Policosanol has been shown to exert anti-coagulant ef ects on platelet function. However, this does not seem to be
the case when administered at 5 or 10 mg per day. Anti-coagulant ef ects appear to start at a dose of 20 mg per
day, with increasing anti-coagulant ef ects at 40 mg per day. Thus, patients taking other anti-coagulants (warfarin,
coumadin, aspirin ) appear to be able to safely take up to 10 mg per day of Policosanol to lower cholesterol without
risk of potentiating the action of anti-coagulant drugs. 19 A dose of 20 mg per day of Policosanol has been shown to
provide the same degree of anti-coagulant activity as 100 mg of aspirin per day in human subjects. 20 This implies
that if an anti-coagulant effect is desired along with a cholesterol lowering ef ect, then Policosanol can be used
alone at a dose of 20 or 40 mg per day. If the patient is already on anti-coagulant therapy, then it is wise to limit the
dose of Policosanol to 10 mg per day, where a cholesterol lowering ef ect is desirable.
Dosage and Standardized Grade
Cholesterol Lowering - To lower cholesterol in patients not taking anti-coagulant therapy (including aspirin) doses of
Policosanol from 5 mg per day to 40 mg per day have been used. Most typically, 10 mg, twice per day is the most
common daily dosage of Policosanol used to treat hypercholesterolemia. In patients using anti-coagulant drugs, it is
best to limit the dose of Policosanol to 5 mg, twice per day. 1,4,7,8,9,19,20,21
Adverse Side Effects, Toxicity and Contraindications
Long term studies with Policosanol in humans has not shown any significant side ef ects and appears to have a safer
profile than statin drugs (HMG-CoA reductase inhibitor drugs) that are commonly prescribed to lower cholesterol.
1,4,7,8,9 A case of erthyma was reported in one trial with diabetics. 18 Animal studies reveal that Policosanol is extremely
safe even when administered to beagle dogs at 180 mg/kg for 52 weeks, which is 620 times higher than the
therapeutic dose of 20 mg per day. 22 Studies in mice showed no adverse ef ects or carcinogenicity at doses of 50-
500 mg/kg administered orally for 18 months. 23 Overall Policosanol is considered to be an extremely safe therapeutic
agent for cholesterol lowering. 4,5,24
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Drug-Nutrient Interactions
1. Anti-coagulant Drugs - Policosanol has been shown to inhibit platelet aggregation and therefore, may potentiate the
ef ects of anti-coagulant drugs such as warfarin, coumadin and aspirin. Studies on humans and animals have not
shown a significant enhancement of anti-platelet activity when Policoasanol has been combined with warfarin or
aspirin. Nevertheless, in the interest of patient safety, it is best not to recommend a daily dosage of more than 5
mg, twice per day in patients on concomitant anti-coagulant therapy, and even then, their prothrombin time should
be properly monitored. 25,26,27,28
2. Beta-Blocker, Anti-Hypertensive Drugs - Human and animal studies reveal that Policosanol can potentiate the
ef ects of beta-blockers used to lower high blood pressure. Thus, blood pressure should be monitored in order to
see if a dose reduction in beta-blocker medication is required once Policosanol supplementation has been
implemented.29
Pregnancy and Lactation
During pregnancy and lactation, the only supplements that are considered safe include standard prenatal
vitamin and mineral supplements. All other supplements or dose alterations may pose a threat to the
developing fetus and there is generally insuf icient evidence at this time to determine an absolute level of
safety for most dietary supplements other than a prenatal supplement. Any supplementation practices
beyond a prenatal supplement should involve the cooperation of the at ending physician (e.g., magnesium
and the treatment of preeclampsia.)
References: Pregnancy and Lactation
1. Encyclopedia of Nutritional Supplements. Murray M. Prima Publishing 1998.
2. Reavley NM. The New Encyclopedia of Vitamins, Minerals, Supplements, and Herbs. Evans and
Company Inc. 1998.
3. The Healing Power of Herbs (2nd edition). Murray M. Prima Publishing 1995.
4. Boon H and Smith M. Health Care Professional Training Program in Complementary Medicine.
Institute of Applied Complementary Medicine Inc. 1997.
