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* Pennington Biomedical Research Center, Baton Rouge, LA and
Procter & Gamble, Cincinnati, OH
2To whom correspondence should be addressed. E-mail: rtulley{at}agcenter.lsu.edu.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-tocopherol, retinol, ß-carotene, lycopene, and lutein + zeaxanthin were analyzed by HPLC. Subjects eating the olestra-containing diet had substantial decreases in serum ß-carotene, lycopene, and lutein + zeaxanthin, which occurred by 12 wk; these changes were found despite correcting for serum total cholesterol or BMI. Serum ß-carotene and lycopene concentrations were below the lower limit of the reference range (<0.186 and <0.298 µmol/L, respectively) at one or more time points. The slight decline in serum -tocopherol concentration, significant at 24 wk, was caused by the decline in serum cholesterol. Retinol concentrations decreased with time in all 3 groups, but were not affected by olestra. We conclude that supplementation with a multivitamin containing vitamins A and E was adequate to prevent olestra-induced decrease in serum -tocopherol and retinol. Olestra-induced decreases in serum ß-carotene, lycopene, and lutein + zeaxanthin were not prevented by the vitamin supplement used in this study.
KEY WORDS: • olestra • vitamin E • vitamin A • carotenoids • fat substitute
Olestra is an indigestible sucrose polyester that contains 6–8 fatty acids per molecule. It was approved by the U.S. FDA in 1996 to replace fats and oils used to prepare snack foods such as corn chips and potato chips (1). Replacement of dietary fat with olestra has been proposed as a method to reduce fat intake and lower cardiac risk factors. Cholesterol absorption and plasma cholesterol concentrations are reduced by olestra (2–9).
One potential disadvantage of olestra is that it decreases absorption of lipophyllic compounds such as fat-soluble vitamins. Daher et al. (10) reported a 19% decline in the mean absorption of [3H]retinyl palmitate in 68 healthy male subjects consuming 32 g olestra in potato chips. In pigs, liver and serum concentrations of vitamin A and vitamin E, as well as serum 25-hydroxyergocalciferal, were decreased with olestra feeding after 4 wk (11,12) and after 26 wk (13). These effects are dose-dependent for the amount of olestra in the diet (14). Vitamin E, 25-hydroxyergocalciferol (25-hydroxyvitamin D2), and phylloquinone (vitamin K) were all decreased in a dose-dependent manner by olestra in humans consuming 8–32 g/d for 8 wk. Similarly, concentrations of carotenoids (ß-carotene, -carotene, lycopene, lutein + zeaxanthin) also decreased, although retinol did not change (15). In humans consuming 12.4 g/d olestra in margarine for 4 wk, Westrate and van het Hof (16) found that olestra reduced plasma ß-carotene concentrations by 34% and lycopene by 52%. Serum concentrations of vitamin E, ß-cryptoxanthin, lutein, and zeaxanthin were also decreased. In this low-dose study, the investigators found reductions of 20% in ß-carotene and 38% in lycopene after 4 wk consumption of 3 g/d olestra (16). Similar reductions in carotenoids were found by Koonsvitsky et al. (17) in free-living adults ingesting 18 g/d olestra.
Supplementation with vitamins A and E during olestra feeding acts to restore serum and liver concentrations of these vitamins in pigs (13,18) and to partially restore serum concentrations of vitamin E in humans (17). The hypothesis that declines in fat-soluble vitamins during ingestion of olestra may be prevented by supplementation was tested in the study presented below. Because no other study has examined the effect of long-term olestra ingestion on fat-soluble vitamins during concurrent administration of supplemental fat-soluble vitamins, our study examined the changes in -tocopherol, retinol, and selected carotenoids (ß-carotene, lycocopene, and lutein + zeaxanthin) over 36 wk in 37 male volunteers receiving daily multivitamin supplements in the Ole Study (19).
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MATERIALS AND METHODS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Experimental design. The study was a double-blind, parallel arms clinical trial. A 3-wk run-in period was instituted in which all subjects received a diet composed of 33% energy from fat, 52% carbohydrate, and 15% protein. After 15 subjects each were assigned to the 3 study diets, control, fat-reduced, or olestra, they were given meals assigned to the appropriate study group (Table 1). The control group ate a diet providing 33% of the energy from fat, 52% carbohydrate, and 15% protein. For the olestra group, one third of the energy from fat was replaced with olestra, to give a total of 25% digestible fat, 58% carbohydrate, and 17% protein. The fat-reduced group ate meals providing 25% of the energy from digestible fat, 58% carbohydrate, and 17% protein. This dietary study continued for 36 wk.
