![[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 * SmithKline Beecham Consumer Healthcare, Parsippany, NJ
2To whom correspondence and reprint requests should be addressed.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
KEY WORDS: • cholesterol • hydroxypropylmethylcellulose • lipoproteins • dietary fibers • humans
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
and 1998
, Haskell et al. 1992
, Jenson et al. 1993
and 1997
). Consumption
in doses adequate to reduce serum cholesterol may be associated with
gastrointestinal (GI) side effects such as bloating, abdominal cramping
and flatulence. These disturbances are thought to result in part from
colonic fermentation, which produces gases and volatile short-chain
fatty acids. In contrast, HPMC is not metabolized by flora in the human
colon and thus might be better tolerated. In a dose titration experiment conducted with mildly hypercholesterolemic subjects, HPMC lowered total and LDL cholesterol (LDL-C) concentrations in a linear fashion. Each 10 g/d increase in HPMC consumption was associated with a decline in LDL-C of ~8%. Although some GI side effects were observed (gas and bloating), these were mild and occurred primarily with the highest dose (30 g/d). Minimal side effects were observed at a dose of 20 g/d, which was associated with a mean reduction of 16% [25 mg/dL (0.65 mmol/L)] in LDL-C.
Findings from another recent study (Maki et al. 1999
)
confirmed the hypocholesterolemic properties of HPMC. Three doses of a
high-molecular-weight HPMC (2.5, 5.0 and 7.5 g/d) were compared with a
cellulose placebo. Reductions in LDL-C of ~12% from baseline
were observed in the 5.0 and 7.5 g/d groups, and the incidences of side
effects in the active treatment arms did not differ from that of the
placebo group.
The mechanisms mediating the hypocholesterolemic effects of HPMC are
incompletely understood. In the intestine, HPMC may form viscous gels,
which interfere with contact between the intestinal wall and luminal
contents. Thus, like some soluble fibers, HPMC may reduce or delay
absorption of cholesterol, bile acids and carbohydrate (Carr et al. 1996
, Eastwood and Morris 1992
,
Turley et al. 1991
, Vahouny and Cassidy 1985
, Vahouny et al. 1980
, Story and Kritchevsky 1976
). Because the availability of these
substances in the intestine would be greatest after a meal, it is
possible that the hypocholesterolemic effect of HPMC might be
influenced by the timing of consumption in relation to food intake.
The purpose of this study was to evaluate the hypocholesterolemic effects of HPMC consumed in the fasting state vs. with meals or snacks. Furthermore, because the high doses of HPMC used in some previous trials (up to 30 g/d) may be unrealistic for long-term consumption, this study used a lower dose (5.0 g/d) of a very high viscosity variant of HPMC.
|
SUBJECTS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
This was a randomized, open-label, parallel group study in free-living hypercholesterolemic male volunteers (n = 51). One group was assigned to ingest 240 mL (8 oz) of orange drink (orange-flavored Tang, Kraft Foods, Northfield, IL) mixed with 2.5 g HPMC twice a day, with meals, for 2 wk. Subjects in the other group were given identical directions except that they were instructed to consume each dose of the HPMC drink at least 2 h after and not <1 h before a meal or snack.
The study consisted of two periods, i.e., a 14-d period for screening and baseline measurements, followed by a 14-d treatment phase during which the subjects consumed the study product.
Subject selection.
The protocol was approved by an Institutional Review Board (Schulman Associates, Cincinnati, OH). The conditions and procedures of the investigation were reviewed with each subject and an informed consent form was signed.
Potential study participants were screened within 3 wk of entering the study. Screening variables included medical history and physical examination, including a 12-lead electrocardiogram, blood pressure, vital signs, and height and weight measurements. Subjects eligible for participation were hypercholesterolemic males between 18 and 85 y of age, without clinical or laboratory findings suggesting the presence of an illness or condition that would confound the study’s results. Individuals were excluded if they were using any medications known to influence lipid metabolism, or dietary fiber supplements.
Serum lipid profiles [total cholesterol, LDL-C, HDL cholesterol (HDL-C) and triglycerides] were obtained from fasting subjects at two baseline visits. Averages from these two sets of lipid values were required to meet the following criteria: LDL-C, 3.36–4.91 mmol/L (130–190 mg/dL) and triglycerides < 3.95 mmol/L (350 mg/dL). If the difference between visit 1 and visit 2 LDL-C values was > 12%, using the larger of the two values as the denominator, the subject was disqualified from participation.
