Natural Alternative To Lower Cholesterol | Heart Health Program

Date: 05/24/2004    Written by: Jon Barron

The Cholesterol Myth

What Is Cholesterol?

Cholesterol is not a fat, but rather a soft, waxy, "fat-like" substance that circulates in the bloodstream. It is vital to life and is found in all cell membranes. It is necessary for the production of bile acids and steroid hormones and Vitamin D. Cholesterol is manufactured by the liver, but is also present in all animal foods. It is abundant in organ meats, shell fish, and egg yolks but is contained in smaller amounts in all meats and poultry. Vegetable oils and shortenings contain no cholesterol.

Cholesterol cannot dissolve in the blood, so your liver combines it with special proteins called lipoproteins to “liquefy” it. The lipoproteins used by the liver are either very low-density lipoproteins (VLDL) or high-density lipoproteins (HDL). (VLDL cholesterol is metabolized in the bloodstream to produce LDL, or low-density cholesterol.)

Note: HDL is called the "good cholesterol" because HDL cholesterol particles prevent atherosclerosis by extracting cholesterol from arterial walls and disposing of them through the liver. LDL cholesterol is called "bad" cholesterol, because elevated LDL cholesterol is associated with an increased risk of coronary heart disease. Thus, high levels of LDL cholesterol and low levels of HDL cholesterol (high LDL/HDL ratios) are considered by most doctors to be risk factors for atherosclerosis, while low levels of LDL cholesterol and high levels of HDL cholesterol (low LDL/HDL ratios) are considered desirable.

It is important to note that the liver not only manufactures and secretes LDL cholesterol into the blood, it also removes it. To remove LDL cholesterol from the blood, the liver relies on special proteins called LDL receptors that are normally present on the surface of liver cells. LDL receptors snatch LDL cholesterol particles from the blood and transport them inside the liver. A high number of active LDL receptors on the liver surfaces are associated with the rapid removal of LDL cholesterol from the blood and low blood LDL levels. A deficiency of LDL receptors is associated with high LDL cholesterol blood levels. But it is also crucial that the cholesterol which has been stored in the liver by the LDL receptors be regularly "flushed" to make room for “new” deposits, or the process comes to a standstill, thus causing levels to soar in the bloodstream.

In point of fact, the liver is responsible for over 80% of your cholesterol level. Diet accounts for less than 20%

The Cholesterol Theory of Heart Disease

According to the cholesterol theory of heart disease (and despite all that you may have heard, it is only a theory), LDL cholesterol in the blood combines with other substances such as cellular waste products, calcium, and fibrin (a clotting material in the blood) to form arterial plaque, which attaches itself to the inner lining of the arteries. Over time, cholesterol plaque causes thickening of the artery walls and narrowing of the arteries, a process called atherosclerosis. Arteries that supply blood and oxygen to the heart muscles are called coronary arteries. When coronary arteries are narrowed by atherosclerosis, they are incapable of supplying enough blood and oxygen to the heart muscle during exertion. Lack of oxygen to the heart muscle (ischemia) causes chest pain. Also formation of a blood clot in the artery can clause complete blockage of the artery, leading to death of heart muscle (heart attack). Atherosclerotic disease of coronary arteries (coronary heart disease) is the most common cause of death in the United States, accounting for about 750,000 deaths annually.

Causes of High Cholesterol

Again, according to the cholesterol theory of heart disease, both heredity and diet have a significant influence on a patient's LDL, HDL and total cholesterol levels. For example, familial hypercholesterolemia is a common inherited disorder whose victims have a diminished number or nonexistent LDL receptors on the surface of liver cells. The resultant decreased activity of the LDL receptors limits the liver's ability to remove LDL cholesterol from blood. Thus, affected family members have abnormally high LDL cholesterol levels in the blood. They also tend to develop atherosclerosis and heart attacks during early adulthood.

