How to Avoid a Broken Heart

How to Avoid a Broken Heart
Using Nutrients to control the leading risk factors of heart disease
by Steve Myers

Coronary artery disease (CAD), cardiovascular disease (CVD), ischemic heart disease and coronary heart disease (CHD) are all synonyms for the general term heart disease (HD), which is actually a group of diseases affecting blood and oxygen flow in the arteries and heart. A broken heart, in this case, is starved of blood and oxygen, causing any number of potentially fatal heart malfunctions or dangerous events, including heart attack, cardiac arrest and stroke. (See next month’s INSIDER for a discussion of cardiac events and mortality.)

Of primary concern is atherosclerosis, a form of arteriosclerosis (“hardening of the arteries”) that manifests as advanced fatty deposits (also called atheromas or plaques) on the interior artery lining (intima or endothelium). The fatty deposits central to atherosclerosis are comprised of lipids, complex carbohydrates, proteins, fibrous tissue and calcium. The formation of plaques begins as a process called atherogenesis, during which fatty streaks deposit lipids in the subendothelium (between the intima lining and muscular portion) of the artery wall. On a cellular level, the blood vessel experiences initial damage, which triggers the inflammatory response that attracts white blood cells to the deposit site in the artery wall.These monocytes enter the wall and become macrophages that consume oxidized cholesterol, forming large foam cells. These foam cells can lead to increased inflammation and increased intima fat deposits, called fatty streaks in early stages. Over time, these deposits slowly and quietly build-up and become a primary contributor to arterial blockage.

Cholesterol lipids are carried by low density lipoprotein (LDL) to the intima, where they can be released and vulnerable to oxidation. In contrast, high density lipoprotein (HDL) carries cholesterol away from atheromas and to the liver for removal. However, lipid or cholesterol health has been exposed as more complex, and researchers have further identified the importance of key components of LDL and HDL.

An indicator of the more dangerous small particle LDL is its structural protein component, apolipoprotein B (apoB). University of Texas, San Antonio, researchers reported while tests for LDL have historically screened for cholesterol, screening for apoB can produce a better indication of LDL particle size, and thus atherosclerosis risk.¹

In addition to cholesterol and apolipoproteins (ApoB and ApoE), LDL and HDL also contain triglycerides, which are split into glycerol and fatty acids by lipases (enzymes that metabolize fats) in the intestines, then are rebuilt into triglycerides in the blood, where they become part of the lipoprotein package. Triglycerides, which are found in high concentration in very low density lipoprotein (VLDL)—the form emerging from the liver—and in lesser amounts in LDL and HDL. A high blood level of triglycerides, called hypertriglyceridemia, has been associated with increased risk of atherosclerosis, adjacent to low-HDL, high-LDL, insulin resistance/diabetes and high blood pressure.

Genetics can certainly play a role in the balance of lipids in the blood, but dietary factors are even more important in lipid health, as they have demonstrated powerful effects and are controllable. In fact, researchers and public health experts routinely suggest a diet rich in whole grains, fruits and vegetables, omega-3 essential fatty acids (EFAs) and unsaturated fats can help prevent CVD.² It is no surprise that most of the supplement ingredients studied for lipid maintenance and vascular health are abundant in this recommended diet.

An ironic twist of the recommended heart healthy diet, fiber—a carbohydrate found in cell walls of plants, including whole grains, vegetables, fruits and legumes—is not even digestible. However, fiber is known to reduce LDL. Medical researchers from the Division of Cardiology Lipid Disorder at the University of Medicine and Dentistry, New Brunswick, N.J., found dietary psyllium supplementation in patients taking 10 mg of simvastatin (one of the cholesterol-lowering statin drugs) is more effective in lowering LDL cholesterol as 20 mg of simvastatin alone;³ similar effects were also noted for total cholesterol and apoB levels.

The wealth of scientific evidence on fiber led the Food and Drug Administration (FDA) to approve two heart health claims for fiber, especially soluble fiber. One claim links high fiber intake to reduced risk of CVD, and the second notes the relationship between reduced CVD risk and soluble fiber from psyllium seeds and oats.

