports no statistically significant association between animal fat intake and risk of cornary heart disease.
  • It reports no statistically significant association between saturated fat intake and risk of cornary heart disease.
  • It reports no statistically significant association between cholesterol intake and risk of cornary heart disease.
  • The reported association between trans fat and coronary heart disease is only statistically significant for the highest consumption of trans fats — but it’s still a very weak statistical association (relative risk = 1.53).

  This study basically reports that all we’ve been told about the association between fat consumption and heart disease is not supported by data collected from 90,000 nurses over a period of 20 years. So either the study data is wrong or the public health establishment has been wrong about fat consumption being associated with heart disease risk. If the study data is wrong, then I doubt the trans fat result. If the public health establishment is wrong then why should we believe it about trans fat when it has been generally wrong about fat consumption for the last two or three decades?

That’s the epidemiology supposedly supporting the proposition that trans fats are so much of a risk for heart disease they need to be labelled. Are you convinced yet?

But there’s more. Check out the authors of the studies discussed above. See if you notice anything unusual (like the underlined names).

• Ascherio A, Hennekens CH, Buring JE, Master C, Stampfer MJ, Willett WC. Trans-fatty acids intake and risk of myocardial infarction. Circulation 1994;89:94-101.
• Bolton-Smith C, Woodward M, Fenton S, Brown CA. Does dietary trans fatty acid intake relate to the prevalence of coronary heart disease in Scotland? Eur Heart J 1996;17:837-45.
• Aro A, Kardinaal AF, Salminen I, et al. Adipose tissue isomeric trans fatty acids and risk of myocardial infarction in nine countries: the EURAMIC study. Lancet 1995;345:273-8.
• Ascherio A, Rimm EB, Giovannucci EL, Spiegelman D, Stampfer M, Willett WC. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States. BMJ 1996;313:84-90.
• Pietinen P, Ascherio A, Korhonen P, Hartman AM, Willett WC, Albanes D, Virtamo J. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men: the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Epidemiol 1997;145:876-87.
• Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Rosner BA, Hennekens CH, Willett WC. Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med 1997;337:1491-9.

ALL THE STUDIES supposedly showing trans fats are associated with heart disease risk involved Alberto Ascherio and Walter Willett.

You may also be interested in knowing who authored the editorial: Alberto Ascherio, Martijn B. Katan, Peter L. Zock, Meir J. Stampfer,and Walter C. Willett.

Should the FDA be taking action because of a duet of scientists whose results are so thin? Has the FDA ever heard of the scientific method and its requirement for independent replication of scientific results?