Beta Sitosterol

 

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Clinical Studies

References


Beta Sitosterol is used for coronary heart disease and hypercholesterolemia, benign prostatic hyperplasia (BPH) and prostatitis, and gallstones. It is also used for enhancing sexual activity and for preventing colon cancer. Beta Sitosterol is also used for boosting the immune system in the common cold and flu (influenza), HIV/AIDS, rheumatoid arthritis, tuberculosis, psoriasis, allergies, fibromyalgia, systemic lupus erythematosus, asthma, alopecia, bronchitis, idiopathic thrombocytopenia purpura (ITP), migraine headache and chronic fatigue syndrome.

Beta Sitosterol is significantly more potent than Saw Palmetto or Pygeum in helping prevent BPH. This is why we are using 200mgs of the high activity Beta Sitosterol per daily dose in  both versions of our Total Balance Men’s Plus.

Beta Sitosterol is a plant sterol with a chemical structure similar to cholesterol. Beta Sitosterol actually inhibits intestinal absorption of cholesterol by competing for the limited space in mixed micelles; cholesterol absorption is decreased by about 50%. Beta Sitosterol reduces blood levels of cholesterol. There is evidence that beta-sitosterol might also have anticancer and immunostimulant effects. Beta Sitosterol can inhibit the growth of human colon cancer cells in vitro.

It has also been effective in reducing symptoms of benign prostatic hyperplasia.

 

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Published Clinical Studiescltop

 1
Randomised, placebo-controlled, double-blind clinical trial of beta-sitosterol in patients with benign prostatic hyperplasia. Beta-sitosterol Study Group.

Berges RR, Windeler J, Trampisch HJ, Senge T.

 

Department of Urology, Ruhr-University, Bochum, Germany.

Medical treatments have become available for benign hypertrophy of the prostate, including alpha-receptor blocking agents and 5-alpha-reductase inhibitors. Drugs derived from plants, for which no precise mechanism of action has been described, are widely used for this purpose in Europe. In a randomised, double-blind, placebo-controlled multicentre study, 200 patients (recruited between April and October 1993) with symptomatic benign prostatic hyperplasia were treated with either 20 mg beta-sitosterol (which contains a mixture of phytosterols) three times per day or placebo. Primary end-point was a difference of modified Boyarsky score between treatment groups after 6 months; secondary end-points were changes in International Prostate Symptom Score (IPSS), urine flow, and prostate volume. Modified Boyarsky score decreased significantly with a mean of -6.7 (SD 4.0) points in the beta-sitosterol-treated group versus -2.1 (3.2) points in the placebo group p < 0.01. There was a decrease in IPSS (-7.4 [3.8] points in the beta-sitosterol-treated group vs -2.1 [3.8] points in the placebo group) and changes in urine flow parameters: beta-sitosterol treatment resulted in increasing peak flow (15.2 [5.7] mL/s from 9.9 [2.5] mL/s), and decrease of mean residual urinary volume (30.4 [39.9] mL from 65.8 [20.8] mL). These parameters did not change in the placebo group (p < 0.01). No relevant reduction of prostatic volume was observed in either group. Significant improvement in symptoms and urinary flow parameters show the effectiveness of beta-sitosterol in the treatment of benign prostatic hyperplasia.

Publication Types:

PMID: 7540705 [PubMed - indexed for MEDLINE]

 

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 2
A multicentric, placebo-controlled, double-blind clinical trial of beta-sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. German BPH-Phyto Study group.

Klippel KF, Hiltl DM, Schipp B.

 

Department of Urology, Allgemeines Krankenhaus Celle, Academic Hospital, Germany.

