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Letters to the Editor |
Department of Molecular Medicine Lawrence Berkeley National Lab Donner Lab, Room 459 University of California Berkeley, CA 94720
Dear Sir:
Kenney et al allude to studies in which there was apparent clinical benefit of programs incorporating very-low-fat diets for the management of coronary artery disease. A recent scientific advisory statement by the American Heart Association Nutrition Committee addressed the current evidence for effects of very-low-fat diets on heart disease risk (1). The statement points out that there are not adequate grounds for ascribing these effects to low fat intake per se, because, as pointed out by Kenney et al, these effects are generally accompanied by other potentially healthful behavioral and dietary changes (2, 3). Moreover, the clinical benefits of these programs have been evaluated either principally or exclusively in groups of patients with preexisting coronary artery disease, many of whom have had abnormal lipoprotein profiles (1–3).
We specifically selected a group of healthy men who, in previous studies, had maintained a normal lipid profile with predominantly large LDL particles (pattern A) while consuming diets containing 20–24% of energy as fat (4). The question that our study addressed was whether a diet with further short-term reductions in total fat intake, with substitution of carbohydrates, and with a total energy intake aimed at maintaining stable body weight, would confer favorable lipoprotein changes or result in a metabolic response leading to a shift to smaller LDL particles (pattern B) as we had observed in subsets of men switched from high-fat to lower-fat diets in previous studies (4, 5). Our findings, therefore, specifically relate to effects of very-low-fat, high-carbohydrate diets on lipoprotein profiles of men whose lipoprotein profiles suggest a low risk of cardiovascular disease. Although the average reported energy intakes of our subjects while consuming their usual diets were lower than those prescribed for the test diet, we observed no weight increases during the study and therefore ascribe the findings to underestimates of energy intake, which are commonly observed with data from food intake records.
As we pointed out, our findings did not address the potential benefits of such diets in men with metabolic traits indicating a higher risk of coronary artery disease (eg, elevated concentrations of total LDLs or LDL pattern B). Indeed, our earlier studies, as well as those of others (6), indicate that these higher-risk individuals, such as those with coronary disease studied by Ornish et al (2), tend to have greater benefits on lipoprotein profiles as a result of dietary fat restriction than do those with normal or low-risk lipoprotein profiles.
We strongly support the recommendation, as described elsewhere (7), that an overall dietary program to reduce cardiovascular risk should emphasize the intake of vegetables, fruit, and whole grains, incorporating an overall energy balance aimed at maintaining a healthy body weight. In this regard, our study was not designed to test these multiple components of an overall dietary program, but to isolate, as effectively as possible, the effects of reduced fat intakes and increased carbohydrate intakes. Although the experimental diet fell short of maintaining basal intakes of fiber and had a high content of simple sugars, our findings may have relevance to those in the population who achieve lower fat intakes by increasing their consumption of prepared low-fat foods with low fiber and high sugar contents and who do not succeed in reducing their total energy intakes. We are planning further studies that address to what extent our findings can be extended to other forms of dietary fat restriction, including diets with a high whole-grain content and in which energy intakes are ad libitum.
We believe that it is not necessary to reiterate that very-low-fat diets do not necessarily promote a pattern B lipid profile. In fact, as stated in our paper, we estimate that 
33% of healthy American men do not express a pattern B lipid profile, even when consuming very-low-fat diets. We also emphasize that in deliberately maintaining stable body weights, we did not address the potential effects of weight reduction (with or without increased exercise) on cardiovascular metabolic risk factors and, in particular, the potential for attenuating or eliminating the adverse changes found in a subset of men whose LDL profile changed from pattern A to pattern B in the present study.
It is also not known to what extent our results may have differed with longer-term consumption of low-fat diets. Noteworthy, however, is that in at least one population with habitual fat consumption lower than that in the average American diet, peak LDL particle size is also smaller (8), in a manner consistent with the predictions based on our short-term feeding studies. Because coronary artery disease risk in these populations is not high, we conclude, as did others (9), that a preponderance of small LDL particles (pattern B) may not confer increased coronary artery disease risk in the absence of elevated concentrations of these or other atherogenic lipoproteins.
We also note that the results of our short-term dietary challenge, while useful in identifying metabolic heterogeneity in the population, cannot yet be extrapolated to clinical outcomes (4). However, on the basis of the strong and well-established relations of lipoproteins to coronary artery disease risk, we feel that our results raise the important possibility that subsets of the healthy population, particularly those with normal lipid metabolic profiles, may not benefit from extreme dietary fat restriction and may even experience lipoprotein changes that would be expected to increase their risk of coronary artery disease.
REFERENCES
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