Milk Thistle / Artichoke Plus Powder


As you age, it becomes critically important to maintain an optimum balance between “good” and “bad” cholesterol, otherwise known as HDL and LDL, in order to maintain a healthy cholesterol profile.

Milk Thistle/Artichoke plus is formulated with extracts of artichoke leaf, Milk thistle seeds, red yeast rice powder and pantethine, the biologically active form of pantothenic acid, to maintain healthy HDL, LDL and total cholesterol levels already within the normal range.



ACACExtract of Amla fruit (Indian gooseberry). This standardized extract contains tannins that have been shown to improve endothelial function and safely help maintain healthy levels of all three key blood lipids — LDL, high-density lipoprotein (HDL), and triglycerides — as well as C-reactive protein. R

  1. Diabetes Metab Syndr Obes. 2013 Jul 26;6:275-84.



Benefits at a Glance

  • Promotes a healthy cholesterol profile
  • Supports an optimum balance between “good” and “bad” cholesterol
  • Supports a healthy heart and cardiovascular system

Balancing Good and Bad Cholesterol

As you age, it becomes critically important to maintain an optimum balance between “good” and “bad” cholesterol, otherwise known as HDL and LDL, in order to maintain a healthy cholesterol profile.

For those who seek a dietary way to support and balance healthy cholesterol levels, researchers have discovered two compounds that help promote healthy levels of both HDL and LDL already within normal range.1-4


Milk Thistle/Artichoke plus is formulated with extracts of artichoke leaf, Milk thistle seeds, red yeast rice powder and pantethine, the biologically active form of pantothenic acid,3 to maintain healthy HDL, LDL and total cholesterol levels already within the normal range.1-4


Artichoke Leaf Extract Optimizes Cholesterol Ratios

Today, health care practitioners believe that an optimal balance between good (HDL) and bad (LDL) cholesterol is key to maintaining a healthy cardiovascular system.5-7 The best way to achieve a healthy cholesterol balance is to optimize HDL and LDL cholesterol levels.

Clinical studies now demonstrate that artichoke leaf extract’s polyphenolic compounds2 support optimal HDL/LDL ratios already within normal range.1,2

Pantethine Supports Healthy Cholesterol Profiles

Pantethine is the biologically active form of pantothenic acid or vitamin B5. Clinical trials show pantethine maintains LDL and total cholesterol already within the normal range, without reducing protective CoQ10 levels.3


  1. Arzneimittelforschung. 2000 Mar;50(3):260-5.
  2. Int J Food Sci Nutr. 2013 Feb;64(1):7-15.
  3. Vasc Health Risk Manag. 2014;10:89-100.
  4. Nutr Res. 2011 Aug;31(8):608-15.
  5. J Am Coll Cardiol. 2009 Dec 29;55(1):35-41.
  6. Kardiol Pol. 2015 May 19. doi: 10.5603/KP.a2015.0086.
  7. Am J Med Sci. 2012 Jan;343(1):40-5


The liver is a large glandular organ, whose functions include decomposition of red blood cells, plasma protein synthesis, hormone production, secretion of bile, and conversion of sugars into glycogen, which it stores. The liver is also responsible for processing many vitamins and nutrients into a form that can be utilized by the body, as well as detoxification of various substances. Modern living involves daily exposure to substances that are toxic to our bodies, which imposes a heavy load on the liver. Therefore, a healthy liver is critical to well-being. Certain lifestyle risks and medical conditions make it all the more important to ensure that the liver is being maintained at its functional best.

In Europe and Asia, herbal liver tonics have been in common use for centuries. The effectiveness of the herbs used has been validated during the past decades through modern research and clinical studies. These herbs generally contain antioxidants, cell membrane-stabilizing agents, bile secretion-enhancing compounds, or nutrients that inhibit the depletion of endogenous antioxidants such as glutathione. Hepatoprotection is beneficial not only for the liver but also for the overall health and vitality of the body.

Silymarin is the major active compound from milk thistle extract (Silybum marianum), a member of the Compositaeor daisy family.1 Silymarin is considered a flavonolignan mixture which is a unique type of bioflavonoid and an antioxidant that scavenges damaging free radicals. Scientific studies show that oral supplementation with silymarin can help support liver function.2-7 Silymarin has been shown to combat lipid peroxidation in the liver.6-9 It has also been demonstrated that silymarin may help promote healthy liver cells.3


  1. Phytother Res. 2010 Oct;24(10):1423-32.
  2. Bratisl Lek Listy. 2012;113(3):145-51.
  3. J Vet Intern Med. 2012 Nov 9. doi: 10.1111/jvim.12002.
  4. J Oncol Pharm Pract. 2012 Sep;18(3):360-5.
  5. Phytomedicine. 2009 May;16(5):391-400.
  6. Int J Clin Pharmacol Ther. 2002 Jan;40(1):2-8.
  7. J Hepatol. 1997 Apr;26(4):871-9.
  8. J Agric Food Chem. 2008 Jun 11;56(11):3966-72.
  9. Arzneimittelforschung. 1998 Mar;48(3):236-9


Inhibiting Cholesterol Synthesis

Pantethine and its metabolites appear to act on the body’s fat and cholesterol metabolism pathways. Pantethine is a derivative of pantothenic acid (vitamin B5), and can serve as a source of the vitamin. One notable function of vitamin B5 is its conversion into coenzyme A, a necessary factor in the metabolism of fatty acids into cellular energy. The pantethine derivative cysteamine may also function to reduce the activity of liver enzymes that produce cholesterol and triglycerides.1 Studies of pantethine consumption have demonstrated significant reductions in total- and LDL cholesterol (up to 13.5%), triglycerides, and elevation of HDL-C in hypercholesterolemic subjects (individuals with high cholesterol)2,3 and diabetic subjects4 when taken at 900-1,200 mg/day, although significant effects on triglycerides have been observed at dosages as low as 600 mg/day.5


Red yeast rice is a traditional preparation of rice fermented by the yeast Monascus purpureus. The yeast produces metabolites (monacolins) that are naturally-occuring HMG-CoA Reductase inhibitors (one of these, monacolin K, is chemically identical to lovastatin6). A comprehensive review of 93 randomized trials including nearly 10,000 patients has demonstrated that commercial preparations of red yeast rice produced reduction in total cholesterol, LDL-C, triglycerides, and an increase in HDL-cholesterol.7 A long-term (4.5 year) multicenter study of nearly 5,000 patients with a previous heart attack and high total cholesterol levels demonstrated that a commercial red yeast rice preparation reduced the incidence of major coronary events, including nonfatal heart attack and cardiovascular mortality, when compared to placebo.8 Red yeast rice extracts have also been shown to be well tolerated and effective in lowering LDL in patients with statin intolerance.9,10

Due to regulations regarding their labeling in the US, standardization of commercial red yeast rice preparations for monacolins is problematic, thus levels of monacolins can vary dramatically between red yeast rice products.11 There are some standardized red yeast rice products that are standardized for monacolin K content.