OBJECTIVE: To report the results of a double-blind, placebo-controlled trial to evaluate Azuprostat, a beta-sitosterol, in patients with symptoms of outlet obstruction caused by benign prostatic hyperplasia (BPH). PATIENTS AND METHODS: A randomized, double-blind and placebo-controlled clinical trial was conducted to assess the efficacy and safety of 130 mg free beta-sitosterol (phytosterol) daily, using the international prostate symptom score (IPSS) as the primary outcome variable. In total, 177 patients with BPH were recruited for 6 months of treatment in 13 study centres. In addition to the relative difference in the IPSS, changes in quality of life, peak urinary flow rate (Qmax) and post-void residual urinary volume (PVR) were recorded. The drug used in the trial consisted of a chemically defined extract of phytosterols, derived for example from species of Pinus, Picea or Hypoxis, with beta-sitosterol as the main component. RESULTS: There were significant (P < 0.01) improvements over placebo in those treated with beta-sitosterol; the mean difference in the IPSS between placebo and beta-sitosterol, adjusted for the initial values, was 5.4 and in the quality-of-life index was 0.9. There were also significant improvements in the secondary outcome variables, with an increase in Qmax (4.5 mL/s) and decrease in PVR (33.5 mL) in favour of beta-sitosterol when adjusted for the changes after placebo. CONCLUSION: These results show that beta-sitosterol is an effective option in the treatment of BPH.

Publication Types:

PMID: 9313662 [PubMed - indexed for MEDLINE]

 

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 3
[Sitosterol in familial hyperlipoproteinemia type II. A randomized double-blind cross-over study]

Oster P, Schlierf G, Heuck CC, Greten H, Gundert-Remy U, Haase W, Klose G, Nothelfer A, Raetzer H, Schellenberg B, Schmidt-Gayk H.

 

The effect of beta-sitosterol on the lipid and lipoprotein level was evaluated in a randomised double-blind cross-over trial in 24 patients with primary familial type II hyperlipoproteinaemia over a period of 16 weeks. All patients completed the trial, however 10 of them had to be excluded from the evaluation due to fluctuations of their body weight or unreliable drug intake. Sitosterol lowered the total cholesterol level by 12.5% (P less than 0.01) from 9.96 mmol/l (3.69 g/l) to 8.37 mmol/l (3.23 g/l). The LDL-cholesterol level was lowered by 19.5% (P less than 0.05). The sitosterol concentration in plasma was consistently lower than 0.3% of total cholesterol. No side effects or tachyphylaxis was observed in the course of the trial. A return to normal of an increased serum cholesterol level by a combination of a lipid lowering diet and sitosterol monotherapy was only achieved in one patient.

Publication Types:

PMID: 182445 [PubMed - indexed for MEDLINE]

 

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 4
A plant food-based diet modifies the serum beta-sitosterol concentration in hyperandrogenic postmenopausal women.

Muti P, Awad AB, Schunemann H, Fink CS, Hovey K, Freudenheim JL, Wu YW, Bellati C, Pala V, Berrino F.

 

Department of Social and Preventive Medicine, University at Buffalo, Buffalo, NY, USA. muti@buffalo.edu

Plant sterols or phytosterols are common components of plant foods, especially plant oils, seeds and nuts, cereals and legumes. The most common phytosterols are campesterol, beta-sitosterol and stigmasterol. Phytosterols have anticarcinogenic properties. Previous studies have suggested that populations with low breast cancer incidence often consume diets high in phytosterols. The present study evaluated whether consumption of a plant food-based diet, low in animal fat, may increase serum phytosterol levels in postmenopausal women. One hundred and four women volunteers were randomized to dietary intervention or control groups. The dietary intervention included intensive dietary counseling to replace animal products with plant-based foods. Subjects in the dietary intervention group participated twice a week for 18 wk in workshops about the preparation and consumption of a plant food-based diet. The absolute change in serum total phytosterol concentration was greater in the dietary intervention group than in the control group. The percent change tended to differ between groups (P = 0.06). However, only for beta-sitosterol did the absolute and percent changes within a group differ significantly between groups (P = 0.0017). The decrease in serum total cholesterol in the dietary intervention group (-14%) was greater than that in the control group (-4%; P = 0.0005). The results of this study show that circulating levels of phytosterols can be affected by dietary modification. These findings indicate that phytosterols, in particular beta-sitosterol, can be used as biomarkers of exposure in observational studies or as compliance indicators in dietary intervention studies of cancer prevention.

