| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Original Research Communication |
1 From the CSIRO Health Sciences and Nutrition, Adelaide, Australia; Unilever Research Laboratories, Vlaardingen, Netherlands; and Flora Foods, Sydney, Australia.
2 Supported by Unilever, Netherlands.
3 Reprints not available. Address correspondence to M Noakes, PO Box 10041, Adelaide, BC SA 5000, Australia. E-mail: manny.noakes{at}hsn.csiro.au.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Objective: Our objective was to assess whether advice to consume specific daily amounts of foods high in carotenoids prevents a reduction in plasma carotenoid concentrations in subjects who consume plant sterol or stanol esters.
Design: Forty-six hypercholesterolemic free-living subjects completed a 3-way, double-blind, randomized crossover comparison. Subjects consumed each of the following 3 spreads (25 g/d) for 3 wk: control-1 (sterol-free), sterol ester-1 (2.3 g plant sterol esters), and stanol ester-1 (2.5 g plant stanol esters). During the 3-wk interventions, subjects were advised to eat 
5 servings of vegetables and fruit/d, of which 1 serving was to be carrots, sweet potatoes, pumpkins, tomatoes, apricots, spinach, or broccoli.
Results: The dietary advice resulted in a 13% increase in plasma ß-carotene in subjects who consumed control-1 (P = 0.04). The plasma ß-carotene concentrations of subjects who consumed control-1 did not differ significantly from those of subjects who consumed stanol ester-1 or sterol ester-1. This result was achieved by an increase of one daily serving of high-carotenoid vegetables or fruit. LDL cholesterol decreased 7.7% and 9.5% after consumption of sterol ester-1 and stanol ester-1, respectively (P < 0.001 for both), and differences between the LDL-cholesterol values obtained were not significant.
Conclusion: Dietary advice to consume an additional daily serving of a high-carotenoid vegetable or fruit when consuming spreads containing sterol or stanol esters maintains plasma carotenoid concentrations while lowering LDL-cholesterol concentrations significantly.
Key Words: Plant sterols • plant stanols • phytosterols • carotenoids • LDL cholesterol
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
38–40% of total energy) (3) and in those having lower fat and cholesterol intakes (25–35% of total energy) (4–6). These findings suggest that the absorption of both dietary cholesterol and biliary cholesterol is inhibited by consumption of plant sterols (6). The products used in these studies contained either plant sterol esters or plant stanol esters incorporated into fat-reduced spreads containing between 35% and 64% fat.
Weststrate and Meijer (3) found that a small quantity (3 g/d) of either plant sterol esters or sitostanol esters significantly lowers lipid-standardized blood carotenoid concentrations by 7%. Although intervention trials supplying ß-carotene have had negative health outcomes (8), there is some evidence that carotenoids may have positive effects on health (7). Thus, it has been recommended that decreases in carotenoids by sterol-enriched spreads be minimized (3). The recently released position statement on plant-sterol-enriched spreads by the National Heart Foundation in Australia makes the following statement: "To minimize decreases in plasma carotenoids, consume plant sterols and stanols in moderation and eat yellow and orange vegetables and fruits daily although the efficacy of this has not been demonstrated" (9).
The first objective of the present study was to establish whether advice to consume specific daily amounts of foods high in carotenoids is effective in preventing the reduction in plasma carotenoid concentrations previously described. Our second objective was to compare the effects on blood lipids of low-fat spreads (40% fat) containing plant sterol esters or stanol esters with those of similar phytosterol-free spreads. An additional, parallel arm of the study compared the effects on blood lipids of a higher fat sterol-containing product with those of a sterol-free product (both products contained 64% fat). The subjects in the study had prior knowledge that they were hypercholesterolemic, and the study was designed to allow them to consume their usual free-living diet, which contained a reduced amount of saturated fat.
|
SUBJECTS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
The study was preceded by a 1-wk baseline period and concluded with a 2-wk period during which subjects reverted to their usual dietary intakes. The functions of the baseline period were to allow subjects to adapt to the consumption of the required amount of spread (provided as control-1) and to provide baseline measurements of plasma carotenoid concentrations while the subjects consumed their usual amount of fruit and vegetables. Before the baseline period, subjects were randomly assigned in groups of 6 to 1 of the 6 treatment orders on the basis of a randomly generated 6-digit number containing each of the numerals 1–6.