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50% at the evening meal. The 2 lower fat diets were designed to provide 11% less of total energy requirements for each individual, as determined during the run-in. Further details are described elsewhere (19). The olestra contained RRR--tocopheryl acetate at 4.44 µmol/g. Each subject was instructed to take 1 vitamin tablet7 (CentrumTM, Whitehall-Robins Health Care) each day at dinner.
Measurements.
Blood samples were collected by venipuncture following overnight fasts at baseline, 12 wk, 24 wk, and 36 wk. The serum was transferred to brown cryovials and frozen at –80°C until analyzed. Cholesterol was analyzed on a Beckman CX7 automated chemistry analyzer using Beckman-Coulter (Beckman-Coulter) reagents. Analysis of retinol, -tocopherol, and the carotenoids was performed according to an in-house modification of the method of Aebischer et al. (20) using a Hewlett Packard 1090 automated HPLC equipped with diode array and fluorescence detectors. The column used was a Primesphere C18-HC, 250 x 4.6 mm, 5 µm particle size (Phenomenex), eluted with acetonitrile:tetrahydrofuran:methanol:1% (w:v) ammonium acetate (684:220:68:28) at a flow rate of 0.7 mL/min. Lutein and zeaxanthin coeluted in our analysis, so all values are expressed in lutein equivalents but represent the sum of lutein and zeaxanthin. Day-to-day precision studies resulted in CVs of 6.9 and 7.1% for -tocopherol at 11.88 and 7.06 µmol/L, respectively; 5.7 and 6.5% for lutein at 0.18 and 0.11 µmol/L, respectively; 5.0 and 9.9% for retinol at 0.92 and 0.55 µmol/L; 10.4 and 10.1% for lycopene at 0.70 and 0.29 µmol/L; and 6.5 and 5.1% for ß-carotene at 1.64 and 0.68 µmol/L. Recovery at 3 concentrations of spiked samples was between 96.8 and 104.1% for all analytes. Daily quality control samples were prepared by using Bio-Rad Lyphocheck chemistry control material, which was split into 2 aliquots, 1 unspiked and the other spiked with high-normal concentrations of each analyte. Samples were analyzed in batch at the end of the study to minimize day-to-day variations.
Materials.
Olestra was provided by Procter & Gamble and prepared in foods in our kitchen. Retinol, -tocopherol, retinyl acetate (internal standard), and lycopene were obtained from Sigma (Sigma-Aldrich); trans ß-carotene was obtained from Aldrich; and lutein and zeaxanthin were obtained from ChromaDex.
Data analyses. ANOVA with a repeated-measures design was used to analyze the data. SAS for Windows, version 8.2 (SAS Institute), was used for all calculations. All subjects participating in the study were analyzed by an intent-to-treat approach and by those who completed the study. The analyses were carried out using the change from baseline and the actual values at each time point. Baseline values for each vitamin were used as covariates in both statistical models. Using these analyses, treatment and time main effects and the time-by-treatment interaction were tested. At each time point, a treatment effect was tested within the same mixed linear model (slice test) and the changes from baseline at each time point within each treatment group were tested against time zero. All pair-wise comparisons were performed using Tukey-Kramer adjustments. To correct for binding by lipids and changes in body fat during the study, the vitamin/carotenoid concentrations were divided by total cholesterol and by BMI, respectively. The same analyses were then carried out for the ratio of each analyte to total cholesterol and BMI. In addition to ratios with cholesterol and BMI, we performed the adjusted analysis with cholesterol, BMI, and/or triglycerides as covariates in the model. The results and conclusions are similar to those presented here and, hence, the data are not shown. Probability values (P) of 0.05 or less were considered significant. Unless otherwise stated, values given are means ± SD.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-tocopherol, retinol, lycopene, or lutein + zeaxanthin. However, the serum ß-carotene concentration was higher in the fat-reduced group (0.37 ± 0.11 µmol/L) than in the olestra group (0.29 ± 0.09 µmol/L) (P = 0.02). As reported elsewhere, all groups lost weight, with the amount of weight loss and body fat loss being highest in the olestra group (6.27 ± 1.66 kg, P < 0.0001), intermediate in the control group (3.81 ± 1.34 kg, P < 0.0001), and lowest in the group eating the fat-reduced diet (1.79 ± 0.81 kg, NS) (19). Cholesterol was also lower than baseline in the olestra group at wk 12 and 24 and increased in the fat-reduced group at wk 36 (21).
