Well that depends a lot on which doctor. who is paying them and how much misguided influence they have on health policy.

Dr Scott Grundy wrote this;

"Dietary Fat: At the Heart of the Matter

The role of dietary fat in the causation of coronary heart disease (CHD) has long been a topic of interest and dispute. In his News Focus article, Gary Taubes discusses what he calls "The soft science of dietary fat" (30 Mar., p. 2536). He reviews the history of the diet-heart issue and concludes that public health recommendations regarding dietary fat have not been based on solid science. He is primarily critical of the "low-fat" recommendation that has long been made by authoritative bodies to the American public. Taubes covers many aspects of the diet-heart issue, but he focuses on the question of whether there has been an overemphasis on fat without sufficient evidence that dietary fat is a major cause of CHD. He points out that recent trends in heart disease mortality both in the United States and worldwide are not well correlated with changes in dietary fat intake. Certainly he makes several astute observations, but in some areas, particularly in cardiovascular epidemiology, he does not appropriately recognize several other factors that confound the role of certain dietary fats in causation of CHD.

In my view, Taubes does not rightly identify saturated fatty acids as the predominant dietary factor contributing to the development of CHD. The significance of saturated fatty acids has been demonstrated by an enormous number of high-quality studies carried out with dietary fat in the fields of animal research, epidemiology, metabolism, and clinical trials (1). Although all questions have not been answered, a clear picture of the metabolic and health effects of saturated fatty acids has emerged. One fact is incontrovertible. As shown in multiple metabolic studies in humans, saturated fatty acids as a class, compared with unsaturated fatty acids and carbohydrate, raise serum low-density lipoprotein (LDL). Evidence is abundant that elevated LDL is a major cause of CHD and that lowering serum LDL levels reduces CHD risk (2). Even moderate reductions in LDL levels, such as those obtained by reducing dietary saturated fatty acids, are projected to substantially reduce risk of CHD in populations (3). Early prospective epidemiological studies gave results that are consistent with these projections (4). For example, in Northern and Eastern Europe, where intake of animal fats (mostly saturated fatty acids) previously was very high, serum LDL levels and CHD rates also were high. Conversely, in Southern Europe, where plant oils (mostly unsaturated fatty acids) are the predominant fat source, serum LDL levels and CHD rates were much lower. These relations were established more than 30 years ago, before increasing social and cultural homogenization in Europe partially obscured the relation of dietary fat to CHD (4). These population results, which in themselves were suggestive although perhaps not definitive, have been confirmed by results of controlled clinical trials. Several trials reveal that substitution of unsaturated fatty acids for saturated fatty acids lowers the incidence of CHD (1).

Although Taubes acknowledges the difference between saturated and unsaturated fatty acids, he does not draw a clear enough distinction in his discussion of dietary fats in general. Consequently, the article obscures the potential for public health benefits of substituting unsaturated for saturated fatty acids in the American diet. Such confusion does a disservice to the public health effort to further reduce the incidence of CHD through a reduction in intake of saturated fatty acids. On the other hand, Taubes does rightly note that other nutritional factors, for example energy imbalance leading to obesity, excessive carbohydrates, and insufficient intake of fruits and vegetables also influence population risk for CHD (1, 2).

Scott M. Grundy
Center for Human Nutrition and the Departments of Clinical Nutrition and Internal Medicine,
University of Texas Southwestern Medical Center,
Dallas, TX 75390-9052, USA.
E-mail: scott.grundy ~utsouthwestern.edu

References and Notes
1. Report of the Dietary Guidelines Committee on the Dietary Guidelines for Americans, 2000 (U.S. Department of Agriculture, Agricultural Research Service, Washington, DC, 2000).
2. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, J. Am. Med. Assoc. 285, 2486 (2001).
3. M. R. Law, N. J. Wald, T. Wu, A. Hackshaw, A. Bailey, Br. Med. J. 308, 363 (1994).
4. A. Keys et al., Am. J. Epidemiol. 124, 903 (1986). "

But the real story (and the dishonesty of Grundy et al) is told here;


"Studies of Dietary Fat and Heart Disease

22 FEBRUARY 2002 VOL 295 SCIENCE

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 diet-heart 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.
DALE ATRENS, Department of Psychology, University of Sydney, Australia.
MARY G. ENIG, Nutritional Sciences Division, Enig Associates, Inc.,
BARRY GROVES,
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,
LARS WERKÖ,
JØRGEN VESTI NIELSEN, Department of Internal Medicine, Karlshamn Hospital, Sweden.
JAN WILSKE, Department of Internal Medicine, Värnamo Hospital, Sweden.
NICOLAI WORM,
*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., Circulation 94, 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)."

Cheers,

Malcolm