2-Way comparison
We used a similarly randomized double-blind crossover design with 2 treatment orders to compare the effects of consuming 25 g/d of each of 2 spreads (64% fat) for 3 wk. One spread contained sterol (sterol ester-2) (Proactiv; Flora Foods, Marrickville, Australia), and the other was sterol-free (control-2) (Flora spread; Flora Foods). As in the 3-way comparison, there was a 1-wk baseline period and a 2-wk follow-up at the end of the last intervention.
The experimental design for the 2 comparisons is shown in Figure 1
. For both comparisons, blood samples were taken on 2 consecutive days at the end of the baseline period and after each intervention period. One blood sample was taken during the 2-wk follow-up period. For both comparisons, the lipid concentrations of these samples (triacylglycerols and total, HDL, and LDL cholesterol) were measured. Plasma carotenoid concentrations were measured only for the 3-way comparison at the end of each intervention period, excluding the follow-up period.
|
Fifty-two and 40 mildly hypercholesterolemic men and women were selected for the 3-way and 2-way comparisons, respectively. Overall, 9 subjects withdrew from the study before it commenced, and 2 subjects withdrew during the study, 1 because of an unrelated hospitalization and the other because of travel commitments. Forty-six and 35 subjects completed the 3-way and 2-way comparisons, respectively, and baseline data for these subjects are presented in Table 1. There were 2 smokers, 1 man and 1 woman. All except 2 women in each comparison were postmenopausal. The study was approved by the CSIRO Health Sciences and Nutrition Human Ethics Committee, and written, informed consent was obtained from the volunteers.
|
. The total fat content, fatty acid composition, and content of free sterols, carotenoids, and 
-tocopherol of the spreads were provided by Unilever Research Laboratory, Vlaardingen, Netherlands and analyzed by methods described by Weststrate and Meijer (3). Subjects were asked to maintain their usual low-saturated-fat diet with minimal variation other than to replace their usual spreads with the required amount of test spread. In addition, from the end of the baseline period, subjects in both the 3-way and 2-way comparisons were advised to eat a diet high in carotenoids. Subjects were specifically advised to consume 5 servings of vegetables and fruit/d and to ensure that 1 of the 5 servings was chosen from a list of 7 foods high in carotenoids. The US carotenoid database was used to select the following 7 carotenoid-rich, commonly consumed fruit and vegetables: carrots, sweet potatoes, pumpkins, tomatoes, apricots, spinach, and broccoli. One serving was deemed to be 125 mL.
|
Food checklists were completed daily, and weighed-food records were completed on 3 d (Sunday, Monday, and Tuesday) every 3 wk; the specific dates were noted on the study calendar given to all subjects. Subjects received detailed instruction by demonstration and in writing on how to accurately document their food intake. The subjects' weights and diets were monitored every 3 wk by the dietitian. Nutrient intakes were calculated with DIET/1 nutrient calculation software (Xyris Software, Highgate Hill, Australia), a computer database of foods in which nutrient composition is based on that of Australian foods and which we modified to include data both from commercial sources and from an analysis of the spreads. Because only ß-carotene equivalents are available for this database, ß-carotene was the only carotenoid for which we were able to compute dietary intake, as follows:
 | (1) |
Measurements
Lipids
After subjects fasted overnight for 12 h, venous blood samples (20 mL) were collected in plain tubes. Serum was separated by low-speed centrifugation at 600 x g for 10 min at 5°C (GS-6R centrifuge; Beckman, Fullerton, CA) and frozen at -20°C. At the end of the study, all samples from each subject were analyzed within the same analytic run. Total cholesterol (10) and triacylglycerol (11) concentrations were measured on a Cobas-Bio centrifugal analyzer (Roche Diagnostica, Basel, Switzerland) by using enzymatic kits (Roche Diagnostica, Basel, Switzerland) and standard control sera. Plasma HDL-cholesterol concentrations were measured after precipitation of apolipoprotein B–containing lipoproteins by polyethylene glycol 6000. The CVs for the individual lipids were all <5%. The following modification of the Friedewald equation (12) for molar concentrations was used to calculate LDL cholesterol in mmol/L:
 | (2) |
Carotenoids
After subjects fasted overnight, blood samples were collected in tubes containing EDTA as an anticoagulant. The plasma was separated by low-speed centrifugation at 600 x g for 10 min at 5°C (GS-6R centrifuge), frozen immediately in liquid nitrogen, and then stored at -80°C until analysis.