Dietary assessment.
The Eating Pattern Assessment Tool (EPAT; University of Minnesota,
Minneapolis, MN) was completed at randomization and at the
final visit by each subject to assess whether diets changed
significantly during the treatment phase of the study (Peters et al. 1994
). The EPAT is a food-frequency questionnaire
designed to indicate the number of times per week a subject consumes
foods high in fat, saturated fat and cholesterol. Section I of the EPAT
can be scored to determine a subject’s compliance with a low fat diet.
A section I EPAT score of 
28 indicates a consumption pattern
consistent with the National Cholesterol Education Program Step I
guidelines.
Randomization.
Seventy-eight (78) men were screened. Of these, 26 did not qualify for randomization. The reasons for subject ineligibility were as follows: LDL-C too low [<130 mg/dL (3.36 mmol/L)] (n = 5); LDL-C variability >12% (n = 5); LDL-C too high [>190 mg/dL (4.91 mmol/L)] (n = 3); elevated triglycerides (n = 2); anemia (n = 1); and subject chose not to participate (n = 10).
Clinic visits.
Vital signs, weight and blood were obtained from fasting subjects at each clinic visit. Study product was dispensed only at visit 3 (randomization), and compliance was assessed at visits 4 and 5 (wk 1 and 2 of treatment, respectively).
Adverse events were ascertained by the study coordinator via nonleading questions. Adverse events that occurred during the course of the study were documented on case report forms and were categorized on the basis of patient input as mild, moderate or severe.
Lipid measurements.
Blood samples for lipid measurements were obtained by venipuncture at
each clinic visit after a 10- to 12-h fast. Lipid analyses were
completed at a central laboratory (Quest Diagnostic Laboratories,
Woodale, IL). Serum lipid profiles were determined using reference
values standardized with those of the Centers for Disease Control and
Prevention (Myers et al. 1989
). Total cholesterol and
triglycerides were measured enzymatically (Artiss and Zak 1997
, Cole et al. 1997
). HDL-C was measured
following phosphotungstate precipitation of lower density lipoproteins
(Lopes-Virella et al. 1977
). The LDL-C level was
calculated using the following equation (DeLong et al. 1986
): LDL-C (mg/dL) = total cholesterol - HDL-C
- (triglycerides/6.25). This equation loses accuracy when the
serum triglyceride concentration exceeds 400 mg/dL; therefore,
LDL-C values were not calculated when triglycerides were above this
level.
Test product distribution.
Each subject was given a box containing the following: 30 packets of HPMC powder (the full 2-wk study supply, plus two extra days), two bottles of Tang powdered drink mix, one electric mixer, a dose instruction sheet and a daily diary. The diary was used to record timing of all doses of study product consumed and was reviewed by the coordinator at each treatment visit.
Test articles.
HPMC was prepared by Midland Dow Chemical of Midland, MI, and delivered to SmithKline Beecham Consumer Healthcare, Parsippany, NJ for packaging and labeling. The HPMC used in this study (United States Pharmacopeia Substitution Type 2208) was manufactured according to United States Pharmacopeia and Good Manufacturing Practices requirements by Dow Chemical. Its viscosity was determined by modification of the United States Pharmacopeia method for Procedure for Cellulose Derivatives under Viscosity method 911. The modification was to test viscosity of a 10 g/L solution rather than the standard 20 g/L solution, necessitated by the high viscosity of the material used. The viscosity of a 20 g/L solution was then calculated using the Phllipof equation: viscosity = (1 + k · c)8, where k is a constant for a given HPMC and c is the concentration expressed as a fraction. The calculated viscosity at 20 g/L for this batch of HPMC was 362.14 mPa · s.
Compliance.
Compliance was calculated from the number of unused servings supplemented with data from a diary kept by each subject during the treatment period. The study coordinator queried subjects regarding any discrepancies.
Statistical analysis.