Diets rich in oats appear to lower cholesterol and blood pressure.⁴ In fact, scientists from New Orleans’Tulane University reported 8 g/d of water-soluble fiber from oat bran for three months in hypertensive subjects moderately affected their systolic and diastolic blood pressure readings.⁵ An oat-rich diet might even control blood pressure to the point where patients can reduce their dosages of hypertensive drugs.⁶

On lipid maintenance, oat fiber helped improve lipid parameters in two University of Minnesota trials presented in 2004. In the first study, one team of researchers noted oat fiber, specifically its beta-glucan content, lowers cholesterol by way of its promotion of high in vitro intestinal viscosity.⁷ In confirmation of this mechanism, the researchers found oat beta-glucans (as Oat Vantage™, from Nurture Inc.) produced a high viscosity of intestinal contents, leading to a reduction in total liver cholesterol concentration in rats. In the second study, their colleagues investigated the effect of 6 g/d of oat beta-glucan concentrate on lipid parameters—LDL, HDL, total cholesterol, triglycerides, C-reactive protein (CRP), glucose, insulin and homocysteine—in 90 healthy men and women with risky levels of serum cholesterol (greater than 200 mg/L).⁸ After six weeks of supplementation, researchers found oat beta-glucans lower LDL cholesterol in subjects with high serum cholesterol levels, concluding a practical dose of beta-glucans can lower lipids in high-risk populations.

A Lund University, Sweden, trial concluded 5 g/d oat betaglucans in a beverage improved lipid and glucose metabolism, while barley beta-glucans did not.⁹ However, U.S. Department of Agriculture (USDA) research showed intake of 3 g/d or 6 g/d of barley beta-glucans for 17 weeks lowered total and LDL cholesterol and various LDL particle sizes in hypercholesterolemic men and postmenopausal women.¹⁰

Another good source of fiber, as well as vitamins, minerals, amino acids and polyphenols, is nuts, which can directly lower cholesterol. Consumption of 50 g/d to 100 g/d of various nuts—including almonds, peanuts, pecans and walnuts (macadamias excluded)—may significantly decrease both total and LDL cholesterol in normal and hyperlipidemic individuals.¹¹ Additional studies have specifically linked lipid and vascular health benefits with peanuts¹² and walnuts.^13,14

Nuts can also support lipid health by replacing high-cholesterol, saturated fatty acids in the diet. The essential fatty acid (EFA) profile of nuts includes oleic acid, linoleic acid (LA) and alpha linolenic acid (ALA). Research conducted at Penn State University, University Park, showed both LA and ALA decrease LDL, total cholesterol and triglycerides, but ALA was more effective in reducing vascular cell adhesion (inflammation marker) and improving endothelial health.¹⁵ Other scientists added LA regulates LDL metabolism and enhances its clearance, but the omega-3s are critical for endothelial function and platelet sensitivity.¹⁶ An omega-3 fatty acid, ALA may counter atherosclerosis by altering the generation of eicosanoids (proinflammatory cells) and blood pro-coagulant activity.¹⁷

Of omega-3s, marine sources have ruled the lipid research pool. One study involving 229 postmenopausal women with CHD found consumption of two or more servings of fish, or one or more servings of tuna or dark fish, significantly reduced progression of atherosclerosis.¹⁸ Supplementation with fish oil can provide lipid benefits via several antithrombotic, antiatherosclerotic and antiinflammatory mechanisms of action, such as normalizing blood pressure, lowering triglyceride concentrations and improving endothelial function.¹⁹ An eight-week study out of Denmark discovered EFAs from fish oil decreased triglycerides and mean arterial blood pressure, while hydrogenated soy oil decreased HDL.²⁰ Against more advanced stages of atherosclerosis, fish oil supplementation was shown to enhance the stability of plaques—and possibly further CVD events—in 170 patients awaiting surgery to remove such plaques (carotid endarterectomy).²¹ Marine omega-3s can also control inflammatory activities influential in vascular health and atherosclerosis,²² as studies reveal fish oil supplementation can reduce thrombin generation²³ and collagen aggregation,²⁴ enhancing endothelial function, even in healthy subjects.²⁵