Plasma extractions and HPLC chromatography were performed according to the method of Yang and Lee (13). Minor modifications to this method were derived from Khachik et al (14).
Sample preparation and analysis
Only a few samples were processed at a time to minimize the exposure to laboratory conditions. The lighting was minimal throughout sample preparation, and amber vials were used for storage of the final extract. The internal standard (a tocopherol acetate) was added to samples (200 µL) with 200 µL ethanol. Vitamins and carotenoids were extracted with hexane, and the extract was evaporated to dryness under nitrogen. Extracts were then stored at -20°C. Mobile phase was used to redissolve the samples for HPLC analysis. Each volunteer had 4 plasma samples taken during the course of the intervention study. All samples from a volunteer were extracted in duplicate and analyzed in one run on the HPLC instrument to minimize the effect of day-to-day variation. CVs for each of the carotenoids were as follows: lutein, 2.5%; retinal, 2.5%; -tocopherol, 2.9%; lycopene, 2.7%; -carotene, 2.9%; and ß-carotene, 2.7%.
Quality control
A standard reference material (product 968b; National Institute of Standards and Technology, Gaithersburg, MD) was initially tested after preparation of the standards (October 1999). All vitamins and carotenoids in the standard reference material were found to be within the certified ranges at all levels (high, medium, and low).
Quality-control plasma was prepared for this study by pooling 20 mL plasma, which was mixed thoroughly, and 500-µL aliquots were then placed into storage vials; quality-control plasma was run with each batch of samples. Quality-control plasma also was stored at -80°C.
A Shimadzu LC 10 HPLC instrument fitted with a refrigerated auto sampler and an SPD-M10Avp photodiode array detector with a class LC 10 chromatography workstation was used for analysis of the prepared samples (Shimadzu, Kyoto, Japan). Isocratic separations of the fat-soluble vitamins and carotenoids were carried out on a Rainin (4.6 mm inner diameter x 250 mm length) C18 (5-µm spherical particles) reversed-phase column (Rainin, Woburn, MA). The mobile phase was a mixture of acetonitrile (55%), methanol (22%), hexane (11.5%), and dichloromethane (11.5%), and the flow rate was 1.0 mL/min. Ammonium acetate (0.01% wt:vol) was added to the mobile phase for stabilization of the carotenoids. Wavelengths of 292 nm (-tocopherol and -tocopherol acetate), 325 nm (retinol), and 450 and 472 nm (carotenoids) were monitored throughout each run.
Plasma carotenoid concentrations were standardized for plasma lipid (total cholesterol plus triacylglycerol) (15) because the sterol spreads significantly reduced plasma lipids, which are carriers of plasma carotenoids. Trans - and ß-carotene, lycopene, lutein, retinol, -tocopherol, and -tocopherol acetate were all obtained from Sigma Chemical Co, St Louis. Solvents, hexane, methanol, acetonitrile, and dichloromethane were all analytic HPLC grade, and ethanol was 99.5% HPLC-grade absolute ethanol.
