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Original Research Communications |
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Objective: We investigated effects of further reduction in dietary fat in men with persistence of LDL subclass phenotype A during both high- and low-fat diets.
Design: Thirty-eight men who had shown phenotype A after 4–6 wk of both high- and low-fat diets consumed for 10 d a 10%-fat diet (2.7% saturates) with replacement of fat with carbohydrate and no change in cholesterol content or ratio of polyunsaturates to saturates.
Results: In 26 men, phenotype A persisted (stable A group) whereas 12 converted to phenotype B (change group). LDL cholesterol did not differ from previous values for 20–24%-fat diets in either group, whereas in the change group there were higher concentrations of triacylglycerol and apolipoprotein B; greater mass of HDL, large LDL-I, small LDL-III and LDL-IV, and HDL3; lower concentrations of HDL cholesterol, apolipoprotein A-I; and lower mass of large LDL-I and HDL2.
Conclusions: There is no apparent lipoprotein benefit of reduction in dietary fat from 20–24% to 10% in men with large LDL particles: LDL-cholesterol concentration was not reduced, and in a subset of subjects there was a shift to small LDL along with increased triacylglycerol and reduced HDL-cholesterol concentrations.
Key Words: Lipoproteins • low-fat diet • LDL subclasses • HDL • men • coronary artery disease • LDL phenotype
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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We previously carried out 2 studies of effects of high-fat (40–46% fat) and low-fat (20–24% fat) diets on plasma lipoproteins in healthy, normolipidemic men (9, 10). In both studies, the reduction in LDL cholesterol with the low-fat diet was significantly less in men with phenotype A during the high-fat diet than in those with phenotype B. Moreover, in men with phenotype A, there was a shift in LDL particle mass from larger, lipid-enriched LDL to smaller, lipid-depleted LDL subfractions, indicative of a change in LDL composition with minimal change in particle number and consistent with the observation of reduced plasma LDL cholesterol without reduced apolipoprotein (apo) B (11). In one-third of the men with phenotype A, this shift resulted in conversion to phenotype B with the low-fat diet (9–11).
The present study was designed to investigate effects on concentrations and distributions of LDL particles of further short-term reductions in dietary fat (to 10% of energy) in 38 men who were previously determined to have LDL subclass phenotype A with both high-fat (40–46%) and low-fat (20–24%) diets. In particular, we wished to test the extent to which both phenotype A and relative resistance of LDL-cholesterol reduction to reduced dietary fat persisted in these men after the very-low-fat diet.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The distribution of LDL peak density in all 238 men, as determined by analytic ultracentrifugation for both high-fat and low-fat diets (13, 14), is shown in Figure 1
. For each diet, subjects were grouped on the basis of 2 modes, with one grouping comprising subjects with "buoyant-mode" profiles [density (d) 
1038 g/L], designated phenotype A, and the other those subjects with "dense-mode" profiles (d > 1038 g/L), designated phenotype B (14). Of 180 men with phenotype A after consuming the high-fat diet, 62 shifted to phenotype B after consuming the low-fat diet (change group), whereas 118 men remained phenotype A (stable A group). The 58 men with phenotype B during the high-fat diet did not change phenotype during the low-fat diet (stable B group).
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Experimental design
In a crossover design, subjects were randomly assigned to follow their usual diets (with an average of 
35% of energy as fat) or a very-low-fat outpatient diet providing 10% of energy as fat for 10 d each. Subjects then switched to the alternate diet for an additional 10 d, an interval that we found to be sufficient to ensure maximal expression of LDL subclass phenotype B (DM Dreon, RM Krauss, unpublished observations, 1997). Detailed measurements of lipids, lipoproteins, and lipoprotein subclasses were carried out after the usual diet and at the completion of the experimental diet. BMI was calculated from weight and height measurements taken after each diet period.