Indian Gooseberry (Amla; Emblica officinalis) has been used traditionally as a nutrient-dense food in Indian regions, and in Ayurvedic medicine for treating a variety of conditions. Modern scientific inquiry has revealed considerable evidence in support of the medicinal use of this nutritional powerhouse. Analytical studies on extracts of Indian Gooseberry highlight its potent antioxidant properties;12 animal studies carry these findings forward by showing that orally administered amla extract significantly reduce levels of oxidized LDL.13,14 In human studies, extracts of amla have been shown to attenuate elevations in LDL, total cholesterol, and triglycerides, and boost levels of protective HDL.15 In a study examining the antioxidant activity of amla extract in subjects with metabolic abnormalities, four months of supplementation was shown to dramatically bolster plasma antioxidant power and suppress oxidative stress.16

Studies suggest that amla extract may also protect against LDL glycation by modulating blood glucose levels. In diabetic patients amla not only significantly reduced post-prandial glucose levels, but also lowered lipid and triglyceride levels over a 21 day period17. In an animal model of metabolic syndrome induced by a high fructose diet, concomitant administration of amla extract reined in rising cholesterol and triglyceride levels, and also significantly repressed the expression of inflammation-related genes, which are typically elevated in metabolic syndrome models.18 Extracts of the antioxidant-rich fruit also reduce levels of advanced glycation end products (AGEs), which are formed by the same process as glycated LDL.19 By limiting the amount of LDL particles that become glycated, amla may help maintain proper cellular uptake of cholesterol and reduce the amount of LDL-C available to infiltrate the arterial wall.


Plant sterols (phytosterols) are steroid compounds found in plants that function similarly to cholesterol in animals (as components of plant cell membranes, and precursors to plant hormones). Like cholesterol, they can exist as free molecules or as sterol- esters. Esters of sterols have a higher activity and better fat solubility, which allows for lower effective dosages (2-3 g/day as opposed to 5-10 g/day for unesterified sterols).20Sterols themselves are poorly absorbed from the diet, but because of their chemical similarity to cholesterol, they are thought to compete with cholesterol for absorption in the intestines, which has the net effect of reducing LDL levels.21 Sterols may also reduce cholesterol production in the liver, reduce the synthesis of VLDLs, increase LDL particle size, and increase LDL uptake from the blood22,23 HDL and/or very low-density lipoproteins are generally not affected by sterol intake.24

There have been numerous studies of the effects of sterol esters on reducing mean total cholesterol and LDL-C cholesterol in healthy, hypercholesterolemic, and diabetic individuals. An analysis of 57 trials involving over 3600 individuals has reported an average LDL-C reduction of 9.9% at a mean intake of 2.4 g sterol esters/day.25 Sufficient evidence of the cholesterol-lowering effects of sterols has prompted the US Food and Drug Administration to permit the health claim that sterol esters may be associated with a reduced risk of coronary heart disease, when taken at sufficient levels in the context of a healthy diet, one of only 12 permissible health claims granted by this organization26


 Coenzyme Q10 (CoQ10). The generation of chemical energy in the form of ATP by the mitochondrial electron transport chain is essential for the existence of life as we know it. Delicate endothelial cells that line the arterial walls depend on healthy mitochondrial function to control blood pressure and vascular tone. Oxidized or glycated LDL can sabotage endothelial mitochondrial function and damage the endothelial barrier, setting the stage for the atherosclerotic cascade to initiate.27,28 CoQ10 is an integral component of mitochondrial metabolism, serving as an intermediary transporter between two major check points along the road to ATP production. Interestingly, CoQ10 is also the only known endogenously synthesized lipid soluble antioxidant,29and is thus incorporated into LDL particles, where it serves to protect against oxidation. Because of these dual roles insufficient levels of CoQ10 expedite atherogenesis from two angles – by limiting mitochondrial efficiency in endothelial cells and leaving LDL particles vulnerable to oxidative damage.

As noted above, statin drugs, which are typically used to treat high cholesterol, ironically also suppress levels of CoQ10 in the blood.30 Individuals taking a statin drug should always supplement with CoQ10.


Carotenoids are common constituents of the LDL particle. ß-carotene is the second most abundant antioxidant in LDL; other common dietary carotenoids (lycopene, lutein) may be transported by LDL particles as well.31 Together, these three carotenoids have an indispensable role in the protection of LDL particles from oxidative damage; their serum levels have been demonstrated to be the most predictive of the degree of LDL oxidation in humans.32 Carotenoids may also possess additional lipid-lowering activities independent of their antioxidant potential. The best-studied in this respect is lycopene; an analysis of 12 human trials of lycopenereveals an average reduction in LDL-C of approximately 12%.33 Potential mechanisms for this action are suppression of cholesterol synthesis by the inhibition of the HMG-CoA reductase enzyme, or an increase in the rate of LDL degradation.34 Astaxanthin, a carotenoid found in some fish and marine oils, can increase HDL.35


Pomegranate is now widely viewed as a superfruit with a myriad of health benefits, and rightfully so; dozens of placebo controlled clinical trials have been carried out on pomegranate juice, or pomegranate extract. With respect to lipid management, the efficacy of pomegranate is rivaled by very few natural compounds. The high concentration of polyphenols (particularly punicalagins) in pomegranate make it an ideal ingredient for suppressing LDL oxidation.36,37

Consumption of pomegranate polyphenols significantly lowered total and LDL cholesterol concentrations while maintaining HDL levels in subjects with elevated cholesterol profiles.38 Pomegranate also suppresses immunoreactivity against oxidized LDL, a mechanisms which would be expected to limit plaque formation in the intimia.39 In fact, this is exactly what was shown in a long-term study of pomegranate consumption. Subjects received either pomegranate juice or placebo for three years; in the group receiving the placebo, carotid intima media thickness (cIMT; a measure of atherosclerosis) increased by 9% one year after study initiation, while in the group receiving pomegranate, cIMT was reduced by an astonishing 30%. Moreover, pomegranate significantly reduced oxidized LDL concentrations, and increased serum antioxidant activity, compared to placebo, while simultaneously lowering blood pressure. This study also showed that pomegranate nearly doubled the activity of paraoxonase-1 (PON-1), an antiatherogenic enzyme that optimizes the function of HDL and protects lipids from oxidative damage.40 Both groups in this study continued on standard therapy that may have included statins, anti-hypertensives, etc.