Diets that are high in saturated fats and cholesterol decrease the LDL receptor activity in the liver, thereby raising the levels of LDL cholesterol in the blood. Saturated fats are derived primarily from meat and dairy products and according to most doctors can raise blood cholesterol levels. Some vegetable oils made from coconut, palm, and cocoa are also high in saturated fats and are on the medical "no-no" list. On the other hand, most vegetable oils are high in unsaturated fats. Unlike saturated fats, unsaturated fats do not raise blood cholesterol (again according to the theory) and can sometimes lower cholesterol. Olive and canola oil are high in monounsaturated fats, which may have a protective effect against coronary heart disease. Unfortunately, some vegetable oils are converted to saturated fats during a process called "hydrogenation" which can be required for food processing.

Phi-Zymes from Baseline Nutritionals

Note: The concept that you might have to flush cholesterol stored in the liver to make room for new cholesterol coming from the bloodstream did not make its way into the cholesterol theory of heart disease.

How Low

On May 15, 2001, the National Cholesterol Education Panel (NCEP) issued major new clinical practice guidelines on the prevention and treatment of high cholesterol levels in adults, lowering the target optimum level for LDL to less than 100. This was the first major update of the NCEP guidelines since 1993. The NCEP has predicted that the new guidelines will increase the number of Americans requiring treatment for elevated cholesterol levels (from 52 million to 65 million) and will nearly triple the number of Americans who will need to take cholesterol lowering drugs (from 13 million to 36 million).

But for many doctors, 36 million people under experimental drug therapy are not enough. Many “experts” are now pushing to set target limits for LDL to less than 80, which would mandate that tens of millions more Americans be on moderate to high doses of statin drugs for the rest of their lives – despite the fact that these drugs are known to cause significant liver damage.

The Studies

And, of course, there are the usual assortment of FDA approved double blind studies to back these conclusions. In the past 10 years, clinical trials have “conclusively” demonstrated that lowering LDL cholesterol reduces heart attacks and saves lives. The benefits of lowering LDL cholesterol include:

  • Reducing the formation of new cholesterol plaques
  • Eliminating existing plaques
  • Preventing rupture of existing plaques
  • Decreasing the risk of heart attacks
  • Lowering the chance of strokes.

So what's my problem? Quite simply, that cholesterol doesn't cause plaque to accumulate on arterial walls. If it did, why doesn't anyone ever have clogged veins – only clogged arteries? Think about that for a moment. If high levels of cholesterol promoted the formation of plaque and its accumulation on arterial walls, then why doesn't it accumulate on the walls of veins? And the answer is – because the problem is centered in the walls of the arteries, not in the cholesterol circulating in the bloodstream.

Challenging the Theory

To understand what I'm talking about, it's first necessary to understand the beneficial role that arterial plaque plays in the human body (yes, beneficial), because therein lies the key to understanding a key role that cholesterol plays. So what is the role of plaque? It is “repair cement” for arterial walls. That is to say, if there is any damage to the arterial wall, your body will whip up some plaque from the cholesterol, calcium, and fibrin in the bloodstream to repair the damage before the arterial wall develops a leak and you bleed to death internally. Cholesterol isn't part of the problem, it's part of the solution – to a different problem.

With that in mind, let's now look at some of the basic assumptions of the cholesterol theory of heart disease.

  • Does eating a high cholesterol diet automatically lead to heart disease? Absolutely not. Look at the results seen on the Atkins Diet.
  • Does eating a high saturated fat diet automatically lead to heart disease? Again, absolutely not. Consider the traditional Eskimo diet, probably the highest saturated fat diet in the world because of all the whale and seal blubber consumed. And yet Eskimos on that diet have virtually no heart disease – until they shift to a modern Western diet. The same positive results are seen with the Atkins diet with its high consumption of saturated fats. (Both diets, however, are associated with different problems long term. Eskimos, on the traditional diet, for example, have an extremely high rate of osteoporosis because their diet promotes high acid levels in body tissue.)
  • Does lowering cholesterol in the diet automatically reduce cholesterol levels in the bloodstream? Not necessarily.
  • Does lowering cholesterol in the bloodstream reduce the formation of new plaques? In many cases it does, but not necessarily for the reasons promoted. The primary reason may be that you've minimized the ability of the body to effect repairs. You haven't got rid of the problem – merely the ability of the problem to manifest one particular set of symptoms.
  • Do the statin drugs (Advicor, Lescol, Lipitor, Mevacor, Pravachol and Zocor) reduce the incidence of heart attack and stroke? Yes, but as we will discuss shortly, probably not because of their ability to lower cholesterol, and not without significant side effects.