Experimental 10%-fat diet
The nutrient composition of the experimental diet was based on a 10-d menu and was calculated by using the Minnesota Nutrition Data System (NDS) software developed by the Nutrition Coordinating Center (version 2.1; University of Minnesota, Minneapolis) (15, 16). The nutrient contents of the usual and 10%-fat diets are shown in Table 1. The usual diets were composed of a mean of 31.8% of energy from fat (10.8% saturated, 11.8% monounsaturated, and 6.9% polyunsaturated), 52.1% from carbohydrate, and 14% from protein. The very-low-fat, high-carbohydrate experimental diet was designed to supply <10% of energy from fat (2.7% saturated, 3.7% monounsaturated, and 2.6% polyunsaturated), with 75% from carbohydrate (with equal amounts of naturally occurring and added simple and complex carbohydrate) and 15% from protein. The experimental diet provided 35.7 mg cholesterol/1000 kJ, 1.2–1.4 g dietary fiber/1000 kJ, and the ratio of polyunsaturated to saturated fat (P:S) was 1.0. The diet was designed to meet age- and sex-specific recommended dietary allowances for energy, protein, and micronutrients. The subjects were allowed ad libitum consumption of non-energy-containing beverages and they were instructed to maintain their customary level of physical activity.
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Clinical and laboratory measurements
Lipids, lipoproteins, and apolipoproteins
Subjects reported to our clinic in the morning, having abstained for from all food and vigorous activity for 12–14 h. Blood pressure, body weight, and height were measured at the end of each diet period. Plasma samples were prepared within 2 h of collection from venous blood collected in tubes containing Na2EDTA (1.4 g/L), and blood and plasma were kept at 4°C until processed. Plasma total cholesterol and triacylglycerol concentrations were determined by enzymatic procedures on a Gilford Impact 400E analyzer (Gilford, Oberlin, OH). These measurements were consistently controlled with monitoring by the Centers for Disease Control and Prevention standardization program. HDL cholesterol was measured after heparin-manganese precipitation of plasma (17). LDL-cholesterol concentration was calculated with the formula of Friedewald et al (18), unless triacylglycerol concentrations were >400 mg/dL (4.52 mmol/L), in which case, LDL cholesterol was measured by direct quantitation of the ultracentrifugal plasma fraction with d >1006 g/L (19). Apo A-I and apo B concentrations in plasma were determined by an immunoturbidometric assay described previously (20). LDL peak particle diameter was determined by nondenaturing gradient gel electrophoresis of plasma (2, 5–7).
Analytic ultracentrifugation
Lipoproteins were analyzed by analytic ultracentrifugation, a procedure that provides measurements of lipoprotein mass as a function of Svedberg peak flotation rate (S
for lipoproteins with d <1063 g/L, and F1.20 for lipoproteins with d <1210 g/L) (13). Mass concentrations were determined for large, very-low-density lipoproteins (VLDLs) (S100–400), intermediate VLDLs (S 60–100), small VLDLs (S 20–60), large intermediate-density lipoproteins (IDLs) (S 14–20), small IDLs (S 10–14), and of 4 major LDL subclasses, LDL-I (S 7–10), LDL-II (S 5–7), LDL-III (S 3–5), and LDL-IV (S 0–3) (21). For LDL, this procedure provides a measurement of peak flotation rate, as well as density (g/L) and diameter (nm) of the peak LDL for each subject (13). In addition, mass was determined for concentrations of 2 major HDL subclasses, HDL2 (F1.20 3.5–9) and HDL3 (F1.20 0–3.5) (13).
Statistics
Mean lipoprotein measurements are reported separately for the usual and 10%-fat diets and for the previous 20–24%-fat diets. Univariate analyses were by the Kruskal-Wallis test when 2 groups were being compared, and by the Wilcoxon signed-rank test for paired-difference analyses. Correlations were tested by using Spearman's method. Results with P values 0.05 were considered significant. Group averages are always reported as means ± SEs. STATVIEW 4.1 software (Abacus Concepts, Inc, Berkeley, CA) was used to perform all statistical analyses, with two-sided tests of significance.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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. After the 10%-fat diet, there were significant increases in concentrations of triacylglycerol, mass of all VLDL subfractions, and apo B, and decreases in mass of small IDL, LDL cholesterol, HDL cholesterol, mass of HDL2 and HDL3, and apo A-I. There were also decreases in the mass of larger LDL-I and increases in the mass of the smaller LDL-III and LDL-IV subfractions, along with decreases in LDL particle size.