1. Gouni-Berthold I, Berthold HK. Policosanol: Clinical pharmacology and therapeutic significance of a new lipid-lowering agent. Am
Heart J 2002Feb;143(2):356-65
2. Torres O, Agramonte AJ, Illnait J, Más Ferreiro R, Fernández L, Fernández JC. Treatment of hypercholesterolemia in NIDDM with
policosanol. Diabetes Care 1995Mar;18(3):393-7
3. Castaño G, Más R, Roca J, Fernández L, Illnait J, Fernández JC, Selman E. A double-blind, placebo-controlled studyof the effects of
policosanol in patients with intermittent claudication. Angiology 1999Feb;50(2):123-30
4. A Natural Anti-Cholesterol Dietary Supplement: Policosanol. Life Extension Jun2001;7(6):24
5. Prat H, et al. Comparative effects of policosanol and two HMG-CoA Reductase inhibitors on type II hypercholesterolemia. Rev Med
Chil Mar1999;127(3):286-94
6. Menéndez R, Amor AM, Rodeiro I, González RM, González PC, Alfonso JL, et al. Policosanol modulates HMG-CoA Reductase
activity in cultured fibroblasts. Arch med Res 2001Jan-Feb;32(1):8-12
7. Canetti M, Moreira M, Más R, Illnait J, Fernández L, Fernández, JC, et al. A two-year study on the efficacy and tolerability of
policosanol in patients with type II hyperlipoproteinaemia. Int J Clin Pharmacol Res 1995;15(4):159-65
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8. Stusser R, et al. Long-term therapy with policosnol improves treadmill exercise-ECG testing performance of coronary heart disease
patients. Int J Clin Pharmacol Ther 1998;36:469-73
9. Mirkin A, Más R, Martinto M, Boccanera R, Robertis A, Poudes R, et al. Efficacy and tolerability of policosanol in
hypercholesterolemic postmenopausal women. Int J Clin Pharmacol Res 2001;21(1):31-41
10. Más R, Castaño G, Illnait J, Fernández L, Fernández J, Alemán C, et al. Effects of policosanol in patients with type II
hypercholesterolemia and additional coronary risk factors. Clin Pharmacol Ther 1999Apr;65(4):439-47
11. Castaño G, Más R, Fernández JC, Illnait J, Fernández L, Alvarez E. Effects of policosanol in older patients with type II
hypercholesterolemia and high coronary risk. J Gerontol A Biol Sci med Sci 2001Mar;56(3):186-92
12. Castaño G, Más R, Arruzazabala ML, Noa M, Illnait J, Fernández JC, et al. Ef ects of policosanol and pravastatin on lipid profile,
platelet aggregation and endothelemia in older hypercholesterolemic patients. Int J Clin Pharmacol Res 1999;19(4):105-16
13. Prat H, Román O, Pino E. Comparative effects of policosanol and two HMG-CoA Reductase inhibitors on type II
hypercholesterolemia. Rev Med Chil 1999Mar;127(3):286-94
14. Marcello S, Gladstein J, Tesone P, Más R. Current Therapeutic Research 2000Jun;61(6):346-57
15. Castaño G, et al. A double-blind placebo-controlled study of the effects of policosanol in patients with intermittent claudication.
Angiology. Feb1999;50(2):123-30
16. Stüsser R, Batista J, Padrón R, Sosa F, Pereztol O. Long-term therapy with policosanol imporves treadmill exercise-ECG testing
performance of coronary heart disease patients. Int J Clin Pharmacol Ther 1998Sep;36(9):469-73
17. Batista J, Stüsser R, Saéz F, Peréz B. Effect of policosanol on hyperlipidemia dn coronary heart diseases in middle-aged patients. A
14-month pilot study. Int J Clin Pharmacol Ther Mar1996;34(3):134-7
18. Torres O, et al. Treatment of hypercholesterolemia in NIDDM with policosanol. Diabetes Care. Mar1995;18(3):393-7
19. Arruzazabala ML, et al. Effect of policosanol successive dose increases on platelet aggregation in healthy volunteers. Pharmacol
Res Nov1996;34(5-6):181-5
20. Arruzazabala ML, et al. Comparative study of policosanol, aspirin and the combination therapy policosanol-aspirin on platelet
aggreagation in healthy volunteers. Pharmacol Res Oct1997;36(4):293-7
21. Carbajal D, et al. Effect of policosanol on platelet aggregation and serum levels of arachidonic acid metabolites in healthy
volunteers. Prostaglandins Leukot Essent Fatty Acids Jan1998;58(1):61-4
22. Mesa AR, Mas R, Noa M et al. Toxicity of policosanol in beagle dogs: one-year study. Toxicol Lett 1994;73:81-90
23. Aleman CL, Mas R, Hernandez C et al. A 12-month study of policosanol oral toxicity in Sprague Dawley rats. Toxicol Lett
1994;70:77-87
24. Mas R, et al. Effects of policosanol in patients with type II hypercholesterolemia dn additional coronary risk factors. Clin Pharmacol
Ther Apr1999;65(4):439-47
25. Carbajal D, Arruzazabala ML, Valdes S, Mas R. Effect of policosanol on platelet aggreagation and serum levels of arachidonic acid
metabolites in healthy volunteers. Prostaglandins Leukot Essent Fatty Acids Jan1998;58(1):61-4
26. Arruzazabala ML, et al. Comparative study of policosanol, aspirin and the combination therapy policosanol-aspirin on platelet
aggregation in healthy volunteers. Pharmacol Res Oct1997;36(4):293-7
27. Stusser R, Batista J, Padron R, et al. Long-term therapy with policosanol improves treadmill exercise-ECG testing performance of
coronary heart disease patients. Int J Clin Pharmacol Ther Sep1998;36(9):469-73
28. Carbajal D, et al. Interaction policosanol-warfarin on bleeding time and thrombosis in rats. Pharmacol Res Aug1998;38(2):89-91