Marine EFAs, chiefly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are also abundant in krill, tiny crustaceans found in the coldest ocean waters. Krill oil, which contains special phospholipid carriers for EPA and DHA, improved the quality of life in atherosclerosis patients taking 1 g/d for one month and 500 mg/d thereafter (up to 180 days), according to a proprietary, randomized, double blind clinical trial conducted by Neptune Technologies, which supplies NKO™ krill oil. In confirmation, a study published in Alternative Medicine Review in 2004 demonstrated a BMI-dependent daily dose of 2 g to 3 g of krill oil (as NKO) managed hyperlipidemia, reducing total cholesterol, blood glucose, triglyceride and LDL levels, while raising HDL, more effectively than fish oil.²⁶

Flaxseeds contain high amounts of ALA, which can convert in the body to EPA (and possibly DHA), but it also contains LA and oleic fatty acid. An omega-9 fatty acid, oleic acid is most commonly consumed as olive oil, which has some benefits to lipid profile and hypertension. In fact, the highly-touted Mediterranean diet, which is high in olive oil, fruit and vegetable intakes while low in saturated fats (from meats), has often been linked with improved lipid health, including reduced oxidized LDL and increased total antioxidant capacity.³⁰ Olive oil can not only help control lipid peroxidation and the ratio of HDL-to-LDL,³¹ but it can also normalize systolic and diastolic blood pressure in hypertension,^32,33,34 In addition, oleic acid from olive oil (and sunflower oil) can attenuate vascular factors of atherosclerosis, including inflammation,³⁵ and lipid profile and vascular response.³⁶

However, the heart benefit from olive oil may be due to its phenolic content. Spanish researchers noted high-phenolic, extra virgin olive oil improves ischemic reactive hyperemia (arterial blood flow) by mediating parameters of endothelial vasodilation, including oxidative stress and nitric oxide (NO) metabolites.³⁷ Further study has revealed the olive phenol hydroxytyrosol, which contains phenolic isochromans, can inhibit platelet aggregation (sticking to vessel injury site).³⁸ Phenols common in both olive oil and red wine, including hydroxytyrosol, oleuropein and resveratrol, increase antioxidant activity and reduce endothelial cell adhesion,³⁹ in addition to addressing LDL oxidation.⁴⁰

Beyond its reduction of LDL,⁴¹ red wine, a Mediterranean diet staple, has been shown to reduce plasma oxidative stress following a fatty meal in healthy men and women,⁴² and inhibited lipid deposition in the aorta in apoE-deficient mice.⁴³ Red wine polyphenols have also been shown to increase NO synthase expression, leading to vasorelaxation,⁴⁴ as well as improve blood flow-mediated dilation of the brachial artery.⁴⁵ The same beneficial phenols in red wine are also abundant in its predecessor, grapes.

As a group, flavonoids can inhibit LDL oxidation, thrombosis and inflammation as well as improve endothelial function; however, specific flavonoids have also been shown as beneficial. Abundant in richly colored red, blue and purple fruits and vegetables—such as raspberries, strawberries, blackberries, blueberries, bilberries, plums, eggplant, red cabbage, red onion and grapes (red and purple)—anthocyanins, have exacted specific atherosclerotic benefits, improving the transporting of excess cholesterol from peripheral tissues to the liver for biliary excretion.⁵⁰ Similarly, flavanols in cocoa, including catechins and proanthocyanins, have been found in to reduce LDL oxidation⁵¹ and inhibition of thrombosis formation.⁵² In addition, a University of California, San Francisco, (UCSF) review revealed cocoa flavanols can improve endothelial function, lower blood pressure and decrease platelet activation and function.⁵³

Tea also contains flavonols, such as quercetin, which has both antihyperlipidemic and antiatherogenic properties. Scientists from Pomeranian Medical University, Poland, studying rabbits with hyperlipidemia and/or atherosclerosis found quercetin supplementation effectively reduced serum triglycerides and cholesterol in both groups of rabbits after 12 weeks, and decreased plaque size in rabbits with injured carotid arteries after four weeks.⁵⁸ Similarly, Chilean researchers reported quercetin showed more potent in vitro antioxidant activity on LDL than did various phytoestrogens, including daidzein and genistein.⁵⁹

These phytoestrogens are common isoflavones in soy and red clover. Experts contend consumption of soy, a mainstay of the heart-healthy Asian diet, appears to improve plasma lipids, reduce LDL oxidation and improve vascular reactivity.⁶⁰ Soy foods intake has been linked to favorable plasma cholesterol profile, including reduced total and LDL cholesterol in both pre- and postmenopausal women.⁶¹ In 1999, a petition from The Solae Co. led to FDA approval of a health claim linking intake of 25 g/d of soy protein with a reduced risk of CHD.