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. The majority of subjects (n = 26) remained in the phenotype A mode, whereas 12 of the subjects changed into the denser phenotype B mode with LDL peak densities >1038 g/L.
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. With the usual diet, there were few significant group differences for concentrations of plasma lipoproteins. The change group had lower HDL2 mass and apo A-I than did the stable A group.
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. During the 10%-fat diet, the change group had higher concentrations of triacylglycerol and greater mass of all VLDL subfractions than did the stable A group. Mean LDL-cholesterol concentrations were not significantly different between the groups. During the 10%-fat diet, the other significant differences between groups were what would be expected from the LDL subclass phenotypes. The change group had lower concentrations of larger LDL-I and higher concentrations of smaller LDL-III and LDL-IV subfractions, along with smaller LDL peak particle size compared with the stable A group. In addition, the change group had significantly lower concentrations of HDL cholesterol and mass of HDL2. Concentrations of apo B were marginally higher in the change group than in the stable A group.
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). Comparison of Tables 4 and 5
shows that for the change group in the present study, the 10%-fat diet resulted in 2-fold higher triacylglycerol concentrations [2.16 ± 0.18 compared with 0.99 ± 0.07 mmol/L (191.0 ± 15.7 compared with 87.6 ± 6.2 mg/dL), P <0.0001)] and lower HDL-cholesterol concentrations [1.02 ± 0.01 compared with 1.18 ± 0.06 mmol/L (39.4 ± 0.2 compared with 45.5 ± 2.4 mg/dL), P <0.01] and HDL2 mass than the previous 20–24%-fat diets. Both the stable phenotype A and change groups had higher plasma VLDL, apo B, and HDL3 mass concentrations after the 10%-fat diet than during the previous 20–24%-fat diet. The 10%-fat diet did not result in lower LDL cholesterol than the 20–24%-fat diets in either group. However, in the change group, the 10%-fat diet resulted in higher mass of large IDL, and as expected from the change in phenotype, lower mass of large LDL-I, higher mass of small LDL-III and LDL-IV subfractions, and smaller LDL peak particle size.
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. Higher VLDL mass concentrations were correlated with higher LDL-II and LDL-III and lower LDL-I concentrations in the stable A group, and with higher LDL-IV and lower LDL-I concentrations in the change group. Differences in LDL-III were positively correlated with differences in IDL and LDL-II in both groups and inversely correlated with LDL-I in the stable A group. In the change group, higher concentrations of IDL were correlated with higher LDL-II. Finally, higher concentrations of apo B were correlated with higher LDL-II in the stable A group and with higher LDL-II, LDL-III, and IDL in the change group.
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). Differences in triacylglycerol concentration were also positively correlated with differences in apo B in both groups combined (rs = 0.57, P <0.001). In addition, differences in apo B and LDL size were negatively correlated in the change group (rs = -0.61, P <0.05).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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we showed that approximately one-third of men who manifested LDL subclass phenotype A (large, buoyant LDL) while consuming a high-fat diet converted to phenotype B (small, dense LDL) with a reduction in fat to 20–24% of energy. In the present study, we found that an additional 32% of men who had stable phenotype A during a 20–24%-fat diet converted to phenotype B after short-term consumption of a very-low-fat (10% fat), high-carbohydrate diet. Thus, it appears that with progressive reduction in dietary fat and a corresponding increase in carbohydrate, an increasing proportion of men show conversion of LDL subclass distributions from phenotype A to phenotype B. This is illustrated in Figure 4, in which data from this and 2 previous studies (9, 10) were combined, showing a significant inverse relation in men between the prevalence of LDL subclass phenotype B and percentage of energy from fat in isoenergetic diets (ranging from 20% to 46% fat). The regression predicts that with a diet with 10% of energy as fat, approximately two-thirds of men would express phenotype B. This prediction is consistent with the current finding that of the population of 238 men from whom the study subjects were drawn, 120 (50%) expressed phenotype B while consuming diets with 20% or 24% of energy as fat, and an additional 34% of the remaining 50% of subjects (17%) converted to phenotype B with further reduction in dietary fat to 10% of energy (total: 67%).
