![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Chicago Center for Clinical Research, Chicago, IL and * Altus Food Company, Chicago, IL
2To whom correspondence should be addressed. E-mail: kmaki{at}protocare.com
 |
ABSTRACT |
|---|
 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
3.0 g total fat and 1.0 g saturated fat (TOP/ß-glucan treatment) or similar control foods. The serum LDL cholesterol response from baseline to the end of study was significantly larger in the TOP/ß-glucan treated group than in the control group, in which there was no change (-3.7 vs. 0.4%; P = 0.013). Likewise, total cholesterol decreased in the TOP/ß-glucan treatment group and did not change significantly in the controls (-2.3 vs. 0.8%; P = 0.043). Serum HDL cholesterol and triglyceride responses did not differ between the groups. The results of this trial suggest that consumption of a group of low fat, TOP and ß-glucan– containing foods is a useful adjunct in the dietary management of hypercholesterolemia.
KEY WORDS: • hypercholesterolemia • lipids • tall oil • phytosterols • ß-glucan
Coronary heart disease (CHD)3 is the leading cause of death in the United States (1 ). Compelling evidence indicates that the risk of CHD can be decreased by reducing total and LDL cholesterol concentrations (2 –5 ). The National Cholesterol Education Program (NCEP) Step I dietary recommendations, and now the Therapeutic Lifestyle Changes (TLC) diet, emphasize limiting saturated fatty acid and cholesterol intakes. In practice, institution of the NCEP Step I diet has produced reductions in LDL cholesterol of 3 to 10% (6 –11 ). Because this is frequently not large enough to achieve target LDL cholesterol levels, an adjunct to diet therapy is often needed. For this reason, the Adult Treatment Panel III of the NCEP recommends phytosterols (plant sterols) and soluble fiber as adjunctive lipid-lowering therapies (4 ).
Plant sterols are structurally similar to cholesterol and compete with cholesterol for incorporation into micelles in the intestine. Usual levels of phytosterol consumption do not significantly affect cholesterol absorption. When consumed at higher levels, however, these compounds inhibit absorption of exogenous and endogenous cholesterol in the gastrointestinal tract (12 ,13 ). Tall oil– based phytosterols (TOP) are extracted from tall oil, which is a fat-soluble by-product obtained from trees during the pulping process (14 ). Regular consumption of TOP has been shown to significantly lower total and LDL cholesterol concentrations (14 –21 ).
Consumption of ß-glucan has also been shown to reduce total and LDL cholesterol levels (22 –26 ). ß-Glucan is the predominant soluble fiber in oat products. The mechanism by which ß-glucan lowers cholesterol levels may be related to its viscosity, bile salt binding capacity or fermentability (23 ,27 ). A meta-analysis of 19 clinical trials indicates that daily consumption of 3 g ß-glucan can reduce total cholesterol levels by 0.13 to 0.15 mmol/L (25 ).
The present study was conducted to evaluate the effects of a group of low fat food products containing free TOP and oat ß-glucan (from whole oats and bran concentrate) on serum lipid levels in adults with mild-to-moderate hypercholesterolemia.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
Subjects.
Potential participants (21 to 75 y of age) were recruited from the Chicago metropolitan area and prescreened by telephone. Eligibility was further assessed at screening and baseline visits (wk –6, –5, –1 and 0). Subjects had to have LDL cholesterol between 3.36 and 5.17 mmol/L, triglycerides 9.05 mmol/L and a body mass index (BMI) 38.0 kg/m2 at the wk –1 visit. Participants also had to be in apparent good health, as indicated by a physical examination, an electrocardiogram and serum chemistry, hematology and urinalysis panels. Women of childbearing potential were required to have a negative urine pregnancy test and to use an approved method of contraception throughout the study.