29. Molina Cuevas V, et al. Effect of policosanol on arterial blood pressure in rats. Study of the pharmacological interaction with
nifedipine and propranolol. Arch Med Res Mar1998;29(1):21-4
30. Griffith W, MD. Complete Guide to Prescription and Nonprescription Drugs. The Body Press 1999;MHG-CoA Reductase
inhibitors:418-419
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Prebiotics (FOS and other Oligosaccharides)
General Features
Prebiotics is a term used to refer to short-chain polysaccharides (carbohydrates) that are not completely digested by
the human intestinal tract, but rather serve as a food supply for the friendly bacteria of the large bowel (bifodobacteria
and lactobacilli), enhancing their growth and cell division rate.1,2,3
The of icial definition of Prebiotics is stated as “nondigestible food ingredients that beneficially affect the host by
selectively stimulating the growth and activity of one species or a limited number of species of bacteria in the colon”.4
Human studies show that supplementation with FOS (fructo-oligosaccharides) increases bifodobacteria and lactobacilli
populations in the flora of the large intestine while simultaneously reducing the colonies of detrimental bacteria. The
same has been shown for supplementation with two other Prebiotics; namely inulin and galacto-oligosaccharides
(GOS).5-9
Fructo-oligosaccharides (FOS) and inulin consist of short chains of fructose molecules. Galacto-oligosaccharides
consist of short chains of galactose molecules.1,2,3
The estimated average daily intake of FOS from food sources (mostly vegetables) is 800 mg.10 Supplementation
studies demonstrate that 2,000-3,000 mg a day of additional FOS can favourably alter the bacteria populations of the
large bowel.5-9 Higher doses may help to lower cholesterol, triglycerides and help bet er regulate blood glucose in type
II diabetics.11,12
From a standpoint of general wellness, supplementation with Prebiotics or probiotics have been shown to improve
digestion and absorption of some nutrients, enhance detoxification by intestinal mucosal cells, reduce the
concentrations of large bowel mutagens and carcinogens, aid elimination processes and favorably af ect the immune
system of the gut and the systemic immune system. These ef ects are related to favorable changes in the
concentrations of friendly gut bacteria resulting from pre- and probiotic supplementation. In regards to immune
modulation, these positive effects extend to include reduced hypersensitivity reactions secondary to food sensitivities,
improved control of autoimmune conditions and a lessening of skin reactions secondary to food-induced
hypersensitivity reactions.4,13,14
An important feature of prebiotic supplementation is its potential impact on reducing risk of colorectal cancer, which is
the second leading cause of cancer death in North America (combining statistics for men and women), after lung
cancer. Human studies demonstrate that supplementation with Prebiotics (and probiotics) encourages the growth of
lactic acid bacteria (LAB). Experimental data and some epidemiological evidence indicate that increased LAB protects
against colon cancer development. Experimental data demonstrates that Prebiotics increase the proliferation of LAB
which also, through fermentation of Prebiotics and other fiber sources, gives rise to the production of short-chain fatty
acids and lowers the pH of the colon; making it a more acidic environment. Lower pH in the colon is associated with a
reduced risk of colon cancer in various studies. This appears related to an inhibition of certain enzymes that are
known to produce bowel carcinogens. Human studies have shown that prebiotic supplementation reduce
concentrations of components that are genotoxic in human colon cells. Butyrate has been shown to increase the
proliferation of normal cells, while inhibiting the proliferation of cancerous cells. This short-chain fat y acid also induces
apoptosis (programmed cell death) of colon cancer cells, under experimental conditions. It is an important fuel for
colon cells and evidence exists to show that colon cells exposed to various carcinogens are less inclined to be
transformed into malignant cells in the presence of adequate butyrate supply. Butyrate has also been shown to
increase the concentrations of glutathione transferase enzyme in colon cells. “Thus, enzyme induction by butyrate, or
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by the microflora and increased activity by Prebiotics, may be an important mechanism or protection against
carcinogen-enhanced colon cancer.”15
Clinical Application and Mechanism of Action
1. Digestive Disorders, Food Sensitivity and Intolerances, Autoimmune Conditions, Rheumatoid Arthritis,
Skin Conditions
Prebiotics may be used to increase friendly gut bacteria (Bifidobacterium, bifidum and longum, and Lacto bacillus
acidophilus). In these conditions a therapeutic dosage of – 2,000-3,000 mg of FOS per day and/or other Prebiotics
(inulin, GOS) is commonly utilized.5-9