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Human Nutrition and Metabolism

Men and Women Differ in Lipoprotein Response to Dietary Saturated Fat and Cholesterol Restriction¹

Lipid Metabolism Laboratory, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA, and ^* LipoScience, Incorporated, Raleigh, NC

²To whom correspondence should be addressed. E-mail: Ernst.Schaefer{at}tufts.edu.

	ABSTRACT

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
A diet restricted in saturated fat and cholesterol is recommended for subjects with elevated LDL cholesterol concentrations before and during drug therapy. Gender differences in lipoprotein subspecies response to such diets have not been studied in detail. We examined the effects of a diet low in total fat, saturated fat and cholesterol (Therapeutic Lifestyle Changes, TLC, diet: 26% of energy as fat, 4% as saturated fat, and 45 mg cholesterol/4.2 MJ), compared with an average American diet (AAD: 35% of energy as fat, 14% as saturated fat, and 147 mg cholesterol/4.2 MJ), on plasma lipoprotein subspecies in men and women. Each diet period lasted 6 wk. Body weight was kept constant during each diet period. Men (n = 19) and postmenopausal women (n = 14) >40 y old with moderate hypercholesterolemia participated in this study. Plasma lipoprotein concentrations were assessed by standardized methodology, and lipoprotein sizes were determined by gradient gel electrophoresis and NMR spectroscopy. The TLC diet resulted in greater reductions in total cholesterol and plasma apolipoprotein B concentrations in men than in women (-19% vs. -12%, P < 0.05, and -18% vs. -9%, P < 0.05, respectively). Postprandial triacylglycerol and LpAI:AII concentrations were reduced in men, but not in women (-15% vs. 8%, P < 0.05, and -9% vs. -2%, respectively, P < 0.05). Similar decreases in LpAI concentrations and LDL and HDL particle size were observed in men and women. These data are consistent with the concept that middle aged/elderly men may have a more favorable lipoprotein response to a low fat, low cholesterol diet than postmenopausal women.

KEY WORDS: • gender • lipoproteins • lipoprotein subclasses • low fat diet • low cholesterol diet

Coronary heart disease (CHD)² is a major cause of death and disability in both men and women in the United States (1). Significant risk factors for CHD include age, hypertension, diabetes, cigarette smoking, decreased concentrations of HDL cholesterol (HDL-C < 1.03 mmol/L) and elevated concentrations of LDL cholesterol (LDL-C 4.14 mmol/L) (2). Male gender also carries a greater risk of CHD (2). The National Cholesterol Education Program (NCEP) recommended that a diet restricted in saturated fat (<7% of total energy) and cholesterol (<200 mg/d) should be consumed by subjects with established CHD or at risk of developing CHD to lower their LDL-C (2,3).

We and others documented previously that under controlled conditions, a diet restricted in total fat, saturated fat and cholesterol can lower LDL-C concentrations by 15–20%, but also lowers HDL-C concentrations (4–7). There is a high degree of variability in responsiveness to a low fat diet, which is related in part to gender (8–12).

The purpose of this study was to compare the effects of a diet restricted in total fat, saturated fat and cholesterol, relative to those of an average American diet (AAD), on plasma lipoprotein and apolipoprotein (apo) concentrations as well as on lipoprotein subspecies in men and women. Our data indicate that, in middle aged and elderly subjects, men respond to restriction in total fat, saturated fat and cholesterol differently from women. Our study does not provide information on the specific component of the diet that is responsible for the observed gender difference in lipoprotein response.

	SUBJECTS AND METHODS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Study subjects.

Subjects participating in this study (n = 33) were moderately hypercholesterolemic at screening (LDL-C 4.14 mmol/L). Inclusion criteria for enrollment into the study included age 40 y, and all women in the study were postmenopausal. None of the subjects were taking medications known to affect lipoprotein metabolism (cholesterol-lowering medications, hormones, and ß-blockers). At the screening visit, all subjects provided a complete medical history and underwent a physical examination. Subjects with any evidence of thyroid disease, diabetes mellitus, kidney disease or liver disease, as well as subjects who smoked or consumed alcohol were not enrolled into the study.

Subjects were grouped by gender, with 19 men and 14 women. The number of subjects with apo E phenotypes 2/3, 3/3, and 3/4, were 3, 11 and 5, respectively, in men and 3, 8 and 3, respectively, in women. Table 1 shows the characteristics of the subjects at screening. Subjects consumed the AAD for 6 wk and then the Therapeutic Lifestyle Changes (TLC) diet, restricted in total fat, saturated fat and cholesterol, for 6 wk. A period of 2–7 wk, during which subjects could resume their habitual diet, separated the AAD and TLC diet phases. The study protocol was approved by the Tufts University-New England Medical Center Investigation Review Board and all subjects provided informed consent.