Subjects were excluded if they had Type I, III, IV or V secondary hyperlipoproteinemia. Use of hypolipidemic medication (including niacin or its analogs at doses of > 400 mg/d) within 4 wk of the wk –6 visit was also exclusionary, as was the use of hypolipidemic supplements [including plant sterol, (n-3) fatty acids and dietary fiber supplements] within 1 wk of the wk –6 visit. Other exclusionary medications included drugs for regulating hemostasis (except for a stable dose of aspirin), hypoglycemic medications, systemic corticosteroids, androgens, phenytoin, erythromycin and thyroid hormone (except stable-dose replacement therapy for 
2 mo before enrollment).
Poorly controlled hypertension (systolic blood pressure 160 mm Hg and/or diastolic blood pressure 100 mm Hg) was an exclusion criterion for this study, although subjects with adequately controlled hypertension were allowed to participate provided that their dose of antihypertensive therapy had remained constant for 2 mo before the wk –6 visit. The following were also exclusionary: diabetes mellitus or a fasting glucose 1.26 g/L at the wk –5 visit; history of cancer within the previous 5 y (with the exception of nonmelanoma skin cancer or basal cell carcinoma); current or recent history (within 6 mo) of significant atherosclerotic, hepatic, gastrointestinal, pulmonary, endocrine or renal disease; and a recent history (within the past 12 mo) or a strong potential for substance abuse.
Clinic visits.
Subjects visited the clinic at wk –6, –5 and –1 (screening), at wk 0 (baseline) and at wk 2, 5 and 6 (treatment) for assessments of vital signs, height (wk –6 only) and weight, and a fasting serum lipid profile [total, LDL and HDL cholesterol, and triglycerides]. Serum chemistry, hematology and urinalysis panels were completed at wk –5, and a urine pregnancy test (for women of childbearing potential) was performed at baseline (wk 0). An electrocardiogram and a physical examination were performed at wk –1. At wk –6, subjects were instructed to continue their usual diets. At wk –5, they were instructed on the NCEP Step I diet. Compliance with this diet was reinforced at each subsequent visit. The Eating Pattern Assessment Tool (EPAT) (28 ) was completed at wk –6, 0 and 6, to aid in the assessment of dietary fat and saturated fat intakes during dietary counseling. Three-day diet records were dispensed at wk –6, –1 and 5, and collected and analyzed at wk –5, 0 and 6, respectively. Diet records were analyzed using the University of Minnesota Nutrition Data System for Research (NDS-R), version 4.02_30 software (1999).
Subjects were randomized at baseline (wk 0) to one of two double-blind treatments: food products that provided 1.8 g TOP and 2.8 g ß-glucan per day and contained 3.0 g total fat and 1.0 g saturated fat (TOP/ß-glucan treatment) or similar food products that provided < 1.0 g ß-glucan and no TOP (control). Assessments of concomitant medication use and adverse events were performed at each treatment visit (wk 2, 5 and 6).
Study products.
Table 1 presents the nutritional composition of the TOP/ß-glucan and control food products. Food products for each treatment included a cereal, a snack bar and a beverage. Subjects were instructed to consume one of each of these products daily, for a total of three doses of study product per day.
|
The free TOP used in the TOP/ß-glucan food products was supplied by ReducolTM (Novartis Consumer Health SA, Nyon, Switzerland, produced by Forbes Meditech, Vancouver, Canada). Reducol has a composition of 44% sitosterol, 25% sitostanol, 12% campesterol and 6% campestanol. The phytosterol content of each food product was assessed by a method that uses gas chromatography (30
). The sterols were extracted from the food samples with toluene. The toluene was then evaporated and the sterols were silylated with N,O-bis(trimethylsilyl) trifluoroacetamide in pyridine. The silylated sterols were assessed by gas chromatography using 5-
-cholestane as an internal standard.
Laboratory measurements.
Medical Research Laboratories (Highland Heights, KY) performed laboratory measurements including urinalyses and serum chemistry, hematology and lipid profiles. This laboratory participates in the Centers for Disease Control and Prevention lipid standardization program (31 ). Serum chemistry analysis was conducted on the Hitachi 747 (Roche Diagnostics, Indianapolis, IN) and serum hematology testing utilized the Coulter STKS (Coulter Corporation, Miami, FL). Urinalyses were completed using the Clinitek Atlas (Bayer Diagnostics, Tarrytown, NY).