The results of the analysis of -tocopherol showed a main effect of treatment (P = 0.03) (Table 2), with an increase from baseline for the fat-reduced group at wk 12 (P = 0.03) and a decrease for the olestra group at wk 24 (P = 0.04). The treatment-by-time interaction was not significant. The main effect of treatment was abolished when the ratios of -tocopherol to cholesterol (Table 3) or BMI (data not shown) were analyzed. The increase from baseline for the fat-reduced group at wk 12 remained significant (P = 0.047) when corrected for total cholesterol. There was no evidence of substantial change from baseline in the olestra group at any time point after correction for total cholesterol (Table 3). Increases from baseline in the fat-reduced group were significant at all times when corrected for BMI (P < 0.04, data not shown). The treatment effect was tested at each time point for -tocopherol using contrasts within the same statistical model. No differences were found at any of the measured time points. There were no differences between any 2 treatment groups at 12, 24, or 36 wk observed for the actual values, ratios with cholesterol (Table 3), or ratios with BMI (data not shown).
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In contrast with retinol and -tocopherol, the mixed statistical analysis showed a treatment main effect for all 3 carotenoids (P < 0.0001 for all) (Fig. 1).
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For lycopene, the treatment-by-time interaction was significant (P = 0.02). In comparison to the control group, lycopene was decreased for the olestra group at all time points (P < 0.025). There were no differences observed between fat-reduced and control groups at any of the time points. The decrease from baseline in the olestra group was significant at all times (P < 0.0001). Lycopene was lower in the olestra group than in the fat-reduced group at all time points (P < 0.0006). These results were substantiated even when corrected for cholesterol (Table 3) or BMI (data not shown).
The HPLC analysis did not separate lutein and zeaxanthin; thus they are combined for presentaton in Tables 2, and 3. In the analysis of lutein + zeanthaxin, the treatment-by-time interaction was highly significant (P < 0.001). Lutein + zeaxanthin was lower in the olestra group compared to the control group at wk 12 (P = 0.003) and 24 (P = 0.009) but not at wk 36. In addition, the decrease from baseline in the olestra group was significant at all times (P < 0.0001). There were no differences observed between the control and the fat-reduced group at any time points. Lutein + zeaxanthin was higher in the fat-reduced group than in the olestra group at all time points. This difference was significant at wk 12 and 36 (P < 0.001). Correction for cholesterol (Table 3) retained the treatment effects. Differences remained between olestra and the control group at wk 12 (P < 0.05) and between olestra and the fat-reduced group at wk 12 (P = 0.0004) and 36 when corrected for total cholesterol (P < 0.05) or for BMI (P < 0.007, data not shown). Decreases from baseline were still significant at all time points for the olestra group when corrected for total cholesterol (P < 0.0001) or BMI (P < 0.0003, data not shown).
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-tocopheryl acetate at 4.44 µmol/g, and participants received a vitamin supplement that contained 63.5 µmol of vitamin E (all racemic -tocopheryl acetate), vitamin A consisting of 3.14 µmol retinyl acetate, 2.24 µmol ß-carotene, and 0.44 µmol of lutein, but no lycopene or zeaxanthin.
In the olestra group, -tocopherol was reduced by 18% below the control level, but the reduction was significant only at wk 24. It is noteworthy that even though substantial differences were found with treatment, the -tocopherol concentrations for all groups remained within the reference range throughout the study. The reduction we observed compares well with the decrease of 18% found in humans consuming potato chips containing 20 g/d olestra (15). The reductions found in our study occurred despite supplemented vitamin E in olestra and in the daily multiple vitamin.
Although vitamin A (retinol) decreased substantially from baseline in all treatment groups, there were no effects of treatment per se, and the concentrations remained within the reference range for all treatments throughout the study. The reason for this across-the-board decline is puzzling. We conclude, however, that there was no effect of olestra on retinol levels. Although Schlagheck et al. (15) observed no declines in retinol in humans consuming 18 g/d olestra for 8 wk, our results are consistent with theirs in showing no treatment effect of olestra on retinol.