One-way ANOVA was used to evaluate comparability of baseline
characteristics of the two treatment groups. Log-transformed values
were utilized for serum triglycerides because of the skewed
distribution of values. ANOVA with repeated measures was used to assess
possible group effects, time effects and group-time interaction for
lipid values, with the dependent variables in each of these models
being the percentage of change from baseline. Single-sample
t tests were used to determine whether the change from
baseline lipid concentration was significantly different from zero
after wk 1 and 2 of treatment within each group. The frequency of
adverse events between groups was compared using Fisher’s exact test.
McNemar’s test was employed to compare the frequency of adverse events
within groups during wk 1 vs. wk 2. Because compliance data showed a
non-Gaussian distribution, Mann-Whitney U and Wilcoxon’s
signed rank tests were used to test for possible differences between
and within groups, respectively. Due to the number of comparisons
completed, P-values > 0.01 but 0.05 were
considered to be of borderline significance; P-values
0.01 were considered significant.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Data from one subject who withdrew before the first on-treatment
blood draw were not included. The two groups did not differ in age,
height, weight and fasting serum lipids (Table 1
). Median compliance was 
93% at all time points (Table 2
). During wk 1, one subject consumed twice the prescribed dosage of
HPMC. Exclusion of this subject’s data had no material influence on
the study’s results.
|
|
No subjects dropped from the study due to HPMC-related side effects. A total of 45 adverse events, all nonserious, were reported during the treatment phase. These included 36 GI events, two dermatological, three musculoskeletal, four respiratory and one other.
The number of subjects reporting 1 adverse event of any type
during the study was 52 and 23% (P < 0.05) in the
With and Between Meals groups, respectively. Only the GI symptoms were
judged by the investigators to be possibly related to the study product
(see Table 3
). Of these, the number of persons reporting events in the Between Meals
group was 7 (27%) compared with 14 (56%) in the With Meals group
(P < 0.05). During wk 1, GI events were reported by 6
(23%) vs. 11 (44%) subjects in the Between and With Meals groups,
respectively (P < 0.12). During wk 2, the
corresponding frequencies were 4 (15%) vs. 10 (40%; P
< 0.07).
|
Eating Patterns Assessment Tool.
No differences were found between or within groups for either
subsection of the EPAT (see Table 4
).
|
Body weight declined slightly, and to a similar degree, in both groups during treatment. Mean change from baseline to week 2 was -0.36 ± 0.91 kg (P < 0.06) in the Between Meals group and -0.45 ± 1.06 kg (P < 0.05) in the With Meals group. No significant relationship was found between the changes in body weight and the absolute (r = 0.01) or percentage of change in LDL-C (r = 0.03). Similar results were obtained for total cholesterol, HDL-C and triglycerides (data not shown).
Serum lipids.
During treatment, significant changes from baseline occurred in
both groups for total cholesterol, LDL-C, HDL-C and triglycerides
(Table 5
). Total and LDL-C were reduced among all subjects. In both groups,
HDL-C declined significantly (P < 0.01) during wk
1, but the wk 2 concentrations were not significantly different from
baseline. Because LDL-C was depressed to a greater degree than
HDL-C, the LDL-C/HDL-C declined for both groups. In contrast to the
other serum lipids, triglycerides increased with treatment. The
increase was significant (P < 0.05) at wk 1 for the
Between Meals group, but not at wk 2. For the With Meals group, the
increase was significant at wk 2, but not at wk 1 (P < 0.05).
|
, LDL-C tended (P < 0.09) to increase during wk 2
in the Between Meals group, but not among the With Meals subjects
(P < 0.06 for the difference between groups in
response at wk 2).
|
Correlation analysis was completed to evaluate the associations between the percentage of change (at wk 2) in serum triglycerides, HDL-C and LDL-C. The LDL-C response was related to the change in HDL-C (r = 0.50, P < 0.001), but not to change in triglycerides (r = 0.19). In addition, the change in HDL-C was inversely associated with the change in triglycerides (r = -0.42, P < 0.003). Multivariate correlation showed that these relationships did not vary according to group assignment. In addition, both the changes in LDL-C (P < 0.001) and triglycerides (P < 0.003) were significant, independent predictors of the change in HDL-C (multiple r = 0.62).
