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February 2002

Policosanol improves blood flow

Intermittent claudication is a disease characterized by severe occlusion of the arterial system in the lower part of the body.

A study published in the journal Angiology investigated the long-term effects of policosanol administered to patients with moderately severe intermittent claudication. The study consisted of a six-week single-blind, placebo-controlled run-in phase, followed by a two-year double-blind, randomized treatment step. Patients were randomized to receive placebo or policosanol (10 mg twice daily). Walking distances on a treadmill were assessed before and after 6, 12, 18 and 24 months of treatment. After six months of therapy, policosanol significantly increased the initial claudication distance by an average of 36% and the absolute claudication distance by an average of 42%. There were no improvements in the placebo group.

Heart attack and stroke have been associated with high levels of a type of cholesterol known as low-density lipoprotein (LDL) ("bad" cholesterol) and low levels of high-density lipoprotein (HDL) ("good" cholesterol). Reversing these trends can lower the risk for these and other artery-related diseases.

In the policosanol group, the beneficial effects improved after long-term therapy, so that final values showed an average of 62% improvement in the initial claudication distance and 66% in the absolute claudication distance, both significantly greater than those obtained in the placebo group. Policosanol, but not placebo, significantly increased the ankle/arm pressure index. In addition, from month six up to study completion, the frequency of patients reporting improvement of lower limb symptoms was greater in the policosanol group than in the placebo group. The treatment was tolerated well. Eight patients in the placebo group experienced a total of 10 serious adverse events, 8 of which were vascular events, compared with none in the policosanol group.[13]

While intermittent claudication is one of the most severe occlusive arterial diseases, the aging process itself results in diminished circulation throughout the body, indicating a significant potential benefit of policosanol to normal aging humans in addition to cholesterol reduction.


Heart attack and stroke have been associated with high levels of a type of cholesterol known as low-density lipoprotein (LDL) (“bad” cholesterol) and low levels of high-density lipoprotein (HDL) (“good” cholesterol). Reversing these trends can lower the risk for these and other artery-related diseases.

Policosanol is a dietary supplement that can normalize cholesterol as well or better than drugs, without side effects.[14] Efficacy and safety have been proven in numerous clinical trials, and it has been used by millions of people in other countries. Policosanol lowers LDL-cholesterol and raises protective HDL-cholesterol. This compares favorably with cholesterol-lowering drugs which have the drawback of side effects such as liver dysfunction and muscle atrophy. Policosanol is free of these side effects.

What makes policosanol exciting is that it has other actions against heart disease in addition to lowering cholesterol. Like statin drugs, policosanol helps stop the formation of artery lesions.[15] This was proven in studies on rabbits fed a diet designed to create high cholesterol:

“In most policosanol-treated animals, atherosclerotic lesions were not present, and in others, thickness of fatty streaks had less foam cell layers than in controls.”[16]

One of policosanol’s important actions is to inhibit the oxidation of LDL.[17] Oxidized LDL is dangerous. It promotes the destruction of blood vessels by creating a chronic inflammatory response. Oxidized LDL can also provoke metalloproteinase enzymes.[18] These enzymes promote blood vessel destruction, partly by interfering with HDL’s protective effect. Studies show that rats treated with policosanol have fewer foam cells, reflecting less inflammatory response causing less blood vessel destruction.[19,20]

Another action of policosanol is to reduce the proliferation of cells on the lining of the arteries. Healthy arteries are lined with a smooth layer of cells so that blood can race through with no resistance. One of the features of diseased arteries is that this layer becomes thick and overgrown with cells. As the artery narrows, blood flow slows down or is blocked completely. Policosanol was tested for its ability to stop the proliferation of these cells.[21] According to the results, policosanol’s ability to stop cell overgrowth “is in agreement with the antiproliferative effects reported for other lipid-lowering drugs, such as most of the statins.”[22]

Policosanol also inhibits the formation of clots, and may work synergistically with aspirin in this respect. In a comparison of aspirin and policosanol, aspirin was better at reducing one type of platelet aggregation (clumping together of blood cells). But policosanol was better at inhibiting another type. Together, policosanol and aspirin worked better than either alone.[23,24] A related effect is that significant reductions in the level of thromboxane occur in humans after two weeks of policosanol.25 Thromboxane is a blood vessel-constricting agent that contributes to abnormal platelet aggregation that can cause a heart attack or stroke.

Those who have elevated LDL-cholesterol (over 100) or low HDL-cholesterol (under 50) should seek to protect themselves from the number one killer of Americans (cardiovascular disease). Some people can achieve optimal cholesterol levels via dietary modification, while others require intervention with dietary supplements like policosanol or prescription drugs.

Note: Reprints of scientific abstracts can be found in the Life Extension Abstracts section.