ß-Carotene concentrations in the olestra group were below the lower reference range (<0.186 µmol/L) as early as 12 wk. Ingestion of olestra resulted in a reduction in ß-carotene of 66% below control and a 56% reduction from baseline. These changes are comparable to the reductions in ß-carotene of 61% in humans consuming 32 g/d olestra for 8 wk (22) and 62% in free-living humans consuming 8 g/d olestra (15), but 65% greater than the 34% decrease found in humans consuming 12.4 g/d olestra (16). Although our subjects ingested more olestra than the subjects in any of these studies, they also received daily ß-carotene supplements of 2.24 µmol/d. Surprisingly, the 25% fat-reduced diet group had a substantial increase in ß-carotene compared to the control group. One explanation for a source of ß-carotene centers around the foods these subjects may have eaten to prevent the expected weight loss if they had adhered to their low-fat diet (19). Broekmans et al. (23) conducted a 1-y clinical trial in which 380 subjects were randomized into 4 groups to receive 0, 7, 10, or 17 g/d olestra. The dose of 17 g/d decreased ß-carotene by 31%, lycopene by 24%, lutein by 18%, and zeaxanthin by 11% at the 1-y time point. Lower doses of olestra produced smaller decreases in these vitamins. Our doses of olestra were higher than theirs (19.6–45.2 g/d), which may account for the larger decreases.
In the group consuming the olestra-substituted diet, lycopene showed a highly significant decrease from baseline at all time points when compared to the control group. Serum lycopene concentrations went below the lower limit of the reference range (<0.298 µmol/L) after 12 wk and remained near the lower limit of normal for the duration of the study. A decrease of 56% in lycopene versus control and a decrease of 53% from baseline were observed at 12 wk. This compares well to published data, which showed decreases of 52% in humans consuming 12.4 g/d olestra (16).
Lutein + zeaxanthin concentrations declined from baseline, but remained within the reference range. Lutein + zeaxanthin rapidly declined to 25% of control and 28% of baseline, respectively. This compares well to published data, which demonstrate 27% declines of lutein + zeaxanthin in humans consuming 8 g/d olestra for 8 wk (22).
Because -tocopherol and carotenoids are transported in the circulation by lipoproteins that also carry cholesterol, changes in plasma cholesterol concentration will be reflected in the amount of tocopherol and carotenoids in serum (24). Because there were changes in serum cholesterol in subjects eating the low-fat diets in our study, we corrected the concentrations of -tocopherol and the carotenoids for the changes in total cholesterol. Analysis of the data normalized for changes in cholesterol revealed that similar changes occurred in carotenoid levels as in nonnormalized data. Likewise, because the olestra group lost weight, correction for BMI was performed (data not shown). The reductions that we found in carotenoids remained important after this correction.
Reductions in these carotenoids in subjects eating olestra-containing foods may be undesirable. Although supplementation with vitamin E and A in this study appeared to be adequate to sustain normal concentrations of these vitamins, this was not true for the carotenoids. Supplementation with higher levels of carotenoids may be worthy of consideration. The degree of change we found in fat-soluble vitamins and carotenoids tends to agree with the octanol-water partition coefficients for these substances (25).
In conclusion, the supplemental vitamin E and vitamin A most likely prevented any substantial changes in plasma concentrations related to the added olestra. However, serum concentrations of all 3 carotenoids decreased substantially in subjects eating the diet containing olestra. In our study, subjects in the olestra group consumed 20 to 45 g/d olestra, depending on total energy intake. This is high in comparison to the estimated 90th percentile of ingestion of olestra in snack foods (25). For retinol and -tocopherol, it is clear that even at the levels we used, supplementation was more than adequate to prevent any substantial changes. This cannot be said for the carotenoids.
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FOOTNOTES |
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3 Current address: Louisiana State University AgCenter, Baton Rouge, LA 70803.