Statistical analysis
Repeated-measures analysis of variance (ANOVA) was calculated with the type of spread in each intervention arm as the within-subject factor and with sex and order as the between-subject factors. Age, baseline LDL cholesterol, and BMI were inserted into the model as covariates. When a significant treatment effect was detected by repeated-measures ANOVA, main effects were located by paired Student' t tests, and, except where stated, a Bonferroni correction was used to adjust for multiple comparisons. Further ANOVAs were run with dietary fat, saturated fat, and energy intake in each phase as covariates. Bivariate correlation was conducted with the use of Pearson' correlation coefficient. Analyses were performed with SPSS 8.0 for WINDOWS (SPSS Inc, Chicago). Significance was set at P < 0.05.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
. Compliance was excellent in the 3-way comparison: mean spread consumptions were 24.5, 24.7, and 24.9 g during the control-1, sterol ester-1, and stanol ester-1 periods, respectively. The minimum consumption was 22.6 g/d. Dietary intakes were low in total and saturated fat, reflecting the fact that the subjects had known hyperlipidemia and had made prior dietary changes. The 3 spread periods did not differ significantly in any dietary variable. Energy intake tended to decrease from the baseline period, and this decrease was significant for the control-1 spread period; the percentage of energy from fat also decreased significantly from baseline to all intervention periods (P < 0.01). These decreases are probably attributable to the advice to increase intakes of colored fruit and vegetabes. Consistent with that advice, intakes of ß-carotene equivalents significantly increased from the baseline period (P < 0.001) by an average of 72%.
|
Plasma lipids
3-Way comparison
The repeated-measures ANOVA for total and LDL cholesterol for the 3 test spreads was significant (P < 0.001) and was not altered by overall dietary fat or energy intake or changes in saturated fat from period to period, age, BMI , sex, baseline LDL cholesterol, or diet order (Table 4). The correlation between the change from control-1 to sterol ester-1 and control-1 to stanol ester-1 was very high (r = 0.7, P < 0.001) and was not influenced by dietary fat changes. This suggests a high individual repeatability of response. The reduction in total cholesterol with consumption of sterol ester-1 and stanol ester-1 was 6.1% and 7.3%, respectively, compared with consumption of the control spread (P < 0.001 for both). The decrease in the LDL-cholesterol concentration was 7.7% (0.33 mmol/L) with consumption of sterol ester-1 and 9.5% (0.41 mmol/L) with consumption of stanol ester-1 (P < 0.001 for both). The difference between the effects of sterol ester-1 and stanol ester-1 on LDL cholesterol was not significant. Two weeks after cessation of test spreads, LDL cholesterol had increased by 0.35 mmol/L from the sterol ester-1 period (P < 0.001), 0.43 mmol/L from the stanol ester-1 period (P < 0.001), and 0.02 mmol/L from the control-1 period (NS). Triacylglycerol and HDL-cholesterol concentrations were not significantly altered by the spreads.
|
). This was not altered by overall dietary fat or energy intake or changes in saturated fat from period to period, age, BMI, sex, baseline LDL cholesterol, or diet order. There were no significant changes in HDL-cholesterol or triacylglycerol concentrations. The difference in LDL cholesterol between the sterol ester-2 period and the 2-wk follow-up period was 0.49 mmol/L (P < 0.05) whereas the difference between the sterol-free control-2 period and the 2-wk follow-up period was 0.09 mmol/L (NS).
Plasma carotenoid concentrations
Plasma carotenoid concentrations standardized for plasma lipids are shown in Table 5. As total cholesterol concentrations decreased with consumption of the sterol or stanol spreads, the plasma concentrations of -tocopherol, lycopene, and -and ß-carotene decreased significantly (P < 0.001); thus, only adjusted figures were analyzed statistically. Consumption of the different spreads did not significantly change the concentrations of retinol and lutein, which is consistent with their transport by retinol binding protein and HDL (40%), respectively. When the baseline and control-1 periods were analyzed separately (where no change in plasma cholesterol concentration occurred), the concentrations of plasma lutein (P = 0.004), -carotene (P < 0.001), and ß-carotene (P = 0.04) increased by 11%, 29%, and 13%, respectively, which is concordant with the increased dietary intake of the specified fruit and vegetables. Interestingly, the concentration of plasma lycopene did not change significantly. However, when the adjusted figures were used, the concentrations of lutein, -carotene, and ß-carotene were significantly different between spreads once the Bonferroni adjustment was applied. Before adjustment, both the sterol and stanol periods significantly (P < 0.05) lowered the ß-carotene concentration by 9% compared with the control-1 period but not compared with the baseline period. Similarly, -tocopherol concentrations were not significantly different among spread periods or between the spread periods and the baseline period. Thus, the advice to increase the intake of the specified type and amount of fruit and vegetables with consumption of the sterol and stanol spreads completely balanced any effect of the spreads on carotenoid concentrations. There was no relation between the amount of reduction in LDL cholesterol and the change in carotenoid concentrations.