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
In this study, LDL-C fell by 12–13% in both treatment groups during wk 1. During wk 2 of treatment, there was a trend for LDL-C to increase toward baseline among the Between Meals group but not among the With Meals subjects. This upward trend in the Between Meal group was due to a rebound in LDL-C concentrations to levels above baseline in five subjects. These nonresponders were not different from the remainder of the study sample with regard to self-reported dietary intake or HPMC consumption. In addition, body weight did not increase among these subjects; in fact, they tended to have larger reductions in body weight than other subjects. Although not conclusive, these results suggest that the hypocholesterolemic efficacy of HPMC may be greatest when it is consumed in association with a meal.
There are four main mechanisms by which soluble fiber is hypothesized to contribute to cholesterol lowering: 1) interfering with bile acid reabsorption, 2) interfering with cholesterol absorption/reabsorption, 3) delaying carbohydrate absorption, and 4) production of cholesterol-lowering fermentation by-products such as short-chain fatty acids.
Wolever and colleagues (1994)
concluded that
psyllium fiber must be consumed with food in order to have its maximum
cholesterol-lowering effect. They found that 7.6 g/d of psyllium
taken between meals did not influence blood lipid levels, whereas a
similar amount of psyllium consumed in a ready-to-eat cereal
lowered LDL-C by 11.3%. The authors suggested that slowing of
carbohydrate absorption, resulting in reduced insulinemia, may
contribute to the hypocholesterolemic influence of psyllium fiber.
The lack of effect on lipids when psyllium is taken between meals
is consistent with this hypothesis. Additional support comes from
studies that show that consuming several small meals lowers insulin and
LDL-C concentrations compared with consumption of the same foods
over three meals (Fabry and Tepperrman 1970
,
Jenkins et al. 1989
). In this study, HPMC was consumed
with a carbohydrate-containing beverage. Accordingly, the influence
of HPMC on the rate of carbohydrate absorption may not have been lost
completely and may explain the difference in results between our study
and that of Wolever et al. (1994)
.
When consumed in association with a meal, it would be expected that HPMC in the intestinal lumen would have greater exposure to cholesterol (endogenous and exogenous) and bile acids, therefore potentially allowing a greater opportunity for interference with absorption or reabsorption of these materials.
Because HPMC is resistant to colonic fermentation, the results of this
and previous studies demonstrating its cholesterol-lowering effects
(Dressman et al. 1993
, Maki et al. 1999
)
suggest that fermentability is not a necessary factor for a food gum to
show hypocholesterolemic properties. Additional investigation will be
required to determine the mechanisms responsible for the influence of
HPMC on serum lipids and whether it is modulated by the timing of HPMC
consumption relative to food intake.
In agreement with results from a study by Dressman et al. (1993)
, HDL-C was reduced slightly in both groups
(~2–5%). However, because LDL-C was lowered to a greater
degree, the LDL-C/HDL-C ratio declined significantly (~6–8%).
Serum triglycerides tended to increase during treatment, although
the response was quite variable. Nevertheless, the percentage of change
in triglycerides correlated significantly with the percentage of
change in HDL-C. Thus, the change in HDL-C may have been a
secondary event driven by an increase in circulating triglycerides
(Ginsberg 1990
). Although these changes may have been
related to HPMC consumption, consideration must also be given to the
possibility that the carbohydrate content of the delivery medium
(Tang) may have played a role. Numerous studies have demonstrated that
substitution of dietary carbohydrates for fat will increase serum
triglycerides and lower HDL-C. The carbohydrates (sugars) in
Tang provided ~5% of daily energy intake [assuming an average 10.46 MJ (2500 kcal) diet for the study participants] and thus may
have influenced triglyceride levels. The changes in LDL-C and
HDL-C were significantly correlated, and this relationship
maintained significance after adjustment for the change in serum
triglycerides. The latter finding is consistent with an effect of HPMC
consumption on HDL-C. However, in a previous trial, no differences
from baseline or cellulose placebo were observed for HDL-C with
consumption of 2.5, 5.0 or 7.5 g/d of HPMC (Maki et al. 1999
).
The lipid responses observed are unlikely to be explained by changes in body weight. Although a slight decline was observed in both groups, weight change did not correlate with the relative or absolute changes in any of the lipid variables measured.