Polyphenols are a diverse set of phytonutrients that are ubiquitous in the diet. Polyphenol intake has been associate with lower risk of cardiovascular mortality, and may partially explain the health benefits of several common foods (tea, fruits, vegetables, wine, chocolate).41 Flavonoids, the largest and best studied class of polyphenols, include catechins from green tea and chocolate, theaflavins from black tea, soy isoflavones, flavan-3-ol polymers from red wine, and anthocyanidins from grapes and berries. A systematic analysis of over 130 human studies of flavonoids revealed significant improvements in endothelial function (cocoa and black tea polyphenols) and blood pressure (anthocyanidins, isoflavones, cocoa); however, only green tea catechins exhibited significant cholesterol (LDL-C) lowering in this analysis (averaging about 9 mg/dL over 4 studies).42Subsequently, a study of black tea extract in 47 mildly hypercholesterolemic Japanese men and women demonstrated an 8% reduction in total cholesterol and 13% drop in LDL-C after 3 months.43

Other polyphenolic compounds with significant lipid modification potential based on human studies include methylated citrus flavonoids (polymethoxyflavones), which were shown to lower total-cholesterol, LDL-C, and triglycerides by 27%, 25%, and 31%, respectively when combined with tocotrienols in a small pilot trial.44Additionally, the red wine polyphenol resveratrol was shown to incorporate into the LDL particles of human volunteers following ingestion of a high-resveratrol wine, potentially acting as a resident antioxidant.45 This is consistent with resveratrol’s role in the prevention of LDL oxidation observed in humans.46


Curcumin has a variety of protective roles in CVD, potentially reducing oxidative stress, inflammation, and the proliferations of smooth muscle cells and monocytes. 95 Small human trials studies have revealed the effects of curcumin on reducing in lipid peroxidation47,48 and plasma fibrinogen,49 both factors in the progression of atherosclerosis.50 Curcumin may also reduce serum cholesterol by increasing the production of the LDL receptor,51,52 but despite successes in animal models, human data on the antihypercholesterolemic effects of curcumin is conflicting. A small study of 10 healthy volunteers revealed significant decreases in lipid oxidation products (-33%) and total cholesterol (-12%), with a concomitant increase in HDL-C (29%) when using 500 mg curcumin daily for 7 days.53 In two subsequent studies, low-dose curcumin showed a non-significant trend toward lowering total- and LDL-C in acute coronary patients,54 while high dose-curcumin (1-4 g/day) exhibited non-significant increases in total-, LDL-, and HDL cholesterol.55


Enhancing Cholesterol Elimination

Artichoke has traditional usage as a liver protectant and choleretic (compound that stimulates bile flow). In stimulating bile flow, artichoke may aid the body in the disposal of excess cholesterol. In vitro studies suggest its anti-atherosclerotic effects may also be linked to an antioxidant capacity that reduces LDL oxidation, or the ability of one of its constituents, luteolin, to indirectly inhibit HMG-CoA reductase.56

In addition to several uncontrolled human studies and case reports,57 several randomized, controlled trials support the ability of artichoke extract to lower total- and/or LDL-cholesterol. In one trial, artichoke extract (1800 mg/day) for six weeks reduced total cholesterol (-9.9%) and LDL-C (-16.6%) in 71 hypercholesterolemic patients, with no differences in HDL-C or triglycerides.58 In another, also in hypercholesterolemic patients, 1280 mg artichoke extract per day for 12 weeks reduced total cholesterol by 6.1% when compared with a control group. Changes in LDL-C, HDL-C, and triglycerides were insignificant.59 Some studies indicate artichoke supplementation can raise HDL levels.104,105 Artichoke extract also improved parameters of endothelial function in a small human trial.62


Niacin/Nicotinic acid (vitamin B3) is an essential nutrient with roles throughout human metabolism. At dosages substantially above the recommended daily intake (RDI), prescription niacin treatments can significantly raise HDL-C (by 30-35% in some cases, at dosages averaging 2.25 grams/day).61,62 Niacin can also change the distribution of LDL by increasing the amount of large buoyant LDL and reducing the amount of small dense LDL.63 Niacin can also reduce the susceptibility of LDL to oxidation.64

In 2010, the results of seven published studies on the effects of niacin therapy were combined to examine the overall effect. This meta-analysis is considered more powerful than an individual study because it increases the sample size. The results showed that patients taking niacin (compared with a placebo) had significant reductions in nonfatal myocardial infarction and and transient ischemic attack.65

On May 26, 2011, the National Institutes of Health stopped a clinical trial of a prescription-strength level of niacin one year prior to its projected completion. The participants were 3400 patients with stable heart disease, well-controlled LDL, and elevated triglycerides. They added high dose, extended release niacin to their statin therapy. The level of niacin used in the study was much higher than that contained in dietary supplements. As shown in previous studies, the niacin drug successfully elevated HDL and lowered triglycerides, but failed to reduce the risk for heart attack or stroke.

Fish Oil, is a source of omega-3 fatty acids (eicosapentaenoic acid — EPA, and docosahexaenoic acid — DHA), which cannot be synthesized by humans but are nonetheless essential for several metabolic processes. Aside from reductions in the risk of cardiovascular mortality and non-fatal cardiovascular events (supported by studies of tens of thousands of moderate and high risk patients)66, fish oil fatty acids significantly reduce serum triglycerides. Forty-seven studies, comprising over 15,000 patients, have confirmed an average triglyceride reduction of 30 mg/dL, at an average intake of 3.35g EPA+DHA over 24 weeks.67 Triglycerides were reduced in a dose-dependent manner, and were dependent on baseline levels (reductions of greater than 40% were observed in patients with the highest starting triglyceride levels). Slight increases in LDL-C and HDL-C were also observed in these studies, although other large analyses failed to detect any significant effects of fish oil on cholesterol.68 The mechanism by which EPA + DHA lowers triglycerides thought to be by slowing the release of VLDL particles into the plasma, or increasing lipid degradation and clearance of triglyceride-rich lipoproteins from the blood.69 Lowering triglyceride levels is a known strategy for increasing the amount of large buoyant LDL and reducing the amount of small dense LDL.