4 Current address: Louisiana State Crime Laboratory, Baton Rouge, LA 70806.
5 Current address: Bastyr University, Kenmore, WA 98028-4966.
6 Current address: Louisiana State University Health Science Center, New Orleans, LA 70112.
7 The composition of these tablets is as follows: vitamin A as retinyl acetate (3.14 µmol) and ß-carotene (2.24 µmol); vitamin C, 0.34 mmol; vitamin D, 0.02 µmol as ergocalciferol; vitamin E, 63.5 µmol as all racemic -tocopheryl acetate; vitamin K, 0.06 µmol as phytonadione; thiamine, 4.58 µmol; riboflavin, 4.5 µmol; niacin, 0.16 mmol; vitamin B6, 9.7 µmol as pyridoxine hydrochloride; folic acid, 0.91 µmol; vitamin B12, 4.43 µmol as cyanocobalamin; biotin, 0.12 µmol; pantothenic acid, 0.05 mmol; calcium, 0.25 mmol; iron, 0.32 mmol; phosphorus, 3.52 mmol; iodine, 1.18 µmol; magnesium, 4.11 mmol; zinc, 0.23 mmol; selenium, 0.25 µmol; copper, 0.03 mmol; manganese, 0.04 mmol; chromium, 2.31 µmol; molybdenum, 0.78 µmol; chloride, 2.03 mmol; potassium, 2.05 mmol; boron, 13.87 µmol; nickel, 0.08 µmol; silicon, 0.07 µmol; tin, 0.08 µmol; vanadium, 0.20 µmol; lutein, 0.44 µmol. These values represent 100% of the Dietary Reference Intakes except for vitamin K (31%), biotin (10%), calcium (16%), phosphorus (11%), magnesium (25%), selenium (29%), and potassium chloride (2%). No RDA has been established for boron, nickel, silicon, tin, vanadium or lutein.
Manuscript received 13 January 2005. Initial review completed 14 February 2005. Revision accepted 8 March 2005.
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LITERATURE CITED |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Peters, J. C., Lawson, K. D., Middleton, S. J. & Triebwasser, K. C. (1997) Assessment of the nutritional effects of olestra, a nonabsorbed fat replacement: Introduction and overview. J. Nutr. 127:1539S-1546S.
2. Mattson, F. H., Hollenbach, E. J. & Kuehlthau, C. M. (1979) The effect of a non-absorbable fat, sucrose polyester, on the metabolism of vitamin A by the rat. J. Nutr. 109:1688-1693.
3. Jandacek, R. J., Mattson, F. H., McNeely, S., Gallon, L., Yunker, R. & Glueck, C. J. (1980) Effect of sucrose polyester on fecal steroid excretion by 24 normal men. Am. J. Clin. Nutr. 33:251-259.
4. Jandacek, R. J., Ramirez, M. M. & Crouse, J. R., 3rd (1990) Effects of partial replacement of dietary fat by olestra on dietary cholesterol absorption in man. Metabolism 39:848-852.[Medline]
5. Crouse, J. R. & Grundy, S. M. (1979) Effects of sucrose polyester on cholesterol metabolism in man. Metabolism 28:994-1000.[Medline]
6. Fallat, R. W., Glueck, C. J., Lutmer, R. & Mattson, F. H. (1976) Short-term study of sucrose polyester, a nonabsorbable fat-like material, as a dietary agent for lowering plasma cholesterol. Am. J. Clin. Nutr. 29:1204-1215.
7. Mellies, M. J., Jandacek, R. J., Taulbee, J. D., Tewksbury, M. B., Lamkin, G., Baehler, L., King, P., Boggs, D. & Goldman, S., et al (1983) A double-blind, placebo-controlled study of sucrose polyester in hypercholesterolemic outpatients. Am. J. Clin. Nutr. 37:339-346.
8. Mellies, M. J., Vitale, C., Jandacek, R. J., Lamkin, G. E. & Glueck, C. J. (1985) The substitution of sucrose polyester for dietary fat in obese, hypercholesterolemic outpatients. Am. J. Clin. Nutr. 41:1-12.
9. Grundy, S. M., Anastasia, J. V., Kesaniemi, Y. A. & Abrams, J. (1986) Influence of sucrose polyester on plasma lipoproteins, and cholesterol metabolism in obese patients with and without diabetes mellitus. Am. J. Clin. Nutr. 44:620-629.
10. Daher, G. C., Cooper, D. A., Zorich, N. L., King, D., Riccardi, K. A. & Peters, J. C. (1997) Olestra ingestion and retinyl palmitate absorption in humans. J. Nutr. 127:1686S-1693S.
11. Daher, G. C., Cooper, D. A. & Peters, J. C. (1997) Physical or temporal separation of olestra and vitamins A, E, and D intake decreases the effect of olestra on the status of the vitamins in the pig. J. Nutr. 127:1566S-1572S.