An Alternative Theory

I would like to propose now the “arterial damage” theory of heart disease. Quite simply, it says that since your body produces arterial plaque in response to arterial damage, excessive plaque build-up and the concomitant hardening and narrowing of the arteries is the result of excessive damage, scarring, and inflammation in the arterial walls. And why only the arteries and not the veins? Because, as we shall see shortly, arterial walls contain muscle tissue that is particularly susceptible to damage. Veins contain much less muscle tissue and are less likely to suffer damage.. So what causes damage or inflammation to the arterial walls? Well, among other things.

  • High homocysteine levels. Homocysteine is an amino acid produced as a normal byproduct of the breakdown of methionine (from proteins), which is an essential amino acid acquired mostly from eating meat. Homocysteine generates superoxide and hydrogen peroxide, both of which have been linked to damage of the endothelial lining of arterial vessels. Studies have shown that too much homocysteine in the blood is related to a higher risk of coronary heart disease, stroke and peripheral vascular disease.
  • Too much Omega-6 fatty acid in the diet. The body converts linoleic acid, the primary fatty acid found in bottled vegetable oil, to arachidonic acid. The Cox-2 enzyme then converts the arachidonic acid to the hormone-like prostaglandin E2 (PGE2) and to the cytokines interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFa), all of which promote inflammation in the body in general, and in the arterial walls in particular.
  • Eating high levels of meats and animal fat from grain fattened animals saturates the body with large amounts arachidonic acid. As a point of interest, the high levels of arachidonic acid found in most meat are accumulated from the conversion of Omega-6 fatty acids present in the grains used to fatten them. That means that only minimal levels of arachidonic acid are found in range-fed beef. Iif you can find it, range-fed beef is far healthier for you than the more common grain-fed variety.
  • High acid diets. Diets high in meat, sugar, grain, and starch raise acid levels in body tissue – thereby making it hard for the body to clear the lactic acid that builds up in muscle tissue from normal muscle activity. This is a particular problem for arteries since the arterial wall contains muscle tissue (again, veins do not) so that the arteries can be contracted to even out blood pressure when changing position (from lying down to suddenly standing up, for example). The problem is that when the acid doesn't clear, it irritates, inflames, and scars the muscle tissue in the arterial walls.
  • High levels of circulating immune complexes in the blood. Circulating immune complexes (CICs) are created when you eat complex proteins (usually from wheat, corn, and dairy) that cannot be digested thoroughly. They make their way into the bloodstream, where they are treated as allergens by the body and combined with antibodies, thus forming CICs. When the number of CICs climbs beyond the ability of the body to eliminate them all, they are deposited in the body's soft tissue, including the arterial walls, thereby triggering attacks by the body's immune system, which results in inflammation.
  • Inflammation in general. C-reactive protein (CRP) is an inflammatory marker — a substance that the liver releases in response to inflammation somewhere in the body. Studies indicate that men with high levels of CRP have triple the risk of heart attack and double the risk of stroke compared to men with lower CRP levels. In women, studies have shown that elevated levels of CRP may increase the risk of a heart attack by as much as seven times. The statin medicines (Advicor, Lescol, Lipitor, Mevacor, Pravachol and Zocor) reduce levels of CRP. This may be more significant in accounting for the ability of these drugs to statistically lower the incidence of heart disease than the role these drugs play in lowering cholesterol levels.