Prescription fish oil uses a highly concentrated EPA+DHA fish oil ester that provides a dosage of 3.36 g of omega-3 in 4 capsules; its degree of triglyceride reduction (up to 45%) is similar to non-prescription fish oil at a similar dose (usually requiring several more capsules.)69 Non-prescription fish oil supplements sell at a fraction of the price of prescription fish oil and usually require one or more additional capsules to be taken daily to obtain the same amount of EPA/DHA.


Alpha-cyclodextrin is a soluble fiber from corn that has received much attention for its ability to bind to dietary fats and prevent their absorption.87-89 In early animal research, rats fed a high-fat diet had reductions in triglyceride and total cholesterol levels when alpha-cyclodextrin was added to their food. The addition of alpha-cyclodextrin resulted in less weight gain, reductions in plasma cholesterol and triglycerides, restored insulin sensitivity, and normalized leptin levels.88 Results from an animal study found alpha-cyclodextrin lowered total cholesterol, with an apparent ability to selectively lower pro-atherogenic apoB lipoprotein, while leaving protective HDL cholesterol unchanged. Studies in rodent models have also revealed alpha-cyclodextrin may have a special affinity to bind atherogenic saturated and trans-fatty acids rather than unsaturated fatty acids.89,90

Beneficial effects of alpha-cyclodextrin have been borne out in human studies. For instance, in a double-blind placebo-controlled clinical trial, 66 obese diabetic patients took either 2 g alpha-cyclodextrin or placebo with each fatty meal for three months. At the end of the study, subjects with hypertriglyceridemia in the alpha-cyclodextrin group had reductions in total cholesterol levels, while cholesterol levels rose in the placebo group. Adiponectin levels rose in the alpha-cyclodextrin group but fell in the placebo group; and subjects in the alpha-cyclodextrin group maintained their weight, while those in the placebo group gained weight.91 In a controlled clinical trial in 28 healthy adults, taking alpha-cyclodextrin with fat-containing meals for 30 days resulted in significant reductions in levels of total cholesterol, LDL cholesterol, and weight. Weight loss was over 90% greater in the alpha-cyclodextrin group compared with the control group. Insulin and apolipoprotein B levels also fell in the alpha-cyclodextrin group. Importantly, no adverse effects were reported. Alpha-cyclodextrin forms a complex with fats, and while it does increase excretion of fat in the stool, it does not appear to cause the fecal incontinence commonly seen with use of medications that block dietary fat digestion.87,89,92


Probiotics are increasingly recognized for their critical role in regulating immune activity, reducing inflammation throughout the body, and have attracted interest for their ability to reduce LDL cholesterol and cardiovascular risk. A review of research found that, of the probiotic strains studied, Lactobacillus reuteri (L. reuteri) NCIMB 30242 has excellent evidence for reducing cardiac risk by safely lowering levels of total and LDL cholesterol as well as markers of inflammation.93

In a randomized controlled trial, 114 participants with high cholesterol levels who were otherwise healthy consumed either a probiotic yogurt providing 2.8 billion colony forming units of microencapsulated L. reuteriNCIMB 30242 or a control yogurt daily for six weeks. The L. reuteri group had reductions in total cholesterol (9%) and LDL-cholesterol (5%), levels relative to the placebo yogurt group. ApoB100, which at high levels is associated with vascular disease, was significantly reduced in the L. reuteri group.94,95 In another controlled clinical trial on 127 healthy adults with high cholesterol levels, subjects received either capsules of L. reuteriNCIMB 30242 or placebo for nine weeks. Those taking the L. reuteri probiotic had a greater than 9% drop in total cholesterol and a drop in LDL cholesterol levels of over 11.5% compared with placebo. The ratio of apoB-100 to apoA-1 fell by 9% in the L. reuteri-supplemented group compared with placebo. The apoB-100:apoA-1 ratio is a strong predictor of cardiovascular risk, particularly in overweight and obese individuals.96,97 High-sensitivity C-reactive protein and fibrinogen, additional markers of cardiovascular risk, were also significantly reduced relative to placebo.98 Interestingly, later analyses of the results from this study identified two other attributes of L. reuteri: subjects taking the probiotic experienced general improvement in functional gastrointestinal symptoms99 and a significant increase in levels of vitamin D compared with placebo.100

Although the exact mechanism by which L. reuteri NCIMB 30242 improves lipid levels has not yet been fully characterized, it is known that intestinal microbes have a role in regulating cholesterol transport and metabolism, and this effect may in part depend on an ability to break down bile acids in the digestive tract.93,98 Bile acids have a close relationship with intestinal microbiota and help regulate cholesterol synthesis and lipid and glucose metabolism.101,103 By increasing bile acid breakdown and excretion, L. reuteriis thought to stimulate cholesterol-dependent bile acid production in the liver, removing cholesterol from circulation.102