1. Wall Street Journal Nov 21, 2001, page A1. Page One Feature, “Auto Industry Faces Effects of Price Pressure As Economists Debate Possibility of Deflation,” by Norihiko Shirouzu and Jon E. Hilsenrath, Staff Reporters of the Wall Street Journal.

2. Wall Street Journal Nov 21, 2001, page A16. Politics & Policy, “Industry Splits Over Bristol-Myers’s Bid To Protect Top Drug From Generic Sales,” by Gardiner Harris and Laurie McGinley, Staff Reporters of the Wall Street Journal.

3. Bernini F, et al. Safety of HMG-CoA reductase inhibitors: focus on atorvastatin. Cardiovasc Drugs Ther 2001;15(3):211-8.

4. Chazerain P et al. Four cases of tendinopathy in patients on statin therapy. Joint Bone Spine 2001 Oct;68(5):430-3.

5. Federman DG, et al. Fatal rhabdomyolysis caused by lipid-lowering therapy. South Med J 2001 Oct;94(10):1023-6.

6. Omar MA, et al. Rhabdomyolysis and HMG-CoA reductase inhibitors. Ann Pharmacother 2001 Sep;35(9):1096-107.

7. Boger RH. Drug interactions of the statins and consequences for drug selection. Int J Clin Pharmacol Ther 2001 Sep;39(9):369-82.

8. Shek A, et al. Statin-fibrate combination therapy. Ann Pharmacother 2001 Jul-Aug;35(7-8):908-17.

9. Hodgson J. Bayer lapse exposes pharma’s vulnerability. Nat Biotechnol 2001 Oct;19(10):897-8.

10. Castano G, et al. Effects of policosanol 20 versus 40 mg/day in the treatment of patients with type II hypercholesterolemia: a 6-month double-blind study. Int J Clin Pharmacol Res 2001;21(1):43-57.

11. Mirkin A, et al. Efficacy and tolerability of policosanol in hypercholesterolemic postmenopausal women. Int J Clin Pharmacol Res 2001;21(1):31-41.

12. Castano G, et al. Effects of policosanol in older patients with type II hypercholesterolemia and high coronary risk. J Gerontol A Biol Sci Med Sci 2001 Mar;56(3):M186-92.

13. Castano G, et al. A long-term study of policosanol in the treatment of intermittent claudication. Angiology 2001 Feb;52(2):115-25.

14. Mas R, et al. Effects of policosanol in patients with type II hypercholesterolemia and additional coronary risk factors. Clin Pharmacol Ther 1999 Apr;65(4):439-47.

15. Noa M, et al. Effect of policosanol on lipofundin-induced atherosclerotic lesions in rats. J Pharm Pharmacol 1995 Apr;47(4):289-91.

16. Arruzazabala ML, Noa M. Protective effect of policosanol on atherosclerotic lesions in rabbits with exogenous hypercholesterolemia. Braz J Med Biol Res 2000 Jul;33(7):835-40.

17. Menendez R, et al. Oral administration of policosanol inhibits in vitro copper ion-induced rat lipoprotein peroxidation. Physiol Behav 1999 Aug 1;67(1):1-7.

18. Xu XP, et al. 1999. Oxidized low-density lipoprotein regulates matrix metalloproteinase-9 and its tissue inhibitor in human monocyte-derive macrophages. Circulation 99:993-8.

19. Noa M, et al. 1996. Effect of policosanol on foam-cell formation in carrageenan-induced granulomas in rats. J Pharm Pharmacol 48:282-5.

20. Lindstedt L, et al. 1999. matrix metalloproteinases-3, -7, and -12, but not -9, reduce high density lipoprotein-induced cholesterol efflux from human macrophage foam cells by truncation of carboxyl terminus of apolipoprotein A-I. Parallel losses of pre-beta particles and the high affinity component of efflux. J Biol Chem 274:22627-34.

21. Noa M, et al. 1998. Effect of policosanol on damaged arterial wall induced by forceps in rabbits. J Electron Microsc 4:629-30.

22. Negre-Aminou P, et al. 1996. Antiproliferative potencies of 6 vastatins in cultured human cells: involvement of the ras-mediated signalling pathway. 66th Cong Eur Atheroscler Soc (July 13-17, Florence): 120.

23. Arruzazabala ML, et al. 1997. Comparative study of policosanol, aspirin and the combination therapy policosanol-aspirin on platelet aggregation in healthy volunteers. Pharmacol Res 36:293-7.

24. Stusser R, et al. 1998. Long-term therapy with policosanol improves treadmill exercise-ECG testing performance of coronary heart disease patients. Int J Clin Pharmacol Ther 36:469-73.

25. Carbajal D, et al. 1998. Effect of policosanol on platelet aggregation and serum levels of arachidonic acid metabolites in healthy volunteers. Prost Leuk Essen Fatty Acids 58:61-4.