Solutions to Lower Cholesterol Levels

  • Avoid trans fatty acids like the plague. Hydrogenated and partially hydrogenated oils (the trans fatty acids) are the number one killer in the modern diet.
  • Optimize the liver. Do a periodic liver flush that includes the use of lipotropic herbs such as dandelion root to flush accumulated fats and cholesterol from the liver and gallbladder.
  • Lower homocysteine levels. While there is a considerable amount we do not know about homocysteine, we do know how to use nutritional supplements to reduce homocysteine levels. This is done through three independent routes: (1) using folic acid with vitamin B-12, (2) using trimethylglycine (TMG), and (3) through B-6. The first two work through a process called methylation, and the B-6 through transsulfuration. Such a combined approach can normalize homocysteine in 95% of the people studied.
  • Optimize Omega-6 to Omega-3 ratios by eliminating bottled vegetable oils found in your supermarket, except for olive oil, and supplementing with fish oil and flax seed oil, which are high in Omega-3 fatty acids. Much of the problem with inflammatory disorders actually stems from a lopsided imbalance in dietary intake of the omega-6 and omega-3 fatty acids and the resulting cascade in pro-inflammatory activity. The ideal ratio is roughly 1 to 1; however, over the past 30 years, people from industrialized countries have replaced much of their dietary saturated fat (on the mistaken advice of their doctors and the media) with vegetable oil omega-6 fatty acids. Ratios of 20 to 1 and 30 to 1 are now not uncommon. From a biochemical standpoint, this sets the stage for major arterial inflammation. (See this article from our newsletter.)
  • A good antioxidant formula that contains OPCs, can help repair damage to arterial walls.
  • Proteolytic Enzymes. This is one of the most important things you can do. The regular use of proteolytic enzymes can help eliminate CICs from the body, reduce overall inflammation, dissolve accumulated plaque, and repair arterial scar tissue. Although the evidence is purely anecdotal at the moment, we have seen extraordinary results using detox levels of this formula.


So, is there anything to worry about with high cholesterol levels? Yes, sort of.

  • High cholesterol levels are indicative of other problems – sort of like the canary in the coal mine. Among other things, they can be a warning signal for:
    • Liver problems
    • Dietary imbalance
    • High acid levels
    • Chronic inflammation, which may be a factor in the onset of Alzheimer's and cancer in addition to heart disease
  • High cholesterol levels and high levels of saturated fat in the blood "thicken" the blood. If the arteries are wide open, this is not a problem. But if the arterial walls have been narrowed or hardened, the thickened blood significantly increase the odds of a heart attack or stroke. Of course, there are a number of natural ways to thin the blood. Gingko biloba is a blood thinner, as is garlic, as are Proteolytic Enzymes (particularly nattokinase).

The trick, of course, is to take care of the problem, not the warning signal. Artificially suppressing cholesterol levels with statin drugs is a bit like feeling good about your car because you've disconnected your warning lights. Not very bright.

And if you're desperate to lower cholesterol levels without subjecting yourself to the side effects of the statin drugs, supplement with niacin and policosanol. Policosanol is a natural supplement made from sugar cane. It works by helping the liver control its production and breakdown of cholesterol, as well as being a powerful antioxidant that prevents LDL oxidation. Clinical studies show that policosanol is as effective as prescription drugs in lowering cholesterol levels, without their dangerous side effects. And, in addition, it reduces the inflammatory response in the arterial wall.

Just for Fun - Questions for Your Doctor

Remember, the cholesterol theory of heart disease is only a theory – a theory that is increasingly being discredited. For those of you who enjoy tormenting your doctor, or if you just want to see them get flustered and angry, be sure and ask them the following questions.

  • If cholesterol is the main culprit in heart disease, why don't veins ever get narrowed and blocked?
  • If high cholesterol foods are responsible for raising cholesterol levels, then why do people on the high-cholesterol Atkins Diet experience such a significant drop in cholesterol levels?
  • Why do Eskimos who eat a traditional diet of almost pure saturated fat (whale and seal blubber) have almost a zero incidence of heart disease?
  • If the liver is responsible for regulating up to 80% of my cholesterol levels, why would I want to take statin drugs for lowering cholesterol – considering that the number one known side effect of statin drugs is liver damage?