Mild-to-moderate GI signs and symptoms (mainly gas, bloating and
changes in the consistency and frequency of bowel movements) were twice
as common in the With Meals group (24 vs. 12 events; events reported by
52 vs. 23% of subjects, P < 0.05). These side effects
may have occurred due to an increased volume of material in the GI
system. Because the subjects reported bloating/gas, but not flatulence
(flatulence was not reported in the With Meals group), side effects
might have resulted from the greater bulk passing through the colon,
due to the water-holding capacity of the HPMC. These sensations may
have been more pronounced when the HPMC was taken with a meal. The high
degree of tolerability associated with HPMC use is supported by results
from a double-blind, controlled trial among 160
hypercholesterolemic subjects (Maki et al. 1999
). During
a 6-wk treatment period, subjects consumed either a 5.0 g/d cellulose
placebo or 2.5–7.5 g/d of HPMC with meals. The incidence of GI side
effects did not differ between the placebo (cellulose) and treatment
groups. The literature does suggest that not all soluble fibers are
equivalent in terms of side effects (Schulte-Brockholt and Koch 1994
). Although direct comparison data from clinical trials are
not available, it is the authors’ impression that HPMC may be better
tolerated than more fermentable dietary fibers.
The findings of this investigation are consistent with a clinically meaningful hypocholesterolemic effect of HPMC at a dose of 2.5 g twice daily when taken with or between meals. Although timing of HPMC consumption in relation to meals did not appear to be critical for efficacy in most subjects, there was a tendency toward a more consistent response when HPMC was consumed with meals. GI side effects were generally mild and were more common in the With Meals group. In total, these results suggest that HPMC has potential clinical utility in the management of hypercholesterolemia.
|
FOOTNOTES |
|---|
3 Abbreviations used: EPAT, Eating Pattern Assessment Tool; GI, gastrointestinal; HDL-C, HDL cholesterol; HPMC, hydroxypropylmethylcellulose; LDL-C, LDL cholesterol.
Manuscript received November 1, 1999. Initial review completed January 4, 2000. Revision accepted March 6, 2000.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Artiss J. D., Zak B. Measurement of cholesterol concentration. Handbook of Lipoprotein Testing 1997 AACC Press Washington, DC.
2. Carr T. P., Gallaher D. D., Yang C., Hassel C. A. Increased intestinal contents viscosity reduces cholesterol absorption efficiency in hamsters fed hydroxypropylmethylcellulose. J. Nutr. 1996;126:1463-1469
3. Cole T. G., Klotzsch S. G., McNamara J. R. Measurement of triglyceride concentration. Handbook of Lipoprotein Testing 1997 AACC Press Washington, DC.
4. Davidson M. H., Dugan L. D., Burns J. H., Bova J., Story K., Drennan K. B. The hypocholesterolemic effects of beta-glucan in oatmeal and oat bran. A dose-controlled study. J. Am. Med. Assoc. 1991;265:1833-1839[Abstract]
5. Davidson M. H., Maki K. C., Kong J. C., Dugan L. D., Torri S. A., Hall H. A., Drennan K. B., Anderson S. M., Fulgoni V., Saldanha L. G., Olson B. H. Long-term effects of consuming foods containing psyllium seed husk on serum lipids in subjects with hypercholesterolemia. Am. J. Clin. Nutr. 1998;67:367-376[Abstract]
6. DeLong D. M., DeLong E. R., Wood P. D., Lippel K., Rifkind B. M. A comparison of methods for the estimation of plasma low- and very low density lipoprotein cholesterol. The Lipid Research Clinics Prevalence Study. J. Am. Med. Assoc. 1986;256:2372-2377[Abstract]
7. Dressman J .B., Adair C. H., Barnett J. L., Berardi R. R., Dunn-Kucharski V. A., Jarvenpaa K. M., Parr D. D., Sowle C. A., Swidan S. Z., Tobey S. W. High-molecular-weight hydroxypropylmethylcellulose: a cholesterol-lowering agent. Arch. Intern. Med. 1993;153:1345-1353[Abstract]
8.
Eastwood M. A., Morris E. R. Physical properties of dietary fiber that influence physiological function: a model for polymers along the gastrointestinal tract. Am. J. Clin Nutr. 1992;55:436-442
9.