All food and drink for the AAD and the TLC diets were prepared by the Metabolic Research Unit of the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University and were provided to the participants as breakfast, lunch, dinner and snacks. Blood pressure and body weight were measured at least three times per week. Energy intake was adjusted to keep each subject’s body weight constant (±1 kg) throughout the study.

The composition of the AAD diet was similar to diets consumed in the United States (13), and consisted of 35.4% of energy as fat, 14.1% as saturated fat and 147 mg cholesterol/4.2 MJ (Table 2). The TLC diet was composed of 25.5% of energy as fat, 4.0% as saturated fat and 45 mg cholesterol/4.2 MJ. This diet meets the recommendations of the NCEP Adult Treatment Panel III [(2); 25%–35% of energy as total fat, <7% as saturated fat, <200 mg/d cholesterol] and Panel II (3). The complete chemical composition of the diets was assessed by Hazelton Laboratories (Madison, WI) in terms of protein, carbohydrate, fat, fatty acids, and cholesterol, and is shown in Table 2. Food sources for the AAD and TLC diets were similar.

Blood was drawn into 0.15% EDTA tubes after a 12- to 14-h fast. Blood samples for plasma lipid measurements were collected at wk 4, 5 and 6 of the AAD diet and the TLC diet.

VLDL (d <1.006 kg/L) and the d >1.006 kg/L infranatant were separated by ultracentrifugation at 4°C in a Beckman 50.3 Ti rotor at 109,000 x g for 18 h. HDL fractions (HDL and HDL₃) were isolated from plasma by the dextran sulfate-Mg²⁺ method, after precipitation of apo B–containing lipoproteins or apo B–containing lipoproteins and HDL₂ as previously described (14,15).

The plasma concentrations of total triacylglycerol (TG), total cholesterol (TC), HDL-C, HDL₃-C and the 1.006 kg/L infranatant cholesterol were measured on an Abbott Diagnostics Spectrum CCX bichromatic analyzer (Dallas, TX), using Abbott and Miles Technicon enzymatic reagents (16). VLDL, LDL and HDL₂ cholesterol concentrations were calculated as follows: VLDL-C = TC - 1.006 kg/L infranatant cholesterol; LDL-C = 1.006 kg/L infranatant cholesterol - HDL-C; HDL₂-C = HDL-C - HDL₃-C (16). TG concentrations were measured in the fasting state and in the postprandial state. For the measurement of postprandial TG, plasma samples were collected at the end of each diet phase during a constant feeding period during which subjects consumed hourly meals for 20 h with each meal containing 5% of the energy consumed for the day, and food containing the same content for that phase. Ten blood samples were collected between 5 and 20 h after feeding had begun. Within- and between-run CV for the lipid measurements were all < 5%.

Plasma concentrations of apo AI and apo B were measured by noncompetitive ELISA using affinity purified polyclonal antibodies as previously described (17,18). Between- and within-run CV for these assays were 10%.

To determine the plasma concentration of lipoprotein particles containing apo AI without apo AII (LpAI) and of lipoprotein particles containing apo AI and apo AII (LpAI:AII) a differential rocket immunoelectrophoresis assay was used (19). CV between and within run were 4.6 and 1.5%, respectively.

NMR measurements of lipoprotein subclasses.

NMR spectroscopy was used to assess the concentration of different lipoprotein subclasses in Dr. Otvos’ laboratory (20). This methodology is based on the observation that each lipoprotein particle of a given size has a distinctive lipid NMR signal, whose intensity is proportional to its lipid mass concentration. By computer deconvolution of the composite plasma lipid signal envelope, the signal intensities (and hence concentrations) of 15 subclasses of VLDL, LDL and HDL were determined simultaneously. The designations and estimated diameter ranges (in nm) of the subclasses quantified by NMR were as follows: VLDL6, 150 ± 70; VLDL5, 70 ± 10; VLDL4, 50 ± 10; VLDL3, 38 ± 3; VLDL2, 33 ± 2; VLDL1, 29 ± 2; intermediate density lipoprotein (IDL), 25 ± 2; LDL3, 22 ± 0.7; LDL2, 20.5 ± 0.7; LDL1, 19 ± 0.7; HDL5, 11.5 ± 1.5; HDL4, 9.4 ± 0.6; HDL3, 8.5 ± 0.3; HDL2, 8.0 ± 0.2; HDL1, 7.5 ± 0.2. Concentrations of VLDL subclasses are expressed in units of TG (mmol/L) and those of IDL, LDL and HDL subclasses in units of cholesterol (mmol/L) (20).