Click for Related Articles


    Submitted by Gretchen Artemis on
    June 23, 2011 - 6:16pm

    I would like your opinion on a book written by Cadwell B. Esselstyn Jr. MD, called PREVENT AND REVERSE HEART DISEASE: THE REVOLUTIONARY SCIENTIFICALLY PROVEN NUTRITION BASED CURE. His research studies are pretty impressive, and the people who participated in the studies and the results they experienced are nothing short of miraculous.

    Submitted by Mary on
    June 28, 2011 - 6:26pm

    Can you list any independently funded clinical trials of policosanol? I couldn't find any that show the results you describe. Excerpt from another health website:
    almost all of the 80+ double-blind studies on sugarcane policosanol were conducted by a single research group in Cuba that owns the policosanol patent.

    An independent study published in the Journal of the American Medical Association in 2006 did not find any benefit of policosanol,

    Submitted by BaselineFoundation on
    June 29, 2011 - 11:45am

    Hi Mary,

    Although many of the studies were conducted in Cuba and paid for by Dalmer Labs, they were published in peer reviewed journals such as Circulation and the Journal of Clinical Pharmacology. The independent study you refer to was conducted by the Drug Commission of the German Medical Association, which, by definition, may not be necessarily unbiased when it comes to evaluating alternative therapies.

    Lindstedt, L. et al. 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. 1999; 274:22627-34.

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

    Arruzazabala M. L., Carbajal D., Mas R., et al. (1994): Cholesterol-lowering effects of policosanol in rabbits. Biol. Res. 27:205-209.

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

    Menendez R., Arruzazabala M.L., Mas R., et al. (1997): Cholesterol-lowering effect of policosanol on rabbits with hypercholesterolemia induced by a wheat starch-casein diet. Br. J. Nutr. 77:323-932.

    Menendez R., Fernandez L, Del Rio A., et al. (1994): Policosanol inhibits cholesterol biosynthesis and enhances LDL processing in cultured human fibroblasts. Biol. Res. 27:199-203.

    Menendez R., Amor A.M. Gonzilez R.M. Fraga V. and Mds R. (1996): Effect of policosanol on the hepatic cholesterol biosynthesis of normocholesterolemic rats. Biol. Res. 29:253-257.

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

    Arruzazabala M. L., Valdes S., Mas R., et al. (1995): Effect of policosanol succesive dose increase in platelet aggregation healthy volunteers. Pharmacol. Res. 34:181-185.

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

    Valdes S., Arruzazabala M.L., Carbajal D., et al. (1996): Effect of policosanol on platelet aggregation in healthy volunteers. Intern. J. Clin. Pharmacol. Res. 16:67-72.

    Noa M., Herrera M., Magrancr J. and Mas R. (1994): Effect of policosanol on isoprenaline-induced myocardial necrosis in rats. J. Pharm. Pharmacol. 46:282-285.

    Carbajal D, Arruzazabala M. L., Mas R., et al. (1994). Effects of policosanol on experimental thrombosis models. Prostaglandins Leuko. Essent. Fatty Acids 50:249-251.

    Arruzazabala M.L., Carbajal D., Molina V., et al. (1993): Effect of policosanol on cerebral ischemia in mongolian gerbils: Role of prostacyclin and thromboxane A2. Prostaglandins Leukot. Essent. Fatty Acids 49:695-697.

    Negre-Aminou, P. et al. Antiproliferative potencies of 6 vastatins in cultured human cells: involvement of the ras-mediated signalling pathway. Presented at the 66th Congress of the European Atherosclerosis Society 1996; July 13-17, Florence): 120.

    Noa M., Mas R., and Magraner J. (1994): Effect of policosanol on lipofundin-induced lesions in rats. J. Pharm. Pharmacol. 47:289-291.