Cholesterol and triglycerides were measured enzymatically (using reagents that contained cholesterol oxidase, esterase and peroxidase for cholesterol, and lipase, L--glycerophosphate oxidase, peroxidase and glycerokinase for triglycerides) using the Hitachi 747 (Roche Diagnostics). Heparin and manganese chloride were used to isolate HDL cholesterol. LDL cholesterol was calculated using the Friedewald equation (LDL cholesterol = total cholesterol – HDL cholesterol – triglycerides/5) (32
). Because this equation is not valid when the triglyceride concentration is above 10.34 mmol/L, LDL cholesterol was not calculated under these circumstances.
Statistical analyses.
Statistical analyses were conducted using the SAS version 8.0 statistical analysis package (SAS Institute, Cary, NC). Analyses are presented for an intent-to-treat sample. This sample includes all subjects who completed at least one postrandomization assessment of lipids after receiving at least one dose of study product. The last observations were carried forward to impute missing values.
Baseline comparability of treatments for age, height, weight, vital signs measurements and lipid values was assessed by ANOVA. Comparability between treatment groups for gender and race was evaluated by the chi-square test. ANOVA models including treatment as the independent variable were generated to compare responses between groups for the following variables: LDL, total and HDL cholesterol; triglycerides; and the ratio of LDL cholesterol to HDL cholesterol. For these analyses, screening, baseline, and end-of-study values were defined as means of values collected at wk –6 and –5; wk –1 and 0; and wk 5 and 6, respectively. Within-treatment group comparisons were assessed by the single-sample t test.
Differences between treatments in dietary intake were also assessed by ANOVA. Possible differences in the incidence of adverse events were measured with Fisher’s exact (two-tail) test. All tests for significance were performed at = 0.05, two-tailed.
|
RESULTS |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
Two-hundred and sixty-eight people were screened to identify the 112 subjects randomized. Seven (6.3%) of the randomized subjects dropped out of the study before completing the intervention period. Reasons reported for discontinuation of subjects in the TOP/ß-glucan treatment included noncompliance with the protocol (n = 1) and withdrawal of consent (n = 1). Subjects who dropped out of the control did so because of noncompliance with the protocol (n = 1), withdrawal of consent (n = 2) and adverse events [rash on arm and groin, abdominal pain in lower left quadrant (n = 1); angioedema and mouth swelling (n = 1)] judged by the Investigator to be possibly or probably related to the study control products.
Table 2
shows the demographic and baseline characteristics of subjects. Subjects in the TOP/ß-glucan treatment group were significantly older than those assigned to the control group (59.3 ± 1.4 vs. 55.2 ± 1.1 y, respectively; P = 0.028). There were no significant differences between treatments in sex, race, height, weight, BMI or blood pressure. The approximate mean height and weight of subjects were 169 cm and 80 kg, respectively. Subjects had a mean BMI of 
28 kg/m2. Of the subjects in the TOP/ß-glucan treatment group, 51% were female as were 62% in the control group. The majority of subjects (75%) were non-Hispanic White.
|
Dietary analyses.
Results of 3-d diet record analyses at screening, baseline and the end-of-study are presented in Table 3 . Reported intakes of energy, carbohydrate, fat, saturated fatty acids, polyunsaturated fatty acids (PUFA), monounsaturated fatty acids, dietary fiber and cholesterol were not significantly different between treatments at screening or baseline. The percentage of energy (% energy) from protein at screening was slightly higher in the TOP/ß-glucan group than in controls (17.9 ± 0.5 vs. 16.4 ± 0.6%; P = 0.026).
|
Compared to controls, dietary fiber intake in the TOP/ß-glucan treatment group was greater at the end of the treatment period (16.8 ± 1.0 vs. 21.6 ± 1.1 g/d; P = 0.003). Likewise, reported consumption of soluble fiber was greater in the TOP/ß-glucan treatment group (7.4 ± 0.4 g/d) than in the control (5.1 ± 0.3 g/d; P < 0.0001). Differences in intakes of total and soluble dietary fiber matched very closely with those expected based on the composition of the study products.