Lipoprotein particle size determinations.

At the end of each diet phase, plasma samples were obtained to measure HDL and LDL particle size by nondenaturing polyacrylamide agarose gradient gel electrophoresis (2–16% for LDL and 4–30% for HDL) (21,22). Mean HDL particle size and weighted LDL scores were calculated by the equations previously reported (22,23).

Statistical analysis.

Statistical Analysis System software (SAS Institute, Cary, North Carolina) was used to analyze the data. Within each gender, paired Student’s t tests were conducted to test for differences between mean values during the TLC and the AAD diet phases. Individual percentage changes were calculated as (TLC value - AAD value)/AAD value x 100. Differences in lipoprotein response (percentage change) between men and women were tested for significance using Student’s t test. P-values < 0.05 were considered significant.

	RESULTS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The effect of the TLC diet, compared with the AAD diet, on non-HDL lipoproteins in the 19 men and 14 women participating in the study is shown in Table 3. Plasma concentrations of TC and LDL-C were reduced (P < 0.01) by 19 and 21%, respectively, in men and by 12 and 15%, respectively, in women. The reduction in TC concentrations was greater in men than in women (P < 0.05). Fasting plasma TG values were not affected by the TLC diet in men, but were increased 14% in women (P < 0.05). TG concentrations in the constant postprandial state were reduced (P < 0.01) by 15% in men, but not in women. The diet-related postprandial reduction in TG levels was (P < 0.05) greater in men than in women. Plasma apo B concentrations were reduced in men and in women (-18%, -9%, P < 0.01) by the TLC diet, and these changes were also (P < 0.05) greater in men than in women. LDL particle size, as assessed by LDL score on gradient gel electrophoresis, decreased by 11% in men and 21% in women (P < 0.05) (with this methodology, a higher LDL score indicates a smaller LDL size). The reduction in LDL particle size in response to the TLC diet tended (P = 0.09) to be greater in women than in men.

View this table: [in this window] [in a new window]   TABLE 3 Non-HDL lipoprotein concentrations at the end of the average American diet (AAD) and the Therapeutic Lifestyle Changes (TLC) diet in moderately hypercholesterolemic men 40 y old and postmenopausal women according to gender1, 2

View this table: [in this window] [in a new window]   TABLE 4 HDL subclasses concentrations at the end of the average American diet (AAD) and the Therapeutic Lifestyle Changes (TLC) diet in moderately hypercholesterolemic men 40 y old and postmenopausal women according to gender1, 2

Effects of dietary modification on lipoprotein subclasses concentrations, as assessed by NMR, are shown in Figures 1and 2. In men (Fig. 1), the TLC diet reduced IDL, HDL5 and HDL3 subclasses (P < 0.05). In women (Fig. 2), the TLC diet decreased VLDL2 and HDL5 subclasses (P < 0.05). No gender differences were observed in the response of lipoprotein subclasses to diet.

View larger version (21K): [in this window] [in a new window]   FIGURE 1 Distribution of lipoprotein subclasses during the average American diet (AAD; open bar) and therapeutic lifestyle changes (TLC; filled bar) diet phases in men 40 y old with moderate hypercholesterolemia. Upper panel, VLDL subclasses; middle panel, intermediate density lipoprotein (IDL) and LDL subclasses; lower panel, HDL subclasses. Values are mean ± SEM,n = 19. *Significant diet effect, P < 0.05.

View larger version (23K): [in this window] [in a new window]   FIGURE 2 Distribution of lipoprotein subclasses during the average American diet (AAD; open bar) and therapeutic lifestyle changes (TLC; filled bar) diet phases in postmenopausal women with moderate hypercholesterolemia. Upper panel, VLDL subclasses; middle panel, intermediate density lipoprotein (IDL) and LDL subclasses; lower panel, HDL subclasses. Values are mean ± SEM,n = 14. *Significant diet effect, P < 0.05.