    Noa M., Mas R. and Mesa A. del R. (1997): Effect of policosanol in circulating endothelial cell in experimental models in Sprague-Dawley rats and in rabbits. Br. J. Nutr. 49:999-1002.

    Noa M, Mas R, Mesa R. (1998): Effect of policosanol on intimal thickening in rabbit cuffed carotid artery. Int. J. Cardiol. 67(2):125-32,

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

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

    Batista J., Stusser I. L., Penichet M. and Uguet E. (1995): Doppler-ultrasound pilot study of the effects of long-term policosanol therapy on carotid-vertebral atherosclerosis. Curr. Ther. Res. 56:906-914.

    Fraga V., Menendez R., Anior A.M., et al. (1997): Effect of policosanol on in vivo and in vitro rat liver microsomal lipid peroxidation. Arch. Medical Res. 28:355-360.

    Mas R., Menendez R., Fraga V., et al. (1997): Modification of rat lipoprotein peroxidation by oral administration of policosanol. Abstract from the 4th International Conference on Preventive Cardiology, June 29-July3. Can. J. Cardiol. 13:Suppl. B. 310B.

    Hernandez F., Illnait J., Mas R., et al. (1992): Effects of policosanol on serum lipids and lipoproteins in healthy volunteers. Curr. Ther. Res. 51:568-575.

    Pons P., Mas R., Illnait J., et al. (1992): Efficacy and safety of policosanol in patients with primary hypercholesterolemia. Curr. Ther. Res. S2:507-513.

    Pons P., Rodriguez M., Robaina C., et al. (1994): Effects of successive dose increases of policosanol on lipid profile of patients with type-II hypercholesterolemia and tolerability to treatment. J. Clin. Pharmacol. Res. 14:27-33.

    Aneiros E. Calderon B., Mas R., et al. (1993): Effects of successive dose increases of policosanol on the lipid profile and tolerability of treatment. Curr. Ther. Res. 54:304-312.

    Aneiros E. Calderon B., Mas R., et al. (1995), Effect of policosanol in cholesterol-lowering levels in patients with type-II hypercholesterolemia. Curr. Ther. Res. 56:176-182.

    Pons P., Rodriguez M., Mas R., et al. (1994): One-year efficacy and safety of policosanol in patients with type-II hypercholesterolemia. Curr. Ther. Res. 55:1084-1092.

    Castano G., Mas R., Nodarse M., et al. (1995): One-year study of the efficacy and safety of policosanol (5 mg twice daily) in the treatment of type II hypercholesterolemia. Curr. Ther. Res., 56:296-304.

    Canetti M., Morera M., Illnait J., et al. (1995): One year study on the effect of policosanol (5 mg-twice-a-day) on lipid profile in patients with type II hypercholesterolemia. Adv. Ther. 12:245-254.

    Canetti M., Morera M., Illnait J., et al. (1995): A two year study on the efficacy and tolerability of policosanol in patients with type II hypercholesterolemia. Intern. J. Clin. Pharmacol. Res. 15:159-165.

    Canetti M., Morera M., Mas R., et al. (1997): Effects of policosanol on primary hypercholesterolemia: A 3-year open follow-up. Curr. Ther Res. 58:868-75.

    Benitez M., Romero C., Mas R., et al. (1997): A comparative study of policosanol vs pravastatin in patients with type-II hypercholesterolemia. Curr. Ther. Res. 58:859-67.

    Ortensi G., Gladstein J., Vail H. and Tesone P.A. (1997): A comparative study of policosanol vs. simvastatin in elderly patients with hypercholesterolemia. Curr. Ther. Res. 58:390-401.

    Illnait J., Castano G., Mas R. and Fernandez J.C. (1997): A comparative study on the efficacy and tolerability of policosanol and simvastatin for treating type II hypercholesterolemia. Abstract front the 4th International Conference on Preventive Cardiology. June 29-July 3. Can. J. Cardiol. 13:Suppl. B, 342B.

    Alcocer L, Campos A., Mas R. and Fernandez L. (1997): A comparative study of policosanol vs acipimox in patients with type II hypercholesterolemia. Data on file.