PMID: 14652381 [PubMed - in process]

 

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 5
The effects of B-sitosterol (BSS) and B-sitosterol glucoside (BSSG) mixture on selected immune parameters of marathon runners: inhibition of post marathon immune suppression and inflammation.

Bouic PJ, Clark A, Lamprecht J, Freestone M, Pool EJ, Liebenberg RW, Kotze D, van Jaarsveld PP.

 

Dept. Medical Microbiology, Tygerberg, South Africa. pjdb@maties.sun.ac.za

A pilot study was undertaken to investigate the effects of the intake of capsules containing the plant sterols and sterolins (BSS:BSSG mixture) on selected immune parameters of volunteers participating in an ultra-marathon in Cape Town, South Africa. Those runners having received active capsules (n=9) showed less neutrophilia, lymphopenia and leukocytosis when compared to their counterparts having received placebo capsules (n=8): the placebo treated individuals showed significant increases in their total white blood cell numbers as well as in their neutrophils (p=0.03 and 0.03 respectively). Furthermore, statistically significant increases within lymphocyte subsets were observed in the runners having received the active capsules: CD3+ cells increased (p=0.02) as did CD4+ cells (p=0.03). In parallel, the BSS:BSSG capsules decreased the plasma level of IL6 in the runners using the active capsules (p=0.08) and significantly decreased the cortisol: DHEAs ratio (p=0.03), suggesting that these volunteers had less of an inflammatory response and were less immune suppressed during the post-marathon recovery period. These findings justify further investigations into the use of the phytosterols to prevent the subtle immunosuppression associated with excessive physical stress.

Publication Types:

PMID: 10376483 [PubMed - indexed for MEDLINE]

 

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 6
Beta-Sitosterol and beta-sitosterol glucoside stimulate human peripheral blood lymphocyte proliferation: implications for their use as an immunomodulatory vitamin combination.

Bouic PJ, Etsebeth S, Liebenberg RW, Albrecht CF, Pegel K, Van Jaarsveld PP.

 

Department of Medical Microbiology, Faculty of Medicine, University of Stellenbosch, Tygerberg, South Africa.

The phytosterols, beta-sitosterol (BSS), and its glucoside (BSSG) enhance the in vitro proliferative response of T-cells stimulated by sub-optimal concentrations of phytohaemagglutinin (PHA) several fold at extremely low concentrations (femtogram level). A 100:1 (mass:mass) ratio of BSS:BSSG (termed essential sterolin formulation, ESF) showed higher stimulation than the individual sterols at the same concentration. In vivo activity of ESF was also demonstrated when volunteers ingested ESF for 4 weeks. Proliferation of their T-cells, stimulated maximally with PHA, was significantly enhanced (20-920%) when compared to baseline values. In vitro, ESF (1 microgram.ml) was able to significantly enhance the expression of CD25 and HLA-Dr activation antigens on T-cells and increased the secretion, into the medium, of IL-2 and gamma interferon. NK-cell activity was also increased by BSS and BSSG alone, but with EST a higher activity was always found at different effector:target ratios (100:1 12:1).