12. Cooper, D. A., Berry, D. A., Spendel, V. A. & Kiorpes, A. L. (1997) The domestic pig as a model for evaluating olestra’s nutritional effects. J. Nutr. 127:1555S-1565S.
13. Cooper, D. A., Berry, D. A., Spendel, V. A., Jones, M. B., Kiorpes, A. L. & Peters, J. C. (1997) Nutritional status of pigs fed olestra with and without increased dietary levels of vitamins A and E in long-term studies. J. Nutr. 127:1609S-1635S.
14. Cooper, D. A., Berry, D. A., Spendel, V. A., King, D., Kiorpes, A. L. & Peters, J. C. (1997) Olestra dose response on fat-soluble and water-soluble nutrients in the pig. J. Nutr. 127:1573S-1588S.
15. Schlagheck, T. G., Riccardi, K. A., Zorich, N. L., Torri, S. A., Dugan, L. D. & Peters, J. C. (1997) Olestra dose response on fat-soluble and water-soluble nutrients in humans. J. Nutr. 127:1646S-1665S.
16. Westrate, J. A. & van het Hof, K. H. (1995) Sucrose polyester and plasma carotenoid concentrations in healthy subjects. Am. J. Clin. Nutr. 62:591-597.
17. Koonsvitsky, B. P., Berry, D. A., Jones, M. B., Lin, P.Y.T., Cooper, D. A., Jones, D. Y. & Jackson, J. E. (1997) Olestra affects serum concentrations of -tocopherol and carotenoids but not vitamin D or vitamin K status in free-living subjects. J. Nutr. 127:1636S-1645S.
18. Cooper, D. A., Berry, D. A., Jones, M. B., Kiorpes, A. L. & Peters, J. C. (1997) Olestra’s effect on the status of vitamins A, D, and E in the pig can be offset by increasing dietary levels of these vitamins. J. Nutr. 127:1589S-1608S.
19. Bray, G. A., Lovejoy, J. C., Most-Windhauser, M., Smith, S. R., Volaufova, J., Denkins, Y., De Jonge, L., Rood, J. & Levfevre, M., et al (2002) A 9-mo randomized clinical trial comparing fat-substituted and fat-reduced diets in healthy obese men: The Ole study. Am. J. Clin. Nutr. 76:928-934.
20. Aebischer, C. P., Schierle, J. & Schuep, W. (1999) Simultaneous determination of retinol, tocopherols, carotene, lycopene, and xanthophylls in plasma by means of reversed-phase high-performance liquid chromatography. Methods Enzymol. 299:348-362.[Medline]
21. Lovejoy, J. C., Bray, G. A., Lefevre, M., Smith, S. R., Most, M. M., Denkins, V. M., Volaufova, J., Rood, J. C., Eldridge, A. L. & Peters, J. C. (2003) Consumption of a controlled low-fat diet containing olestra for 9 months improves health risk factors in conjunction with weight loss in obese men: the Ole Study. Int. J. Obes. Relat. Metab. Disord. 27:1242-1249.[Medline]
22. Schlagheck, T. G., Kesler, J. M., Jones, M. B., Zorich, N. L., Dugan, L. D., Davidson, M. H. & Peters, J. C. (1997) Olestra’s effect on vitamins D and E in humans can be offset by increasing dietary levels of these vitamins. J. Nutr. 127:1666S-1685S.
23. Broekmans, W. M., Klopping-Ketelaars, I. A., Westrate, J. A., Tijburg, L. B., Van Poppel, G., Vink, A. A., Berendschot, T. T., Bots, M. L., Castenmiller, W. A. & Kardinaal, A. F. (2003) Decreased carotenoid concentrations due to dietary sucrose polyesters do not affect possible markers of disease risk in humans. J. Nutr. 133:720-726.
24. Rock, C. L., Thornquist, M. D., Kristal, A. R., Patterson, R. E., Cooper, D. A., Neuhouser, M. L., Neumark-Sztainer, D. & Cheskin, L. J. (1999) Demographic, dietary and lifestyle factors differentially explain variability in serum carotenoids and fat-soluble vitamins: Baseline results from the sentinel site of the olestra post-marketing surveillance study. J. Nutr. 129:855-864.
25. Cooper, D. A., Webb, R. & Peters, J. (1997) Evaluation of the potential for olestra to affect the availability of dietary phytochemicals. J. Nutr. 127:1699S-1709S.
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