Lipids.
Table 4
details the lipid concentrations at screening, baseline and the end-of-study, and the percentage changes from screening to baseline and from baseline to the end-of-study. There were no significant differences between treatments at screening for total, LDL or HDL cholesterol concentrations, the LDL/HDL cholesterol ratio, or triglyceride levels. Subjects in both groups entered the study with a mean LDL cholesterol level of 4.14 mmol/L. After diet counseling, the LDL cholesterol concentration changed significantly in the TOP/ß-glucan group (-3.7 ± 1.0%, P = 0.0004), but not in the control group (-0.3 ± 1.5%). A further reduction of 3.7 ± 1.2% (P = 0.002) compared to baseline occurred in the TOP/ß-glucan group during treatment, whereas LDL cholesterol levels were unchanged in control subjects (0.4 ± 1.5%). The difference in response between groups tended to be significant for the screening to baseline period (P = 0.077) and was significant for the baseline to end-of-study period (P = 0.013).
|
No significant changes occurred in HDL cholesterol or triglyceride concentrations during the trial in the TOP/ß-glucan treatment group. Significant within-group changes from baseline in HDL cholesterol (-3.9 ± 1.1%, P = 0.0006) and triglyceride levels (median change = 7.9%, P = 0.002) occurred in the control group. The LDL/HDL cholesterol ratio responses differed (P = 0.003) between groups: -1.8 ± 1.3 (NS) vs. 4.8 ± 1.7% (P = 0.007) in the TOP/ß-glucan and control groups, respectively.
Adverse events.
With the exception of an increased incidence of rhinitis in the TOP/ß-glucan treatment group (17.5 vs. 7.3% for control; P = 0.026), there were no other statistically or clinically important differences between treatments in the incidence of adverse events overall or for any body system. All reported cases of rhinitis in the TOP/ß-glucan group were considered mild in severity and judged by the Investigator to be unrelated to the study product.
|
DISCUSSION |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
This trial was not designed to evaluate the separate contributions of the active ingredients in the study products (TOP and ß-glucan). Rather, the study aim was to assess the efficacy of a group of commercially available functional food products that would reduce LDL cholesterol when incorporated into a therapeutic diet.
There is substantial evidence to suggest that sterol/stanol and ß-glucan–containing foods effectively reduce elevated levels of LDL cholesterol (14 –26 ). In previous studies, daily consumption of 2 to 3 g/d plant sterols or stanols was shown to lower total and LDL cholesterol levels by 5 to 15% (15 ,18 –20 ). Results from studies using ß-glucan from oats suggest that consumption of 2 to 3 g/d will lower the LDL cholesterol concentration by 4 to 5% (33 ). Differences between the active and control study products in TOP and ß-glucan for the present study were 1.8 and 2.0 g/d, respectively. Therefore, the observed LDL cholesterol response was at the low end of the expected range, given results from previous trials.
Roughly one-half of adults in the United States have elevated cholesterol levels (34 ). Each 5% reduction in LDL cholesterol in the population would decrease the number of people who qualify for drug therapy by 5 to 7 million (34 ,35 ). Therefore, dietary interventions that produce modest but sustained reductions in LDL cholesterol have the potential to have an important public health impact. The NCEP ATP III guidelines encourage the use of phytosterols and soluble fiber as therapeutic options to enhance LDL cholesterol lowering (4 ). In the current study, the addition of the TOP/ß-glucan– containing foods had an additional effect on LDL cholesterol that was equivalent to the influence of the initial diet counseling.