	DISCUSSION

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

Only a few studies have examined the role of gender on the response of lipoprotein subspecies to diet in humans (24,25). Some studies showed that LDL-C lowering in response to low fat, low saturated fat diets was greater in men than in women (8,9,11,12), whereas other studies did not find a gender difference in LDL-C response (26). In a large study with >4000 subjects, the mean reduction in LDL-C in response to the Pritikin Program (<10% of total fat, exercise, and weight reduction over a 3-wk period) was 25% in men and 19% in women, and this gender difference was significant (8). In the Pritikin Program, body weight reduction was also achieved by design during dietary treatment, and body weight changes may have affected the degree of LDL-C response to the diet. In a recent study in which we examined the data from five controlled, isoweight (designed to maintain body weight constant) dietary studies using NCEP Step 2 diets, a nonsignificant trend for greater LDL-C reductions in men than in women was observed (-19 vs. –16%, respectively, P = 0.058) (10). No gender difference in LDL-C response was observed in a study conducted in 63 women and 99 men with hypercholesterolemia who were instructed to follow an American Heart Association step 1 diet (<30% fat, <300 mg cholesterol/d) for 8 wk (27). Similarly, no difference in LDL response to four different low fat diets was observed in 33 women and 30 men with hypercholesterolemia (28). The variability in findings in the current literature may be due to the fact that a large number of subjects may be needed to detect a statistical significance in LDL, or other lipoprotein, response to diet. We showed previously that the degree of LDL-C response to a TLC diet varies greatly among individuals, possibly due to gene-diet interactions (10). In addition, strict adherence to the diet may be a factor in this variability, and controlled studies are best suited to assess the role of diet on lipoprotein changes. In the current study, consumption of a TLC diet under controlled, isoweight conditions significantly reduced LDL-C in both men and women, and this reduction tended to be greater in men than in women (P = 0.08). We also observed a significant reduction in LDL particle size in both men and women. This reduction was likely due to a selective reduction in the larger LDL fractions, as shown by the NMR analysis of LDL subclasses. We reported previously that LDL particle size is reduced, in men and women combined, during consumption of a TLC diet compared with an AAD (29).

Interestingly, although men experienced a significant reduction in postprandial TG concentrations when consuming the TLC diet, this variable tended to increase in women (P = 0.10). This differential response resulted in a significant gender effect. Our results are consistent with a previous observation by Kovar et al. (30) that postprandial TG levels are higher in men than in women consuming a high fat diet, but no such difference is observed when men and women consume a low fat diet.

It is likely that the differential postprandial TG metabolism we observed in our subjects is responsible at least in part for the gender difference in the response of the HDL subclasses to the TLC diet. The TLC-associated reduction in HDL₂-C in women was almost twice that in men. HDL₂ are large HDL particles, containing both LpAI and LpAI:AII. NMR analysis of HDL subclasses indicated that the larger HDL5 subclass was particularly and significantly reduced by the TLC diet, and this reduction was greater in women than in men. Because a significantly greater reduction in the Lp AI:AII fraction was also observed in men than in women, our data indicate a selective reduction of large LpAI and LpAI:AII HDL in men, and of large Lp A-I in women with the TLC diet. In a previous study of eight subjects (men and women) consuming a TLC diet with an elevated fish content, reductions in Lp AI:AII particles, but not Lp AI particles, were reported (31). Elevated fish consumption alters plasma TG metabolism (32). Therefore the discrepancy in results between our study and that of Cheung et al. (31) may be explained by the difference in the composition of the TLC diet. In a study of hypercholesterolemic subjects, Walden et al. (24) reported that consumption of a TLC diet was associated with a reduction in HDL₂-C concentrations that was significantly greater in women than in men. These results are consistent with our observation of a reduction in HDL₂ subclasses that was almost twice as large in women than in men. Other investigators have examined alterations in LDL and HDL subclasses, as assessed by gradient gel electrophoresis (33,34). In a study of moderately overweight men, a combined program of dietary modification (step 1 diet), exercise and weight loss over a 1-y period significantly increased large HDL particles only in the group that experienced weight loss (BMI reduction of 2.8 kg/m²), whereas the diet group without exercise did not experience such changes (33). In addition, Dreon et al. (34) observed a significantly greater reduction in LDL-C and apo B levels in response to a low fat diet in men with small LDL particles that in men with a larger LDL particles.

In conclusion, our data are consistent with the concept that middle-aged and elderly men have a more favorable lipoprotein response to a TLC diet than do postmenopausal women. Due to the protective role played by HDL in the atherogenesis process (35,36), it is not known whether the reductions in HDL-C and HDL subclasses that we observed in our study are of relevance in terms of patients’ risk of CHD.

	FOOTNOTES

 
¹ Supported by grant HL39236 from the National Heart, Lung, and Blood Institute, National Institutes of Health, and contract 53–3K06–5-10 from the U.S. Department of Agriculture Research Service.

³ Abbreviations used: AAD, average American diet; apo, apolipoprotein; C, cholesterol; CHD, coronary heart disease; IDL, intermediate density lipoprotein; LpAI, HDL containing apo A-I only; LpAI:AII, HDL containing apo AI and A-II; NCEP, National Cholesterol Education Program; TC, total cholesterol; TG, total triacylglycerol; TLC, therapeutic lifestyle changes.

Manuscript received 22 May 2003. Initial review completed 14 July 2003. Revision accepted 19 August 2003.

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TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 

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