Fabry P., Tepperrman J. Meal frequency—a possible factor in human pathology. Am. J. Clin. Nutr. 1970;23:1059-1068
10. Ginsberg H. N. Lipoprotein physiology and its relationship to atherogenesis. LaRosa J. C. eds. Endocrinology and Metabolism Clinics of North America: Lipid Disorders 1990;vol. 19:211-228 W. B. Saunders Company Philadelphia, PA.
11. Haskell W. L., Spiller G. A., Jensen C. D., Ellis B. K., Gates J. E. Role of water-soluble dietary fiber in the management of elevated plasma cholesterol in healthy subjects. Am. J. Cardiol. 1992;69:433-439[Medline]
12. Jenkins D.J.A., Wolever T.M.S., Vuksan V., Brighenti F., Cunnane S. C., Rao A. V., Jenkins A. L., Buckley G., Patten R., Singer W., Corey P., Josse R. G. Nibbling versus gorging: metabolic advantages of increased meal frequency. N. Engl. J. Med. 1989;321:929-934[Abstract]
13. Jensen C., Haskell W., Whittam J. Long-term effects of water-soluble dietary fiber in the management of hypercholesterolemia in healthy men and women. Am. J. Cardiol. 1997;79:34-37[Medline]
14. Jensen C. D., Spiller G. A., Gates J. E., Miller A. F., Whittam J. H. The effect of acacia gum and a water-soluble dietary fiber mixture on blood lipids in humans. J. Am. Coll. Nutr. 1993;12:147-154[Abstract]
15.
Lopes-Virella M. F., Stone P., Ellis S., Colwell J. A. Cholesterol determination in high-density lipoproteins separated by three different methods. Clin. Chem. 1977;23:882-884
16. Maki K. C., Davidson M. H., Malik K. C., Albrecht H. H., O’Mullane J., Daggy B. P Cholesterol lowering with hydroxypropylmethylcellulose. Am. J. Cardiol. 1999;84:1198-1203[Medline]
17. Myers G. L., Cooper G. R., Winn C. L., Smith S. J. 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. 1989;9:105-135[Medline]
18. Peters J. R., Quitter E. S., Brekke M. L., Admire J., Brekke M. J., Mullis R. M., Hunninghake D. B. The Eating Pattern Assessment Tool: a simple instrument for assessing dietary fat and cholesterol intake. J. Am. Diet. Assoc. 1994;94:1008-1013[Medline]
19. Schulte-Brockholt A., Koch T. Constipation. Bayless T. M. eds. Current Therapy in Gastroenterology and Liver Disease 4th ed. 1994:362-363
20. Story J. A., Kritchevesky D. Comparison of the binding of various bile acids and bile salts in vitro by several types of fiber. J. Nutr. 1976;106:1292-1294
21. Turley S. D., Daggy B. P., Dietschy J. M. Cholesterol-lowering action of psyllium mucilloid in the hamster: sites and possible mechanisms of action. Metabolism 1991;40:1063-1073[Medline]
22. Vahouny G. V., Cassidy M. M. Dietary fibers and absorption of nutrients. Proc. Soc. Exp. Biol. Med. 1985;180:432-446[Medline]
23. Vahouny G. V., Tombes R., Cassidy M. M., Kritchevsky D., Gallo L. L. Dietary fibers. V. Binding of bile salts, phospholipids and cholesterol from mixed micelles by bile acid sequestrants and dietary fibers. Lipids 1980;15:1012-1018[Medline]
24.
Wolever T.M.S., Jenkins D.J.A., Mueller S., Boctor D. L., Ransom T.P.P., Patten R., Chao E.S.M., McMillan K., Fulgoni V. Method of administration influences the serum cholesterol-lowering effect of psyllium. Am. J. Clin. Nutr. 1994;59:1055-1059
This article has been cited by other articles:
|
|
 |
|
  K. C. Maki, M. L. Carson, M. P. Miller, M. Turowski, M. Bell, D. M. Wilder, T. M. Rains, and M. S. Reeves Hydroxypropylmethylcellulose and Methylcellulose Consumption Reduce Postprandial Insulinemia in Overweight and Obese Men and Women J. Nutr., February 1, 2008; 138(2): 292 - 296. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