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
2 g stanol esters. The advantage of this mix is that it does not require chemical manipulation after extraction from its source, which is also in abundant supply.
Although the average reduction in LDL cholesterol attributed to phytosterols is estimated to be 13%, there is considerable variability, as noted above, ranging from <2% to 33% (21). If experiments on subjects with familial hypercholesterolemia are excluded, this figure is closer to 11%. In a review of 14 randomized double-blind trials, Law (22) estimates that 2 g plant sterol esters or stanol esters reduces LDL cholesterol differentially by age, with an average reduction of 0.54 mmol/L in persons aged 50–59 y, 0.43 mmol/L in those aged 40–49 y, and 0.33 mmol/L in those aged 30–39 y. Differences in efficacy may also be related to factors such as the nature and form of the phytosterols used, the dose, the background diet, and subject variability in age and in efficiency of cholesterol absorption (23).
The reduction of plasma carotenoid concentrations by spreads containing phytosterols was reported previously. Weststrate and Meijer (3) compared a sitostanol ester spread with esterified sterols from soybean, sheanut, or rice bran and found that all reduced lipid-standardized carotenoids to a variable extent (9–43%) and that the reduction was not related to the magnitude of lipid reduction. Gylling et al (24) reported a 25% reduction in plasma ß-carotene concentrations in subjects who consumed 2.6 g sitostanol-ester-fortified spread/d. Furthermore, daily consumption of 0.83, 1.61, and 3.24 g plant sterol equivalents in spread (8% free plant sterols = 13.33% of esterified plant sterols as the molecular weight of free plant sterols = 60% esterified plant sterols) decreased lipid-standardized plasma concentrations of - plus ß-carotene by 8%, 5.5%, and 14.9%, respectively, and plasma lycopene nonsignificantly by 7–10% (2). In contrast, Hallikainen et al (25) evaluated the effects of 2 low-fat stanol ester spreads containing 2.2–2.3 g total stanols and found no significant change in lipid-standardized - and ß-carotene or lycopene concentrations when subjects were concomitantly advised to follow a low-fat, low-cholesterol diet. Although the authors argue that the high nutrient (and implicitly carotenoid) density of the background diet in their study may have affected the outcome, reported dietary intakes of ß-carotene equivalents do not support this (6).
The finding that an increase in dietary carotenoid intake negated a potential decrease in plasma carotenoids in subjects consuming either sterol ester-2 or stanol ester-1 has not been shown previously. This result was achieved by advising subjects to consume 5 servings of fruit and vegetables/d and to ensure that 1 of those servings had a high carotenoid content. The spreads themselves contributed a negligible amount of carotenoids (only 125–225 µg/25-g serving). Dietary carotenoid intake data are limited because dietary carotenoid values are highly variable, and comparison of calculated and analyzed data have noted considerable discrepancies, with analyzed diet data amounting to only 50–60% of calculated values (26). These discrepancies may be due to real differences in food composition, to losses occurring during food preparation, or to differences in analytic methods. However, in the present study, we were concerned with changes in the dietary intake of carotenoids rather than with absolute intake, suggesting that the specific dietary advice regarding fruit and vegetable consumption was relevant for this population.
The fact that the dietary advice resulted in a 13% increase in plasma ß-carotene in subjects consuming the control spread suggests that current dietary intakes of carotenoids fall somewhat below those in the present study. This result was achieved with a 72% increase in calculated dietary ß-carotene equivalents and is consistent with the reported low bioavailability of carotenoids (27). High intakes of dietary fiber are reported to impair bioavailability (28), and the high intakes of dietary fiber of our subjects at baseline (26–30 g) may also have impaired carotenoid absorption. The increase in fruit and vegetable consumption was associated with a 2–4-g increase in dietary fiber intakes from the baseline period that was suggestive of a small increase in fruit and vegetable intake of 1–2 servings/d. Therefore, even in the context of a high-fiber diet, dietary advice to increase consumption of high-carotenoid vegetables or fruit by 1 serving/d should suffice to maintain plasma carotenoid concentrations when phytosterol-enriched spreads are consumed.