Very little LDL cholesterol reduction occurred in the control group after initiation of the NCEP Step I diet (change = -0.3%). Subjects in the active treatment group showed a more typical response (-3.7%). Because this was a double-blind, placebo-controlled trial, it is likely that this difference represents a chance occurrence. Notably, the diet record analyses suggest that in both the control and TOP/ß-glucan groups, intakes of fat, saturated fat and cholesterol during the treatment period were significantly reduced beyond the levels consumed after counseling on the NCEP Step I diet. The control group experienced a small increase in triglycerides (median change = 7.9%, P = 0.002) and a small decline in the HDL cholesterol concentration (change = -3.9%, P = 0.0006). This is most likely due to greater carbohydrate and lower fat intakes as a result of consuming the low fat, high carbohydrate study foods, which apparently displaced other higher fat items from the diet. Increased triglycerides and reduced HDL cholesterol are well-documented effects of replacing dietary fat with carbohydrate (36 ). As a result of the decline in HDL cholesterol concentration, the LDL/HDL cholesterol ratio rose significantly among control subjects during the treatment period (4.8%, P = 0.007). Despite consumption of foods with similar macronutrient composition, the TOP/ß-glucan treatment group did not show significant adverse changes in triglycerides, HDL cholesterol or the LDL/HDL cholesterol ratio.
As the food industry develops products intended for use as adjunctive cholesterol-lowering therapies, it is important that they keep the needs of consumers in focus. People are unlikely to consider a product for long-term use unless it tastes good and is practical to consume. The group of TOP/ß-glucan– containing foods used in the present study included a cereal, a snack bar and a beverage. Mean compliance with consumption of these products was > 95%, suggesting that the taste of these products was acceptable and that they were easily incorporated into a low fat diet. Therefore, these foods can be recommended with the expectation that people will consider them for long-term use.
In conclusion, the results of the present study provide evidence that consumption of a group of low fat, TOP and ß-glucan–containing foods is a useful adjunct in the dietary management of hypercholesterolemia.
|
FOOTNOTES |
|---|
3 Abbreviations used: ATP, Adult Treatment Panel; BMI, body mass index; CHD, coronary heart disease; EPAT, Eating Pattern Assessment Tool; NCEP, National Cholesterol Education Program; NDS-R, Nutrition Data System for Research; TOP, tall oil– based phytosterols.
Manuscript received 10 July 2002. Initial review completed 26 July 2002. Revision accepted 25 November 2002.
|
LITERATURE CITED |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
1. National Heart, Lung, and Blood Institute (NHLBI) (2000) Morbidity and Mortality: 2000 Chart Book on Cardiovascular, Lung, and Blood Diseases 2000 U.S. Department of Health and Human Services, National Institutes of Health Rockville, MD.
2. Downs, J. R., Clearfield, M., Weis, S., Whitney, E., Shapiro, D. R., Beere, P. A., Langendorfer, A., Stein, E. A., Kruyer, W. & Gotto, A. M., Jr (1998) Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. J. Am. Med. Assoc. 279:1615-1622.
3. Krauss, R. M., Eckel, R. H., Howard, B., Appel, L. J., Daniels, S. R., Deckelbaum, R. J., Erdman, J. W., Jr., Kris-Etherton, R., Goldberg, I. J., Kotchen, T. A., Lichtenstein, A. H., Mitch, W. E., Mullis, R., Robinson, K., Wylie-Rosett, J., Sachiki, S., Suttie, J., Tribble, D. L. & Bazzarre, T. L. (2000) AHA Dietary Guidelines. Revision 2000: a statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation 102:2284-2299.
4. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (2001) Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). J. Am. Med. Assoc. 102:2284-2299.
5. Scandinavian Simvastatin Survival Study Group (1994) Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: The Scandinavian Simvastatin Survival Study (4S). Lancet 344:1383-1389.[Medline]
6. Davidson, M. H., Kong, J. C., Drennan, K. B., Story, K. & Anderson, G. H. (1996) Efficacy of the National Cholesterol Education Program Step I Diet: a randomized trial incorporating quick-service foods. Arch. Intern. Med. 156:305-312.