  1. McCarty MF. Inhibition of acetyl-CoA carboxylase by cystamine may mediate the hypotriglyceridemic activity of pantethine. Medical Hypotheses 2001;56(3):314-317.
  2. Bertolini S, Donati C, Elicio N, Daga A, Cuzzolaro S, Marcenaro A, Saturnino M, Balestreri R. Lipoprotein changes induced by pantethine in hyperlipoproteinemic patients: adults and children. Int J Clin Pharmacol Ther Toxicol 1986 Nov;24(11):630-7
  3. Gaddi A, Descovich GC, Noseda G, et al. Controlled evaluation of pantethine, a natural hypolipidemic compound, in patients with different forms of hyperlipoproteinemia. Atherosclerosis 1984 Jan;50(1):73-83
  4. Donati C, Bertieri RS, Barbi G. Pantethine, diabetes mellitus and atherosclerosis. Clinical study of 1045 patients Clin Ter 1989 Mar 31;128(6):411-22
  5. Tonutti L, Taboga C, Noacco C. Comparison of the efficacy of pantethine, acipimox, and bezafibrate on plasma lipids and index of cardiovascular risk in diabetics with dyslipidemia. Minerva Med 1991 Oct;82(10):657-63
  6. Cunningham E. Is Red Yeast Rice Safe and Effective for Lowering Serum Cholesterol? J Am Diet Assoc 2011 Feb.;111(2):324.
  7. Liu J, Zhang J, Shi Y, Grimsgaard S, Alraek T, Fønnebø V. Chinese red yeast rice(Monascus purpureus) for primary hyperlipidemia: a meta-analysis of randomized controlled trials. Chin Med 2006;1(1):4.
  8. Lu Z, Kou W, Du B, Wu Y, Zhao S. Effect of Xuezhikang, an extract from red yeast Chinese rice, on coronary events in a Chinese population with previous myocardial infarction. The American journal of … 2008;
  9. Becker D, Gordon R, Halbert S et al. Red yeast rice for dyslipidemia in statin-intolerant patients: a randomized trial. Ann Intern Med. 2009 Jun 16;150(12):830-9, W147-9.
  10. Halbert SC, French B, Gordon RY, et al. Tolerability of red yeast rice (2,400 mg twice daily) versus pravastatin (20 mg twice daily) in patients with previous statin intolerance. Am J Cardiol 2010 Jan.;105(2):198-204.
  11. Gordon RY, Cooperman T, Obermeyer W, Becker DJ. Marked variability of monacolin levels in commercial red yeast rice products: buyer beware! Arch Intern Med 2010 Oct.;170(19):1722-1727.
  12. Nampoothiri SV et al. In vitro antioxidant and inhibitory potential of Terminalia bellerica and Emblica officinalis fruits against LDL oxidation and key enzymes linked to type 2 diabetes. Food Chem Toxicol. 2011 Jan;49(1):125-31.
  13. Kim HJ et al. Influence of amla (Emblica officinalis Gaertn.) on hypercholesterolemia and lipid peroxidation in cholesterol-fed rats. J Nutr Sci Vitaminol (Tokyo). 2005 Dec;51(6):413-8.
  14. Yokozawa T et al. Amla (Emblica officinalis Gaertn.) prevents dyslipidaemia and oxidative stress in the ageing process. Br J Nutr. 2007 Jun;97(6):1187-95.
  15. 75. Akhtar MS et al. Effect of Amla fruit (Emblica officinalis Gaertn.) on blood glucose and lipid profile of normal subjects and type 2 diabetic patients. Int J Food Sci Nutr. 2011 Apr 18.
  16. Chen TS et al. Supplementation of Emblica officinalis (Amla) extract reduces oxidative stress in uremic patients. Am J Chin Med. 2009;37(1):19-25.
  17. Kim HY et al. The protective role of amla (Emblica officinalis Gaertn.) against fructose-induced metabolic syndrome in a rat model. Br J Nutr. 2010 Feb;103(4):502-12.
  18. Rao TP et al. Amla (Emblica officinalis Gaertn.) extracts reduce oxidative stress in streptozotocin-induced diabetic rats. J Med Food. 2005 Fall;8(3):362-8.
  19. Badimon L, Vilahur G, Padro T. Nutraceuticals and atherosclerosis: human trials. Cardiovasc Ther 2010 Aug.;28(4):202-215.
  20. Shrestha S, Freake HC, McGrane MM, Volek JS, Fernandez ML. A combination of psyllium and plant sterols alters lipoprotein metabolism in hypercholesterolemic subjects by modifying the intravascular processing of lipoproteins and increasing LDL uptake. J Nutr 2007 May;137(5):1165-1170.
  21. Badimon L, Vilahur G, Padro T. Nutraceuticals and atherosclerosis: human trials. Cardiovasc Ther 2010 Aug.;28(4):202-215.
  22. Normén L, Holmes D, Frohlich J. Plant sterols and their role in combined use with statins for lipid lowering. Curr Opin Investig Drugs. 2005;6:307–16.
  23. Electronic Code of Federal Regulations (
  24. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA 2001;285(19):2486-2497.
  25. Lichtenstein AH. Summary of American Heart Association Diet and Lifestyle Recommendations Revision 2006. Arteriosclerosis, Thrombosis, and Vascular Biology 2006 Oct.;26(10):2186-2191.
  26. Ulbricht C, Basch E, Szapary P, et al. Natural Standard Research Collaboration. Guggul for hyperlipidemia: a review by the Natural Standard Research Collaboration. Complement Ther Med 2005 Dec.;13(4):279-290.
  27. Reaven P, Witztim J. Oxidized Low Density Lipoproteins in Atherogenesis: Role of Dietary Modification. Annual Reviews in Nutrition 1996 Feb.;16:51-70.
  28. Karppi J, Nurmi T, Kurl S, Rissanen TH, Nyyssönen K. Lycopene, lutein and beta-carotene as determinants of LDL conjugated dienes in serum. Atherosclerosis 2010 Apr.;209(2):565-572.
  29. Ried K, Fakler P. Protective effect of lycopene on serum cholesterol and blood pressure: Meta-analyses of intervention trials. Maturitas 2011 Apr.;68(4):299-310.
  30. Fuhrman B, Elis A, Aviram M. Hypocholesterolemic effect of lycopene and beta-carotene is related to suppression of cholesterol synthesis and augmentation of LDL receptor activity in macrophages. Biochem Biophys Res Commun 1997 Apr.;233(3):658-662.
  31. Yoshida H, Yanai H, Ito K, et al. Administration of natural astaxanthin increases serum HDL-cholesterol and adiponectin in subjects with mild hyperlipidemia. Atherosclerosis 2010 Apr.;209(2):520-523.
  32. Badiou S et al. Vitamin E supplementation increases LDL resistance to ex vivo oxidation in hemodialysis patients. Int J Vitam Nutr Res. 2003 Jul;73(4):290-6.
  33. Tesoriere L et al. Oral supplements of vitamin E improve measures of oxidative stress in plasma and reduce oxidative damage to LDL and erythrocytes in beta-thalassemia intermedia patients. Free Radic Res. 2001 May;34(5):529-40.
  34. Li D, Saldeen T, Romeo F, Mehta JL. Relative effects of alpha- and gamma-tocopherol on low-density lipoprotein oxidation and superoxide dismutase and nitric oxide synthase activity and protein expression in rats. J Cardiovasc Pharmacol Ther. 1999 Oct;4(4):219-26.
  35. McCarty MF. Gamma-tocopherol may promote effective no synthase function by protecting tetrahydrobiopterin from peroxynitrite. Med Hypotheses. 2007;69(6):1367-70.
  36. Saito F, Iwamoto S, Yamauchi R. Reaction products of gamma-tocopherol with (E)-4-oxo-2-nonenal in acidic acetonitrile. Biosci Biotechnol Biochem. 2010;74(1):168-74.
  37. Singh I, Turner AH, Sinclair AJ, Li D, Hawley JA. Effects of gamma-tocopherol supplementation on thrombotic risk factors. Asia Pac J Clin Nutr. 2007;16(3):422-8.
  38. Aviram M, Dornfeld L, Kaplan M, et al. Pomegranate juice flavonoids inhibit low-density lipoprotein oxidation and cardiovascular diseases: studies in atherosclerotic mice and in humans. Drugs Exp Clin Res 2002;28(2-3):49-62.