In 2005, researchers from Wake Forest University, Winston-Salem, N.C., studying adult monkeys discovered long-term consumption of soy protein containing a modest amount of isoflavones inhibits the early progression of coronary atheromas, without affecting endothelium-dependent or -independent arterial function.⁶³ In another animal study, rats fed soy protein isolate (SPI) or casein for eight weeks displayed reduced plasma triglyceride and cholesterol levels, as SPI modulated genes involved in lipid and energy metabolism.⁶⁴ A 23-trial meta-analysis confirmed the ability of soy and its isoflavones to lower serum total cholesterol, LDL cholesterol, and triacylglycerol, and significantly increase HDL cholesterol.⁶⁵

Both soy protein and rice protein have demonstrated protection against development of atherosclerotic plaques. A Japanese trial comparing a purified diet of soy and rice protein with an animal protein (casein) diet in apoE-deficient mice found the plant proteins more effectively inhibited lesion formation, unrelated to gender and serum cholesterol.⁶⁶

The role of isoflavones in soy’s lipid benefits is not clear. In one Canadian study, while soy protein decreased total cholesterol and triglycerides in hyperlipidemic subjects more effectively than animal protein, isoflavones had no such effect.⁶⁷ However, another Canadian study determined both high- and low-soy isoflavone diets can lower total cholesterol and improve the LDL-to HDL ratio in hyperlipidemic subjects;⁶⁸ while a Tokyo trial found a high-isoflavone soy diet more effectively lowered LDL than a low-isoflavone diet.⁶⁹

Further study revealed higher intake of soy phytochemicals, including isoflavones and lignans, lowers triglyceride levels⁷⁰ and aortic stiffness.⁷¹

Isoflavones in red clover have produced comparable results on plasma lipid health. Studies involving red clover supplementation have resulted decreased triglycerides and increased HDL,⁷² and reduced total and LDL cholesterol in menopausal women;⁷³ red clover has shown similar benefits in men.⁷⁴

The roster of heart healthy flavonoids is robust. Citrus bioflavonoids, including naringin, hesperidin, nobiletin and tangeretin, appear to reduce total and LDL cholesterol, as well as triglycerides.⁷⁵ Rabbit studies have shown naringin, abundant in grapefruit, increases serum antioxidant activity similar to the most effective cholesterollowering drugs,^76,77 and reduces aortic fatty acid streaks in highcholesterol diets.⁷⁸ Nobiletin, from tangerine peel, was found to reduce plasma concentrations of LDL and inhibit macrophage foam-cell formation;⁷⁹ while fellow tangerine bioflavonoid tangeretin showed hypertriglyceridemic actions on apoB-containing lipoprotein metabolism by reducing apoB secretion in a study led by KGK Synergize.⁸⁰ Hesperidin, most common in lemons and oranges, normalized blood pressure and heart rate in a trial involving hypertensive rats.⁸¹

In addition to bioflavonoids, citrus fruits contain limonoids, which have demonstrated some heart benefits. In early 2005, USDA Agricultural Research Service scientists found the limonoid limonin, which is as abundant in orange juice as vitamin C, is readily accessed in the human body, where it can limit high cholesterol by inhibiting apoB production in the liver.⁸²

Other phytochemical-rich fruits also improve lipid health. According to a study conducted at University of Hawaii, Honolulu, bitter melon juice, from the edible fruit of the plant Momordica charantia, substantially inhibited apoB secretion and triglyceride synthesis that may be involved in the plasma lipid- and VLDL-lowering effects observed in animal studies.⁸³ Likewise, pomegranate juice has multiple mechanisms of action against CVD. Pomegranate may inhibit atheroma development by inhibiting LDL oxidation via direct interaction with the lipoprotein and accumulating in arterial macrophages.⁸⁴ A compound study of healthy males found two weeks of pomegranate juice consumption decreased LDL aggregation in one study arm, while similar supplementation in mice reduced foam cells and decreased atheroma size by 45 percent in the other study arm.⁸⁵ Recent UCSF research reported pomegranate juice (as POM, from POM Wonderful) significantly increased blood flow in CVD patients, without affecting lipids, glucose or blood pressure.⁸⁶