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The dietary factors responsible for LDL subclass phenotype changes are not understood. High-carbohydrate, low-fat diets are known to result in increased plasma concentrations of larger, more triacylglycerol-rich VLDL particles (11, 25). It may be that those subjects whose LDL phenotype changed from A to B were more responsive to this effect because with the low-fat diet, this group had 2-fold higher concentrations of triacylglycerol and higher concentrations of all VLDL fractions, particularly the largest VLDL particles, compared with the stable A group. Although it is thought that increased intake of carbohydrates, particularly simple sugars, is a major factor responsible for increased hepatic triacylglycerol production, it is not known whether reduced dietary fat intake contributes to these lipoprotein changes as well, perhaps as a result of reduced triacylglycerol clearance (24).
Despite the relations of triacylglycerol and VLDL changes to changes in LDL subclass profiles, we have not found baseline triacylglycerol concentration to be a significant predictor of low-fat diet–induced change in LDL subclass phenotype (11). Given the evidence for major gene effects on LDL particle distributions (26–28), it is possible that genetically influenced metabolic variations not related to plasma triacylglycerol concentrations determine susceptibility to conversion from phenotype A to phenotype B during low-fat diets, and that different genetic or metabolic traits operate to promote this conversion at differing fat intakes (Figure 4).
The present study was also designed to test the LDL-cholesterol response to a very-low-fat diet in men who had previously shown relatively small changes in total LDL with manipulation of dietary fat content. Consistent with our previous results in subjects with phenotype A consuming high-energy, low-fat diets (9, 10), reduced concentrations of LDL cholesterol with the 10%-fat diet were not accompanied by reductions in plasma apo B. Although this reflects in part small increases in VLDL and IDL-apo B, it is principally indicative of a shift from larger, cholesterol-rich to smaller, cholesterol-poor particles, without a significant reduction in LDL particle number. As noted above, the conversion from phenotype A to B in a subset of men is a more pronounced manifestation of this phenomenon. It is possible that other compositional differences in LDL particles, such as exchange of triacylglycerol for cholesteryl ester (29, 30), also could have contributed to the reduction in LDL cholesterol with consumption of the 10%-fat diet.
Because the present study involved short-term administration of diets with extreme variations in fat and carbohydrate content, it is not possible to draw conclusions as to possible long-term metabolic or clinical consequences of the lipoprotein subclass responses to the very-low-fat diets observed here. In addition, potential differences in metabolic effects of complex compared with simple sugars (31) and the tendency for ad libitum consumption of low-fat diets to promote weight loss need to be considered. The present results suggest, however, that in healthy normolipidemic men with LDL subclass phenotype A consuming average American diets, lipoprotein changes induced by further restriction of dietary fat and isoenergetic substitution of carbohydrates are not indicative of reduced risk of coronary artery disease; in a subset of men who convert to phenotype B, the changes are suggestive of an increase in coronary disease risk.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported in part by the National Dairy Promotion and Research Board and administered in cooperation with the National Dairy Council and NIH Program Project grant HL-18574 and grant HL-5734 from the National Heart, Lung, and Blood Institute through the US Department of Energy under contract no. DE-AC03-76SF00098.
3 Address reprint requests to RM Krauss, Ernest Orlando Lawrence Berkeley National Laboratory, University of California, 1 Cyclotron Road, Donner Laboratory, Room 459, Berkeley, CA 94720. E-mail: rmkrauss{at}lbl.gov.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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