    Pons P., Illnait J., Mas R., et al. (1997): A comparative study of policosanol versus probucol in patients with hypercholesterolemia. Curr. Ther. Res. 58:26-35.

    Torres O., Agramonte A. J., Illnait J., et al. (1995): Treatment of hypercholesterolemia in NIDDM with policosanol. Diabetes Care 18:393-397.

    Crespo N., Alvarez R., Mas R., et al. (1997): Effect of policosanol on patients with non-insulin-dependent diabetes mellitus and hypercholesterolemia: A pilot study. Curr. Ther. Res. 58:44-51.

    Castano G., Tula L., Canetti M., et al. (1996): Effects of policosanol in hypertensive patients with type II hypercholesterolemia. Curr. Ther. Res. 57:691-699. 

    Pons P., Jimenez A., Rodriguez M., et al. (1993): Effects of policosanol in elderly hypercholesterolemic patients. Curr. Ther. Res. 53:265-269.

    Castano G., Canetti M., Morera M., et al. (1995): Efficacy and tolerability of policosanol in elderly patients with type-II hypercholesterolemia: A 12 months study. Curr. Ther. Res. 56:819-828.

    Zordoya R., Tula L., Castano G., Mas R., et al. (1996): Effects of policosanol on hypercholesterolemic patients with disturbances on serum biochemical indicators of hepatic function. Curr. Ther. Res. 57:568-577.

    Davalos J.M., Mederos H., Rodriguez J., et al. (1996): Effect of policosanol in hypercholesterolemia due to nephrotic syndrome. X Latinoamerican Congress of Nephrology and Hypertension, 14 September, Santiago de Chile, Chile.

    Arruzazabala M. L., Carbajal D., Mas R. and Valdes S. (1997): Comparative study of policosanol, aspirin and the combination therapy policosanol-aspirin on platelet aggregation in healthy volunteers. Pharmacol Res 36(4):293-7.

    Stusser R., Batista J., Padron 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(9):469-73.

    Fernandez L., Mas R., Illnait J., Fernandez J.C. (1998): Policosanol: Results of a postmarketing surveillance study of 27,879 patients. Curr. Ther. Res. 59:7717-22.

    Aleman C.L., Mas R., Rodeiro I., et al. (1992): Acute, subchronic and chronic toxicology of policosanol in rats. Toxicol. Letters. Suppl.2:248.

    Rodriguez C., Mesa R., Mas R., et al. (1994): Study of policosanol oral chronic toxicity in male monkeys (Maraca arctoidcs). Food and Chem. Toxicol. 32:565-575.

    Mesa A. del R., Mas R., Noa M., et al. (1994): Toxicity of policosanol in Beagle dogs: one year study. Toxicol. Lett. 73:131-90.

    Aleman C.L., Mas R., Hernandez C., et al. (1994): A 12 months study of policosanol oral toxicity in Sprague-Dawley rats. Toxicol. Lett. 70:77-87.

    Aleman C.L., Noa M., Cerejido E., Mis R., Rodeiro L Hcrnindez C. and Briffis F. (1995): Carcinogenicity of policosanol in mice: A 18 months study. Fd. and Client. Toxicol., 33:573-578.

    Aleman C.L., Mas R., Noa M., et al. (1994): Carcinogenicity of policosanol in Sprague Dawley rats: A 24 months study. Teratog. Carcinog. and Mutag., 14:239-249.

    Rodriguez M.D. and Garcia H. (1994): Teratogenic and reproductive studies of policosanol in the rat and rabbit. Teratog., Carcinog. and Mutag., 14:107-113.

    Rodriguez M.D., Garcia H. (1998): Evaluation of peri- and post-natal toxicity of Policosanol in rats. Teratog Carcinog Mutagen 18(1):1-7.

    Rodriguez M.D., Sanchez M., Garcia H. (1997): Multigeneration reproduction study of policosanol in rats. Toxicol. Lett. 90:97-106. 61. Carbajal D, Arruzazabala M. L., Mas R., et al. (1998): Interaction policosanol-warfarin on bleeding time and thrombosis in rats. Pharmacol Res 38(2):89-91.