  39. Sezer ED, Akçay YD, Ilanbey B, Yildirim HK, Sözmen EY. Pomegranate wine has greater protection capacity than red wine on low-density lipoprotein oxidation. J Med Food 2007 Jun.;10(2):371-374.
  40. Esmaillzadeh A et al. Cholesterol-lowering effect of concentrated pomegranate juice consumption in type II diabetic patients with hyperlipidemia. Int J Vitam Nutr Res. 2006 May;76(3):147-51.
  41. Fuhrman V et al. Pomegranate juice inhibits oxidized LDL uptake and cholesterol biosynthesis in macrophages. J Nutr Biochem. 2005 Sep;16(9):570-6.
  42. Aviram M et al. Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation. Clin Nutr. 2004 Jun;23(3):423-33.
  43. Badimon L, Vilahur G, Padro T. Nutraceuticals and atherosclerosis: human trials. Cardiovasc Ther 2010 Aug.;28(4):202-215.
  44. Hooper L, Kroon PA, Rimm EB, et al. Flavonoids, flavonoid-rich foods, and cardiovascular risk: a meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition 2008 Jul.;88(1):38-50.
  45. Jujita H, Yamagami T. Antihypercholesterolemic effect of Chinese black tea extract in human subjects with borderline hypercholesterolemia. Nutr Res 2008, 28:450–456.
  46. Roza J, Xian-Liu Z. Effect of citrus flavonoids and tocotrienols on serum cholesterol levels in hypercholesterolemic subjects. Health Med 2007;
  47. Urpí-Sardà M, Jáuregui O, Lamuela-Raventós RM, et al. Uptake of diet resveratrol into the human low-density lipoprotein. Identification and quantification of resveratrol metabolites by liquid chromatography coupled with tandem mass spectrometry. Anal. Chem. 2005 May;77(10):3149-3155.
  48. Nigdikar S, Williams N, Griffin B. Consumption of red wine polyphenols reduces the susceptibility of low-density lipoproteins to oxidation in vivo. The American journal … 1998;
  49. Ramirez Boscá A, Soler A, Gutierrez MC. Antioxidant curcuma extracts decrease the blood lipid peroxide levels of human subjects. Age; Volume 18, Number 4, 167-169.
  50. Ramirez Boscá A, Carrión-Gutiérrez MA, et al. Effects of the antioxidant turmeric on lipoprotein peroxides: Implications for the prevention of atherosclerosis. Age1997 Jul.;20(3):165-168.
  51. Ramirez Boscá A, Soler A, Carrión-Gutiérrez MA, et al. An hydroalcoholic extract of Curcuma longa lowers the abnormally high values of human-plasma fibrinogen. Mech Ageing Dev 2000 Apr.;114(3):207-210.
  52. Wongcharoen W, Phrommintikul A. The protective role of curcumin in cardiovascular diseases. Int. J. Cardiol. 2009 Apr.;133(2):145-151.
  53. Dou X, Fan C, Wo L, et al. Curcumin up-regulates LDL receptor expression via the sterol regulatory element pathway in HepG2 cells. Planta Med 2008 Sep.;74(11):1374-1379.
  54. Peschel D, Koerting R, Nass N. Curcumin induces changes in expression of genes involved in cholesterol homeostasis. J Nutr Biochem 2007 Feb.;18(2):113-119.
  55. Soni KB, Kuttan R. Effect of oral curcumin administration on serum peroxides and cholesterol levels in human volunteers. Indian J. Physiol. Pharmacol. 1992 Oct.;36(4):273-275.
  56. Alwi I, Santoso T, Suyono S, et al. The effect of curcumin on lipid level in patients with acute coronary syndrome. Acta Med Indones 2008 Oct.;40(4):201-210.
  57. Baum L, Cheung SKK, Mok VCT, et al. Curcumin effects on blood lipid profile in a 6-month human study. Pharmacol. Res. 2007 Dec.;56(6):509-514.
  58. Brown JE, Rice-Evans CA. Luteolin-rich artichoke extract protects low density lipoprotein from oxidation in vitro. Free Radic Res 1998 Sep.;29(3):247-255.
  59. Wider B, Pittler MH, Thompson-Coon J, Ernst E. Artichoke leaf extract for treating hypercholesterolaemia. Cochrane Database Syst Rev 2009;(4):CD003335.
  60. Englisch W, Beckers C, Unkauf M, Ruepp M, Zinserling V. Efficacy of Artichoke dry extract in patients with hyperlipoproteinemia. Arzneimittelforschung 2000 Mar.;50(3):260-265.
  61. Bundy R, Walker AF, Middleton RW, Wallis C, Simpson HCR. Artichoke leaf extract (Cynara scolymus) reduces plasma cholesterol in otherwise healthy hypercholesterolemic adults: a randomized, double blind placebo controlled trial. Phytomedicine 2008 Sep.;15(9):668-675.
  62. Lupattelli G, Marchesi S, Lombardini R, et al. Artichoke juice improves endothelial function in hyperlipemia. Life Sci 2004 Dec.;76(7):775-782.
  63. Morgan JM, Capuzzi DM, Baksh RI, et al. Effects of extended-release niacin on lipoprotein subclass distribution. Am J Cardiol 2003 Jun.;91(12):1432-1436.
  64. Zema MJ. Gemfibrozil, nicotinic acid and combination therapy in patients with isolated hypoalphalipoproteinemia: a randomized, open-label, crossover study. J Am Coll Cardiol 2000 Mar.;35(3):640-646.
  65. Florentin M, Tselepis AD, Elisaf MS, et al. Effect of non-statin lipid lowering and anti-obesity drugs on LDL subfractions in patients with mixed dyslipidaemia. Curr Vasc Pharmacol 2010 Nov.;8(6):820-830.
  66. Ganji SH, Qin S, Zhang L, Kamanna VS, Kashyap ML. Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells. Atherosclerosis 2009 Jan.;202(1):68-75.
  67. Duggal JK, Singh M, Attri N, et al. Effect of niacin therapy on cardiovascular outcomes in patients with coronary artery disease. J. Cardiovasc. Pharmacol. Ther. 2010 Jun.;15(2):158-166.
  68. Marik PE, Varon J. Omega-3 dietary supplements and the risk of cardiovascular events: a systematic review. Clin Cardiol 2009 Jul.;32(7):365-372.
  69. Eslick GD, Howe PRC, Smith C, Priest R, Bensoussan A. Benefits of fish oil supplementation in hyperlipidemia: a systematic review and meta-analysis. Int. J. Cardiol. 2009 Jul.;136(1):4-16.
  70. Shafiq N, Singh M, Kaur S, Khosla P, Malhotra S. Dietary treatment for familial hypercholesterolaemia. Cochrane Database Syst Rev 2010;(1):CD001918.
  71. McGowan MP, Proulx S. Nutritional supplements and serum lipids: does anything work? Curr Atheroscler Rep 2009 Nov.;11(6):470-476.
  72. Gauhar R, Hwang SL, Jeong SS, et al. Heat-processed Gynostemma pentaphyllum extract improves obesity in ob/ob mice by activating AMP-activated protein kinase. Biotechnology letters. 2012;34(9):1607-1616.
  73. Nguyen PH, Gauhar R, Hwang SL, Dao TT, Park DC, Kim JE, . . . Oh WK. New dammarane-type glucosides as potential activators of AMP-activated protein kinase (AMPK) from Gynostemma pentaphyllum. Bioorganic & medicinal chemistry. Nov 1 2011;19(21):6254-6260.
  74. Winder WW, Ukropcova B, Deutsch WA, et al. AMP-activated protein kinase, a metabolic master switch: possible roles in type 2 diabetes. Am J Physiol. 1999;277(1 Pt 1):E1-10.
  75. Park SH, Huh TL, Kim SY, et al. Antiobesity effect of Gynostemma pentaphyllum extract (actiponin): a randomized, double-blind, placebo-controlled trial. Obesity (Silver Spring). 2014 Jan;22(1):63-71.
  76. Dong Y, Zhang M, Wang S, et al. Activation of AMP-activated protein kinase inhibits oxidized LDL-triggered endoplasmic reticulum stress in vivo. Diabetes. 2010 Jun;59(6):1386-96