7. Bae, C.-Y., Keenan, J. M. & Wenz, J. (1991) A clinical trial of the American Heart Association step one diet for treatment of hypercholesterolemia. J. Fam. Pract. 33:249-254.[Medline]
8. Geil, P. B., Anderson, J. W. & Gustafson, N. J. (1995) Women and men with hypercholesterolemia respond similarly to an American Heart Association step 1 diet. J. Am. Diet. Assoc. 95:436-441.[Medline]
9. Kris-Etherton, P. M. (1999) A new role for diet in reducing the incidence of cardiovascular disease: evidence from recent studies. Curr. Atheroscler. Rep. 1:185-187.[Medline]
10. Ginsberg, H. N., Kris-Etherton, P. & Dennis, B. (1998) Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects: The Delta Study, protocol 1. Arterioscler. Thromb. Vasc. Biol. 18:441-449.
11. Walden, C. E., Retzlaff, B. M. & Buck, B. L. (1997) Lipoprotein lipid response to the National Cholesterol Education Program Step II Diet by hypercholesterolemic and combined hyperlipidemic women and men. Arterioscler. Thromb. Vasc. Biol. 17:375-382.
12. Ling, W. H. & Jones, P.J.H. (1995) Minireview of dietary phytosterols: a review of metabolism, benefits, and side effects. Life Sci 57:195-206.[Medline]
13. Ikeda, I. & Sugano, M. (1983) Some aspects of mechanisms of inhibition of cholesterol absorption by ß-sitosterol. Biochim. Biophys. Acta 732:651-658.[Medline]
14. Jones, P.J.H, Ntanois, F. Y., Raeini-Sarjaz, M. & Catherine, V. A. (1999) Cholesterol-lowering efficacy of a sitostanol-containing phytosterol mixture with a prudent diet in hyperlipidemic men. Am. J. Clin. Nutr. 69:1144-1150.
15. Weststrate, J. A. & Meijer, G. W. (1998) Plant sterol-enriched margarines and reduction of plasma total- and LDL-cholesterol concentrations in normocholesterolaemic and mildly hypercholesterolaemic subjects. Eur. J. Clin. Nutr. 52:334-343.[Medline]
16. Moghadasian, M. H. & Frohlich, J. J. (1999) Effects of dietary phytosterols on cholesterol metabolism and atherosclerosis: clinical and experimental evidence. Am. J. Med. 107:588-594.[Medline]
17. Jones, P.J.H., Howell, T., MacDougall, D. E., Feng, J. Y. & Parsons, W. (1998) Short-term administration of tall oil phytosterols improves plasma lipid profiles in subjects with different cholesterol levels. Metabolism 47:751-756.[Medline]
18. Hendricks, H.F.J, Westrate, J. A., van Vliet, T. & Meijer, G. W. (1999) Spreads enriched with three different levels of vegetable oil sterols and the degree of cholesterol lowering in normocholesterolaemic and mildly hypercholesterolaemic subjects. Eur. J. Clin. Nutr. 53:319-327.[Medline]
19. Hallikainen, M. A., Sarkkinen, E. S., Gylling, H., Erkkila, A. T. & Uusitupa, M.I.J. (2000) Comparison of the effects of plant sterol ester and plant stanol ester-enriched margarines in lowering serum cholesterol concentrations in hypercholesterolaemic subjects on a low-fat diet. Eur. J. Clin. Nutr. 54:715-725.[Medline]
20. Maki, K. C., Davidson, M. H., Umporowicz, D. M., Schaefer, E. J., Dicklin, M. R., Ingram, K. A., Chen, S., McNamara, J. R., Gebhart, B. W., Ribaya-Mercado, J. D., Perrone, G., Robins, S. J. & Franke, W. C. (2001) Lipid responses to plant sterol-enriched reduced-fat spreads incorporated into a NCEP Step 1 diet. Am. J. Clin. Nutr. 74:33-43.