PMID: 9172012 [PubMed - indexed for MEDLINE]

 

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Referencesre

  1. Awad AB, Chen YC, Fink CS, Hennessey T. Beta-sitosterol inhibits HT-29 human colon cancer cell growth and alters membrane lipids. Anticancer Res 1996;16(5A):2797-804.
  2. Berges RR, Windeler J, Trampisch HJ, et al. Randomised, placebo-controlled, double-blind clinical trial of beta-sitosterol in patients with benign prostatic hyperplasia. Beta-sitosterol Study Group. Lancet 1995;345(8964):1529-32.
  3. Oster P, Schlierf G, Heuck CC, et al. [Sitosterol in familial hyperlipoproteinemia type II. A randomized, double-blind, cross-over study]. [Article in German] Dtsch Med Wochenschr 1976;101(36):1308-11.
  4. Becker M, Staab D, Von Bergmann K. Treatment of severe familial hypercholesterolemia in childhood with sitosterol and sitostanol. J Pediatr 1993;122(2):292-6.
  5. Wilt TJ, MacDonald R, Ishani A. beta-sitosterol for the treatment of benign prostatic hyperplasia: a systematic review. BJU Int 1999;83:976-83.
  6. Klippel KF, Hiltl DM, Schipp B. A multicentric, placebo-controlled, double-blind clinical trial of beta-sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. Br J Urol 1997;80(3):427-32.
  7. Salen G, Shefer S, Nguyen L, et al. Sisterolemia. J Lipid Res 1992;33(7):945-55.
  8. Ntanios FY, Jones PJ, Frohlich JJ. Effect of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor on sterol absorption in hypercholesterolemic subjects. Metabolism 1999;48(1):68-73.
  9. Bouic PJ, Etsebeth S, Liebenberg RW, et al. Beta-sitosterol and beta-sitosterol glucoside stimulate human peripheral blood lymphocyte proliferation: implications for their use as an immunomodulatory vitamin combination. Int J Immunopharmacol 1996;18(12):693-700.
  10. Schlierf G, Oster P, Heuck CC, et al. Sitosterol in juvenile type II hyperlipoproteinemia. Atherosclerosis 1978;30(4):245-8.
  11. Awad AB, von Holtz RL, Cone JP, et al. Beta-sitosterol inhibits growth of HT-29 human colon cancer cells by activating the sphingomyelin cycle. Anticancer Res 1998;18(1A):471-3.
  12. Nguyen LB, Shefer S, Salen G, et al. Competitive inhibition of hepatic sterol 27-hydroxylase by sitosterol: decreased activity in sitosterolemia. Proc Assoc Am Physicians 1998;110(1):32-9.
  13. Salen G, Shore V, Tint GS, et al. Increased sitosterol absorption, decreased removal, and expanded body pools compensate for reduced cholesterol synthesis in sitosterolemia with xanthomatosis. J Lipid Res 1989;30(9):1319-30.
  14. Patel SB, Honda A, Salen G. Sitosterolemia: exclusion of genes involved in reduced cholesterol biosynthesis. J Lipid Res 1998;39(5):1055-61.
  15. Bouic PJ, Clark A, Lamprecht J, et al. The effects of B-sitosterol (BSS) and B-sitosterol glucoside (BSSG) mixture on selected immune parameters of marathon runners: inhibition of post marathon immune suppression and inflammation. Int J Sports Med 1999;20(4):258-62.
  16. Hidaka H, Kojima H, Kawabata T, et al. Effects of an HMG-CoA reductase inhibitor, pravastatin, and bile sequestering resin, cholestyramine, on plasma plant sterol levels in hypercholesterolemic subjects. J Atheroscler Thromb 1995;2(1):60-5.
  17. Anon. W&B Associates Inc. website. URL http://www.wandb.com/cholesterol.6.htm (Accessed 30 March 2000).
  18. Schwartzkopff W, Jantke HJ. [Dose-effect of beta-sitosterin in type IIa and IIb hypercholesterolemias]. [Article in German]. MMW Munch Med Wochenschr 1978;120(47):1575-8.
  19. Becker M, Staab D, Von Bergman K. Long-term treatment of severe familial hypercholesterolemia in children: effect of sitosterol and bezafibrate. Pediatrics 1992;89(1):138-42.
  20. Micromedex Healthcare Series. Englewood, CO: MICROMEDEX Inc.