    Submitted by Guestarlene on
    June 30, 2011 - 10:03am

    I have a question. I have LDL of 136 and homocysteine of 11.6. My HDL is 81. my crp is o.48. Do you think that is bad?

    Submitted by Guest Virginia on
    November 28, 2011 - 2:10pm

    I had a blood test with the following results: IFG: "high"; triglycerides: 160 "high"; APOB: 175 "high". Does this show "size" of molecule? I understand that if they are "large", they "bounch" around and not as much of a concern, whereas if they are small it is more of a concern. Can you explain this more?
    My recent tests: Total cholesterol, 2/11: 209; 8/11: 311. HDL both times were 67 and 63. Triglycerides, 2/11: 140; 8/11: 193. LDL, 2/11: 114; 8/11: 209. Ratio: 2/11: 3.1; 8/11: 4.9. I do not want to take statins. Thank you.

    Submitted by Guest on
    June 27, 2012 - 7:10am

    Heart attack risk in dieting (Daily Express p1). People on extreme Atkins-style diets are putting themselves at risk of potentially fatal heart disease and strokes, experts warned yesterday. The controversial low carbohydrate-high protein eating plan is said to have dangerous long-term health effects. More than 43,000 Swedish women aged 30 to 49 were assessed over 15 years and 1,270 suffered a “cardiovascular event” such as heart disease, stroke and narrowing of the arteries. Cutting daily carbohydrate intake by just 20g, equivalent to a small bread roll, and increasing protein by 5g, or one boiled egg, increased the risk of cardiovascular disease by five per cent. But when the diet is followed to excess, the chances of heart disease, stroke or narrowed arteries soared by 60 per cent, it was claimed. Young women on such a strict regime are ¬particularly in danger, with increased risk of disease for years after coming off the diet. Professor Pagona Lagiou, of the University of Athens, who carried out the research, said: “Low-carbohydrate, high-protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are associated with increased risk of cardiovascular disease.” The research is published in the BMJ. Also reported in the Daily Mirror p31, The Daily Telegraph p8 and the Daily Mail p7.

    Submitted by Joan Zarbatany on
    January 17, 2015 - 5:32am
    Toronto ,

    I just noticed in this article that you mention "detox levels" of proteolytic enzymes. I take 3 phiZymes in the morning upon awakening and 3 before bedtime - all on an empty stomach. I'd be very interested in knowing what are considered to be "detox levels". Thank you for your kind reply to this question.

    Submitted by BaselineFoundation on
    January 20, 2015 - 12:40pm

    The back of the product gives more detailed information, or you can write to Baseline Nutritionals directly for any product related questions.  Thanks!

    Submitted by al dell on
    April 11, 2016 - 12:56pm
    burlington ,

    what is the material, generally, that restricts blood flow in the lowers legs ... and possibly is responsible for poorly-functioning valves. the result appears to be fluid buildup (seems more like water than blood) that then causes swelling and several other related abnormalities.
    what natural means could be employed daily to 'unclog' these smaller pathways? ... to reduce/eliminate the swelling, restore proper blood flow, allow for better functioning valves.
    apologize for the long message, but do not know the proper terminology. appreciate your help. bp=130/72, p=56, w=172#, h=73", age=74, and diet=fruit/nuts/seeds/veg's/grains/whole eggs + fish. only liquid is coffee+ h2o for processing. many txs, al.

    Submitted by BaselineFoundation on
    April 13, 2016 - 12:01pm

    Did you see this part of the article?

    • Proteolytic Enzymes. This is one of the most important things you can do. The regular use of proteolytic enzymes can help eliminate CICs from the body, reduce overall inflammation, dissolve accumulated plaque, and repair arterial scar tissue. Although the evidence is purely anecdotal at the moment, we have seen extraordinary results using detox levels of this formula.

Add New Comment