21. Davidson, M. H., Maki, K. C., Umporowicz, D. M., Ingram, K. M., Dicklin, M. R., Schaefer, E., Lane, R. W., McNamara, J. R., Ribaya-Mercado, J. D., Perrone, G., Robins, S. J. & Franke, W. C. (2001) Safety and tolerability of esterified phytosterols administered in reduced-fat spread and salad dressing to healthy adult men and women. J. Am. Coll. Nutr. 20:307-319.
22. Glore, S. R., Van Treeck, D., Knehans, A. W. & Guild, M. (1994) Soluble fiber and serum lipids: a literature review. J. Am. Diet. Assoc. 94:425-436.[Medline]
23. Davidson, M. H. & McDonald, A. (1998) Fiber: forms and functions. Nutr. Res. 18:617-624.
24. Davidson, M. H., Dugan, L. D., Burns, J. H., Bova, J., Story, K. & Drennan, K. B. (1991) The hypercholesterolemic effects of ß-glucan in oatmeal and oat bran. J. Am. Med. Assoc. 265:1833-1839.
25. Ripsin, C. M., Keenan, J. M., Jacobs, D. R., van Horn, L., Liu, K., Turnbull, W. H., Thye, F. W. & Kestin, M. (1992) Oat products and lipid-lowering. A meta-analysis. J. Am. Med. Assoc. 267:3317-3325.
26. Nicolosi, R., Bell, S. J. & Bistrian, B. R. (1999) Plasma lipid changes after supplementation with ß-glucan fiber from yeast. Am. J. Clin. Nutr. 70:208-212.
27. Marlett, J. A., Hosig, K. B., Vollendorf, N. W. & Shinnick, F. L. (1994) Mechanism of serum cholesterol reduction by oat bran. Hepatology 20:1450-1457.[Medline]
28. Peters, J. R., Quiter, E. S. & Brekke, M. L. (1994) The Eating Pattern Assessment Tool: A simple instrument for assessing dietary fat and cholesterol intake. J. Am. Diet. Assoc. 94:1008-1013.[Medline]
29. AOAC Method 995.16. (2000) Beta-D-Glucan in Barley and Oats, Streamlined Enzymatic Method.. Horwitz, W eds. Official Methods of Analysis of AOAC International. 17th edition. 2000 AOAC International Press Gaithersburg, MD .
30. Kasturi, P. (2001) Determination of Sterols and Stanols in Foods by Gas Chromatography. Internal Quaker methods paper 2001 Quaker Foods & Beverages Barrington, IL.
31. Myers, G., Cooper, G., Winn, C. & Smith, S. (1989) The Centers for Disease Control–National Heart, Lung, and Blood Institute Lipid Standardization Program. An approach to accurate and precise lipid measurements. Clin. Lab. Med. 9:105-135.[Medline]
32. Friedwald, W., Levy, R. & Frederickson, D. (1972) Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin. Chem. 18:499-502.[Abstract]
33. Food and Drug Administration (1997) Food labeling: health claims, oats, and coronary heart disease. Fed. Regist. 62:3584-3681.
34. Sempos, C. T., Cleeman, J. I., Carroll, M. D., Johnson, C. L., Bachorik, P. S., Gordon, D. J., Burt, V. L., Briefel, R. R., Brown, C. D. & Lippel, K. (1993) Prevalence of high blood cholesterol among US adults. An update based on guidelines from the second report of the National Cholesterol Education Program Adult Treatment Panel. J. Am. Med. Assoc. 269:3009-3014.
35. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (1993) Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). J. Am. Med. Assoc. 269:3015-3023.
36. Abassi, F., McLaughlin, T., Lamendola, C., Kim, H. S., Tanaka, A., Wang, T., Nakajima, K. & Reaven, G. M. (2000) High carbohydrate diets, triglycerides-rich lipoproteins, and coronary heart disease risk. Am. J. Cardiol. 85:45-48.[Medline]
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
) from screening to baseline and from baseline to end-of-study12