  77. Steinberg GR, Kemp BE. AMPK in health and disease. Physiol Rev. 2009; 89: 1025-78.
  78. Viollet B, Horman S, Leclerc J, Lantier L, Foretz M, Billaud M, et al. AMPK inhibition in health and disease. Crit Rev Biochem Mol Biol. 2010; 45(4):276-95.
  79. Umeno A, Horie M, Murotomi K, Nakajima Y, Yoshida Y. Antioxidative and Antidiabetic Effects of Natural Polyphenols and Isoflavones. Molecules. May 30 2016;21(6).
  80. Devi KP, Rajavel T, Nabavi SF, Setzer WN, Ahmadi A, Mansouri K, Nabavi SM. Hesperidin: A promising anticancer agent from nature. Industrial Crops and Products. 2015;76:582-589.
  81. Li C, Schluesener H. Health-promoting effects of the citrus flavanone hesperidin. Critical reviews in food science and nutrition. Feb 11 2017;57(3):613-631.
  82. Roohbakhsh A, Parhiz H, Soltani F, Rezaee R, Iranshahi M. Neuropharmacological properties and pharmacokinetics of the citrus flavonoids hesperidin and hesperetin–a mini-review. Life sciences. Sep 15 2014;113(1-2):1-6.
  83. Jia S, Hu Y, Zhang W, Zhao X, Chen Y, Sun C, . . . Chen K. Hypoglycemic and hypolipidemic effects of neohesperidin derived from Citrus aurantium L. in diabetic KK-A(y) mice. Food Funct. Mar 2015;6(3):878-886.
  84. Rizza S, Muniyappa R, Iantorno M, Kim JA, Chen H, Pullikotil P, . . . Quon MJ. Citrus polyphenol hesperidin stimulates production of nitric oxide in endothelial cells while improving endothelial function and reducing inflammatory markers in patients with metabolic syndrome. The Journal of clinical endocrinology and metabolism. May 2011;96(5):E782-792.
  85. Zhang J, Sun C, Yan Y, Chen Q, Luo F, Zhu X, . . . Chen K. Purification of naringin and neohesperidin from Huyou (Citrus changshanensis) fruit and their effects on glucose consumption in human HepG2 cells. Food chemistry. Dec 01 2012;135(3):1471-1478.
  86. Homayouni F, Haidari F, Hedayati M, Zakerkish M, Ahmadi K. Hesperidin Supplementation Alleviates Oxidative DNA Damage and Lipid Peroxidation in Type 2 Diabetes: A Randomized Double-Blind Placebo-Controlled Clinical Trial. Phytotherapy research : PTR. Aug 14 2017.
  87. Sun Q, Wedick NM, Tworoger SS, Pan A, Townsend MK, Cassidy A, . . . van Dam RM. Urinary Excretion of Select Dietary Polyphenol Metabolites Is Associated with a Lower Risk of Type 2 Diabetes in Proximate but Not Remote Follow-Up in a Prospective Investigation in 2 Cohorts of US Women. The Journal of nutrition. Jun 2015;145(6):1280-1288.
  88. Salden BN, Troost FJ, de Groot E, Stevens YR, Garces-Rimon M, Possemiers S, . . . Masclee AA. Randomized clinical trial on the efficacy of hesperidin 2S on validated cardiovascular biomarkers in healthy overweight individuals. The American journal of clinical nutrition. Dec 2016;104(6):1523-1533.
  89. Jarosz PA, Fletcher E, Elserafy E, Artiss JD, Jen KL. The effect of alpha-cyclodextrin on postprandial lipid and glycemic responses to a fat-containing meal. Metabolism: clinical and experimental.Oct 2013;62(10):1443-1447.
  90. Artiss JD, Brogan K, Brucal M, Moghaddam M, Jen KL. The effects of a new soluble dietary fiber on weight gain and selected blood parameters in rats. Metabolism: clinical and experimental. Feb 2006;55(2):195-202.
  91. Wagner EM, Catherine Jen KL, Artiss JD, Remaley AT. Dietary alpha-cyclodextrin lowers LDL-C and alters plasma fatty acid profile in LDLr-KO mice on a high-fat diet. Metabolism: clinical and experimental.2008;57(8):1046-1051.
  92. Gallaher DD, Gallaher CM, Plank DW. Alpha-Cyclodextrin selectively increases fecal excretion of saturated fats. The FASEB Journal.April 1, 2007 2007;21(5):A730.
  93. Grunberger G, Jen KL, Artiss JD. The benefits of early intervention in obese diabetic patients with FBCx: a new dietary fibre. Diabetes/metabolism research and reviews.Jan 2007;23(1):56-62.
  94. Comerford KB, Artiss JD, Jen KL, Karakas SE. The beneficial effects of alpha-cyclodextrin on blood lipids and weight loss in healthy humans. Obesity (Silver Spring, Md.).Jun 2011;19(6):1200-1204.
  95. DiRienzo DB. Effect of probiotics on biomarkers of cardiovascular disease: implications for heart-healthy diets. Nutrition reviews. Jan 2014;72(1):18-29.
  96. Jones ML, Martoni CJ, Parent M, Prakash S. Cholesterol-lowering efficacy of a microencapsulated bile salt hydrolase-active Lactobacillus reuteri NCIMB 30242 yoghurt formulation in hypercholesterolaemic adults. The British journal of nutrition. May 2012;107(10):1505-1513.
  97. Semekovich CF, Goldman L. (ed.). Goldman-Cecil Medicine. Twenty-Fifth edition. Chapter 206: Disorders of Lipid Metabolism; 1389-1397.e3. Copyright 2016 Saunders, an imprint of Elsevier Inc. Accessed 7/7/2016.
  98. Lu M, Lu Q, Zhang Y, Tian G. ApoB/apoA1 is an effective predictor of coronary heart disease risk in overweight and obesity. Journal of biomedical research. 2011;25(4):266-273.
  99. Walldius G, Frank S and Kostner G (eds.). Biochemistry, Genetics and Molecular Biology. Chapter 5: The apoB/apoA-I Ratio is a Strong Predictor of Cardiovascular Risk. 10/3/2012. Accessed 7/7/2016.
  100. Jones ML, Martoni CJ, Prakash S. Cholesterol lowering and inhibition of sterol absorption by Lactobacillus reuteri NCIMB 30242: a randomized controlled trial. European journal of clinical nutrition. Nov 2012;66(11):1234-1241.
  101. Jones ML, Martoni CJ, Ganopolsky JG, Sulemankhil I, Ghali P, Prakash S. Improvement of gastrointestinal health status in subjects consuming Lactobacillus reuteri NCIMB 30242 capsules: a post-hoc analysis of a randomized controlled trial. Expert Opin Biol Ther. Dec 2013;13(12):1643-1651.
  102. Jones ML, Martoni CJ, Prakash S. Oral supplementation with probiotic L. reuteri NCIMB 30242 increases men circulating 25-hydroxyvitamin D: a post hoc analysis of a randomized controlled trial. The Journal of clinical endocrinology and metabolism. Jul 2013;98(7):2944-2951.
  103. Staels B, Fonseca VA. Bile Acids and Metabolic Regulation: Mechanisms and clinical responses to bile acid sequestration. Diabetes care. Nov 2009;32(Suppl 2):S237-245.
  104. Kumar M, Nagpal R, Kumar R, et al. Cholesterol-lowering probiotics as potential biotherapeutics for metabolic diseases. Experimental diabetes research. 2012;2012:902917.
  105. Haidari F, Heybar H, Jalali MT, Ahmadi Engali K, Helli B, Shirbeigi E. Hesperidin supplementation modulates inflammatory responses following myocardial infarction. Journal of the American College of Nutrition. 2015;34(3):205-211.
  106. Rondanelli M, Giacosa A, Opizzi A, et al. Beneficial effects of artichoke leaf extract supplementation on increasing HDL-cholesterol in subjects with primary mild hypercholesterolaemia: a double-blind, randomized, placebo-controlled trial. Int J Food Sci Nutr. 2013 Feb;64(1):7-15.
  107. Nazni P, Poongodi Vijayakumar T, Alagianambi P, Amirthaveni M. Hypoglycemic and Hypolipidemic Effect of Cynara Scolymus among Selected Type 2 Diabetic Individuals. Pakistan J of Nut. 2006;5(2):147-151.



