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Letters to the Editor |
Pritikin Longevity Center, 2811 Wilshire Boulevard, Suite 410, Santa Monica, CA 90403
Department of Physiological Sciences, University of California Los Angeles, Los Angeles, CA 90095
Ocean View Medical Group, Loews Hotel, 1700 Ocean Avenue, Santa Monica, CA 90401
Dear Sir:
Dreon et al (1) concluded that "There is no apparent lipoprotein benefit of reduction in dietary fat from 20–24% to 10% in men with large LDL particles...." They also suggest that switching from an average American diet to a very-low-fat diet "in a subset of men who convert to phenotype B, [is] suggestive of an increase in coronary disease risk." However, Ornish et al (2) observed regression of atherosclerosis in subjects consuming a very-low-fat (VLF) diet even though their serum triacylglycerol concentrations increased and their HDL-cholesterol concentrations decreased (lipoprotein changes often associated with an increase in small dense LDL particles, also known as pheno- type B or pattern B). In contrast, Ornish et al (2) observed the progression of atherosclerosis in subjects consuming a more moderate-fat diet, even in those subjects who were taking cholesterol-lowering drugs. Many years ago, Morrison (3) showed a dramatic reduction in both cardiovascular disease and in all-cause mortality in subjects consuming a VLF diet compared with those consuming an average American diet. We know of no comparable clinical trials showing that diets with 
20–30% of energy as fat lead to regression of atherosclerosis, a reduction in all-cause mortality, or both. Should suggestive evidence from Dreon et al's short-term trial outweigh evidence from these much longer clinical trials with harder endpoints (eg, overall mortality and cardiovascular disease mortality)?
There is little doubt that pattern B is associated with an increased risk of atherosclerosis in people who eat a moderate-to-high-fat diet. But what is the evidence that a change in LDL status from pattern A to pattern B as a result of restricting dietary fat promotes atherosclerosis?
A low HDL-cholesterol concentration is associated with an increased risk of ischemic heart disease (IHD), and restriction of dietary fat generally leads to a drop in HDL cholesterol. However, in countries where VLF diets are the norm, the incidence of IHD is much lower than in the United States, despite significantly lower HDL-cholesterol concentrations. In hamsters, it was shown that reverse cholesterol transport is not impaired by fat restriction despite a nearly 50% reduction in HDL (4). Perhaps there are other metabolic changes associated with the change to pattern B when fat is restricted that reduce the risk of atherogenesis when a VLF diet is consumed? For example, Parks et al (5) showed a significant reduction in the susceptibility of LDL to oxidation in subjects consuming a diet containing 10% of energy as fat (10%-fat diet) even though there was little change in LDL particle size.
In addition, it would be incorrect to generalize from Dreon et al's results and conclude that all VLF diets inevitably lead to an increased number of small, dense LDL particles (pattern B). Indeed, at the Pritikin Center we found that the LDL status of 6 of 22 subjects actually changed from pattern B to pattern A (a predominance of large LDL particles) while consuming a VLF diet, which is the exact opposite of the trend observed by Dreon et al (6). There are several possible factors that may have contributed to the opposite trends observed during the 2 diets, even though both provided 
10% of energy as fat. One reason we saw a trend away from pattern B at the Pritikin Center is exercise. Exercise tends to raise HDLs and lower triacylglycerols and thus may also reduce the predominance of small, dense LDL particles. However, there are 3 possible differences between Dreon et al's 10%-fat diet and the 10%-fat diet we used or in the way the diets were fed that might explain the opposite trends observed.
If the point of Dreon et al's study is that a VLF, energy-dense, low-fiber diet consisting largely of refined sugars and white flour is of questionable value for many, if not most, normolipidemic individuals, we agree. However, if Dreon et al believe that their data show that a more vegetarian, high-fiber, VLF diet is likely to increase atherosclerosis and IHD in normolipidemic individuals relative to an average American diet, we disagree. The peculiar nature of the VLF diet used in Dreon et al's study coupled with the fact that it provided a higher energy intake than the subjects' usual diet make it inappropriate to suggest or imply that all VLF diets promote pattern B, an increased risk of IHD, or both.
REFERENCES
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