22 FEBRUARY 2002 VOL 295 SCIENCE

Studies of Dietary Fat
and Heart Disease
IN HIS LETTER ABOUT THE ARTICLE “THE
soft science of dietary fat” (News Focus,
G. Taubes, 30 Mar. 2001, p. 2536), Scott
M. Grundy says that saturated fatty acids
(SFA) are the main dietary cause of coronary
heart disease (CHD) (“Dietary fat: at
the heart of the matter,” 3 Aug., p. 801),
and he cites two reviews in support (1, 2).
In one of the reviews, there are no references
(1); in the other, of which Grundy is a
co-author, most of the references do not appear
to be supportive of his statement (2).
For instance, the authors say that “populations
consuming diets high in saturated fats
have relatively high levels of serum cholesterol
and carry a high prevalence of coronary
heart disease” (2, p. 34), referring to
12 studies (3–14). In the eight cohort studies
(3–10), only one had examined the association
between SFA and serum cholesterol
(10), five found no increased SFA consumption
among CHD patients (3, 4, 6, 9, 10), and
one found a smaller consumption (7). In addition,
three of the 12 studies were reports
from a project comparing the incidence of
CHD in native Japanese living in Japan with
Japanese-Americans living in the United
States (12–14). Although it is correct that the
Japanese-Americans, on average, had higher
cholesterol, ate more saturated fat, and had a
higher incidence of CHD, the determining
factor for heart disease was not their cholesterol
levels or their diets, but how acculturated
they were to Western culture (13).
Grundy also writes in his letter that
lowering serum LDL cholesterol by dietary
means reduces CHD risk. But the study he
cites did not specifically address this question
(15), and more to the point, meta-analyses
of all controlled and randomized trials
that have used modification of dietary fat
as the only type of intervention have shown
that neither the incidence of nonfatal CHD,
nor coronary or total mortality, was lowered
significantly (16, 17).
Grundy’s way of presenting scientific
data is not unique. An analysis of three influential
reviews in this field showed that
insignificant findings in favor of the dietheart
connection were systematically inflated,
and unsupportive studies were either
not included or they were quoted as if
they were supportive (18).
UFFE RAVNSKOV,* Magle Stora Kyrkogata 9, S-
22350 Lund, Sweden.
CHRISTIAN ALLEN, 660 Research Drive, Frederick, MD 21703, USA.
DALE ATRENS, Department of Psychology, University of Sydney, Australia.
MARY G. ENIG, Nutritional Sciences Division, Enig Associates, Inc.,
11120 New Hampshire Avenue, Silver Spring, MD 20904–2633, USA.
BARRY GROVES, Kohima, Lyneham Road, Milton under Wychwood,
Oxford OX7 6LP, UK. JOEL
M. KAUFFMAN, Department of Chemistry and Biochemistry, University
of the Sciences, Philadelphia, PA, USA.
ROLF KRONELD, University of Åbo (Turku), Finland.
PAUL J. ROSCH, New York Medical College, Yonkers, NY, USA.
RAY ROSENMAN,† 2200 PacificAvenue, San Francisco, CA 94115, USA.
LARS WERKÖ,‡ Eriksbergsgatan 30, S-11430 Stockholm, Sweden.
JØRGEN VESTI NIELSEN, Department of Internal Medicine,
Karlshamn Hospital, Sweden.
JAN WILSKE, Department of Internal Medicine,Värnamo Hospital, Sweden.
NICOLAI WORM, Maxhoehe 40, D-82335 Berg, Germany
*To whom correspondence should be addressed. E-mail: uffe.ravnskov@swipnet.se
†Former director of cardiovascular research, SRI International.
‡Former head of the Department of Medicine, Sahlgren’s Hospital, Gothenburg;
former scientific director at Astra Company; and former head of Swedish Council
on Technology Assessment in Health Care, Stockholm.
References and Notes
1. Expert Panel on Detection, Evaluation, and Treatment
of High Blood Cholesterol in Adults, J. Am. Med. Assoc.
285, 2486 (2001).
2 Report of the Dietary Guidelines Committee on the
Dietary Guidelines for Americans, 2000(U.S. Department
of Agriculture, Agricultural Research Service,
Washington, DC, 2000).
3. R. B. Shekelle et al., N. Engl. J. Med. 304, 65 (1981).
4. D. Kromhout, C. D. L. Coulander, Am. J. Epidemiol.
119, 733 (1984).
5. D. L. McGee et al., Am. J. Epidemiol. 119, 667 (1984).
6. L. H. Kushi et al., N. Engl. J. Med. 312, 811 (1985).
7. P. Pietinen et al., Circulation94, 2720 (1996).
8. K. L. Esrey, L. Joseph, S. A. Grover, J. Clin. Epidemiol.
49, 211 (1996).
9. F. B. Hu et al., N. Engl. J. Med. 337, 1491 (1997).
10. R. B. Singh et al., J. Am. Coll. Nutr. 17, 342 (1998).
11. A. W. Caggiula, V. A. Mustad, Am. J. Clin. Nutr. 65
(suppl.), 1597S (1997).
12. A. Kagan et al., J. Chronic Dis. 27, 345 (1974).
13. M. G. Marmot et al., Am. J. Epidemiol. 102, 514 (1975).
14. R. M.Worth et al., Am. J. Epidemiol. 102, 481 (1975).
15. M. R. Law et al., Br. Med. J. 308, 363 (1994).
16. U. Ravnskov, J. Clin. Epidemiol. 51, 443 (1998).
17. L. Hooper et al., Br. Med. J. 322, 757 (2001).
18. U. Ravnskov, J. Clin. Epidemiol. 48, 713 (1995).