Policosanol improves blood flow


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.

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.

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.

Policosanol is a dietary supplement that can normalize cholesterol as well or better than drugs, without side effects.1 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.2 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.”3

One of policosanol’s important actions is to inhibit the oxidation of LDL.4 Oxidized LDL is dangerous. It promotes the destruction of blood vessels by creating a chronic inflammatory response. Oxidized LDL can also provoke metalloproteinase enzymes.5 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.6,7

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.8 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.”9

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.10,11A related effect is that significant reductions in the level of thromboxane occur in humans after two weeks of policosanol.12 Thromboxane is a blood vessel-constricting agent that contributes to abnormal platelet aggregation that can cause a heart attack or stroke.




  1. 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.
  2. Noa M, et al. Effect of policosanol on lipofundin-induced atherosclerotic lesions in rats. J Pharm Pharmacol1995 Apr;47(4):289-91.
  3. 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.
  4. 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.
  5. 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.
  6. Noa M, et al. 1996. Effect of policosanol on foam-cell formation in carrageenan-induced granulomas in rats. J Pharm Pharmacol 48:282-5.
  7. 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 Chem274:22627-34.
  8. Noa M, et al. 1998. Effect of policosanol on damaged arterial wall induced by forceps in rabbits. J Electron Microsc 4:629-30.
  9. 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.
  10. 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.
  11. 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.
  12. 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.

 *These statements have not been evaluated by the Food and Drug Administration.
These products are not intended to diagnose, treat, cure, or prevent any disease.

Additional information

Weight 1 lbs
Dimensions 2 × 2 × 4 in

8 oz,, 5 lbs,, 44 lbs,


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