Lipid-standardized plasma lycopene did not increase during the control period even though tomatoes, which were commonly consumed by the subjects in both cooked and raw form, were listed as one of the high-carotenoid foods. Studies examining changes in serum lycopene after dietary supplementation suggest that plasma concentrations will change only marginally after a 4-wk period (29). Yeum et al (30), however, found that supplementation with 10 servings of fruit and vegetables/d significantly increased all plasma carotenoids including lycopene after 15 d. It was also suggested that high intakes of ß-carotene may antagonize the bioavailability of lycopene (31), but several studies did not find this to be the case (32,, 33).
In summary, low-fat sterol- and stanol-containing spreads lowered plasma LDL concentrations by 7.3–9.4% in subjects consuming a low-fat diet. The daily consumption of an average of one extra daily serving of high-carotenoid fruit or vegetables elevated plasma concentrations of - and ß-carotene and maintained concentrations of lipid-standardized plasma carotenoids in subjects consuming sterol-enriched spreads.
|
ACKNOWLEDGMENTS |
|---|
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  V. S. Retelny, A. Neuendorf, and J. L. Roth Nutrition Protocols for the Prevention of Cardiovascular Disease Nutr Clin Pract, October 1, 2008; 23(5): 468 - 476. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Naumann, J. Plat, A. D.M. Kester, and R. P. Mensink The Baseline Serum Lipoprotein Profile Is Related to Plant Stanol Induced Changes in Serum Lipoprotein Cholesterol and Triacylglycerol Concentrations J. Am. Coll. Nutr., February 1, 2008; 27(1): 117 - 126. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. G. Moruisi, W. Oosthuizen, and A. M. Opperman Phytosterols/Stanols lower cholesterol concentrations in familial hypercholesterolemic subjects: a systematic review with meta-analysis. J. Am. Coll. Nutr., February 1, 2006; 25(1): 41 - 48. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. M. Clifton, M. Noakes, D. Ross, A. Fassoulakis, M. Cehun, and P. Nestel High dietary intake of phytosterol esters decreases carotenoids and increases plasma plant sterol levels with no additional cholesterol lowering J. Lipid Res., August 1, 2004; 45(8): 1493 - 1499. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Noakes, P. R. Foster, J. B. Keogh, and P. M. Clifton Meal Replacements Are as Effective as Structured Weight-Loss Diets for Treating Obesity in Adults with Features of Metabolic Syndrome J. Nutr., August 1, 2004; 134(8): 1894 - 1899. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Richelle, M. Enslen, C. Hager, M. Groux, I. Tavazzi, J.-P. Godin, A. Berger, S. Metairon, S. Quaile, C. Piguet-Welsch, et al. Both free and esterified plant sterols reduce cholesterol absorption and the bioavailability of {beta}-carotene and {alpha}-tocopherol in normocholesterolemic humans Am. J. Clinical Nutrition, July 1, 2004; 80(1): 171 - 177. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Quilez, M. Rafecas, G. Brufau, P. Garcia-Lorda, I. Megias, M. Bullo, J. A. Ruiz, and J. Salas-Salvado Bakery Products Enriched with Phytosterol Esters, {alpha}-Tocopherol and {beta}-Carotene Decrease Plasma LDL-Cholesterol and Maintain Plasma {beta}-Carotene Concentrations in Normocholesterolemic Men and Women J. Nutr., October 1, 2003; 133(10): 3103 - 3109. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Naumann, J. Plat, and R. P. Mensink Changes in Serum Concentrations of Noncholesterol Sterols and Lipoproteins in Healthy Subjects Do Not Depend on the Ratio of Plant Sterols to Stanols in the Diet J. Nutr., September 1, 2003; 133(9): 2741 - 2747. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Y. Ntanios, Y. Homma, and S. Ushiro A Spread Enriched with Plant Sterol-Esters Lowers Blood Cholesterol and Lipoproteins without Affecting Vitamins A and E in Normal and Hypercholesterolemic Japanese Men and Women J. Nutr., December 1, 2002; 132(12): 3650 - 3655. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