Although pomegranate is known for its ellagic acid content, its polyphenolic content—delphinidin, cyaniding, pelargonidin and punicalagin—has been the focus of numerous atherogenesis studies. These phenols have been shown to lower total and LDL cholesterol,⁸⁷ as well as decrease carotid intima-media thickness (IMT).⁸⁸

Pomegranates are also noted for their powerful free radical scavenging,⁸⁹ a benefit associated with numerous other lipid healthy phtyochemical ingredients. Colorful fruits and vegetables contain carotenoids, including lycopene, beta-carotene, astaxanthin, betacryptoxanthin, lutein and zeaxanthin. As a group, carotenoids appear particularly proficient at scavenging singlet oxygen and peroxyl radicals generated by lipid peroxidation.⁹⁰

A review of lycopene trials revealed the tomato-borne compound can protect against LDL oxidation,⁹¹ an effect more pronounced with tomato oleoresin, according to in vitro study.⁹² In addition to its antioxidant benefits, lycopene might also affect LDL degradation and particle size, and improve endothelial health.⁹³ A study conducted at the Japanese Women’s University, Tokyo, showed tomato juice increased lycopene concentrations in both HDL and LDL cholesterol, protecting the lipids from peroxidation.⁹⁴ Data from the Kuopio Ischaemic Heart Disease Risk Factor Study, conducted in Finland, linked low lycopene intake in men to increased carotid IMT.⁹⁵

Fellow carotenoid lutein can also help impede atherosclerosis development. Scientists at the Keck School of Medicine at University of Southern California (USC), Los Angeles, found increased lutein intake slowed IMT progression, inhibited LDL migration to the artery wall and reduced atheroma size by 43 percent in apoE-deficient mice.⁹⁶ A similar UCLA cohort study involving 573 men and women found higher plasma levels of lutein, alpha-carotene, beta-cryptoxanthin and zeaxanthin reduced atherosclerotic progression, as measured by IMT.⁹⁷

The antioxidant carotenoid astaxanthin has also exhibited atherosclerotic benefits, according to a handful of Japanese trials. In one such trial, researchers reported astaxanthin limited LDL oxidation both in cell cultures and human subjects.⁹⁸ Another trial found 14 days of oral astaxanthin supplementation (as AstaREAL®. from Fuji Health Sciences) decreased arterial blood pressure in hypertensive rats by inducing vasorelaxation via NO-mediation.⁹⁹ A third study showed 6 mg/d of astaxanthin supplementation (as AstaREAL) improved blood rheology (transit time) after 10 days.¹⁰⁰ A Linkoping University, Sweden, study showed 500 mg of vitamin E (as alpha-tocopherol) combined with 100 mg astaxanthin (as AstaREAL) per kg of feed improved plaque stability by decreasing macrophage infiltration and apoptosis in atherosclerotic rabbits.¹⁰¹

Vitamin E has been combined with vitamin C in a few studies to address parameters of atherosclerosis development and progression. Finnish researchers reported six years of combined supplementation of vitamins E and C in hypercholesterolemic men and women resulted in decreased carotid IMT.¹⁰⁹ In a Slovakian study, a mixture of vitamins E and C and fellow antioxidants beta-carotene and selenium increased the antioxidant activity in CVD patients, leading to reduced lipid peroxidation.¹¹⁰ On its own, increased vitamin C intake has been linked to normalized endothelial function in CVD patients,¹¹¹ while two studies failed to find a connection between acute or chronic vitamin C supplementation and hypertension.^112,113

Vitamin-like antioxidant coenzyme Q10 (CoQ10) can also help limit atherosclerosis risk factors. An Australian review of CoQ10 hypertension research concluded supplementation with the coenzyme could help lower both systolic and diastolic blood pressure.¹¹⁴ Another review, investigating numerous antihypertension supplements, concluded CoQ10 has demonstrated consistent benefits to hypertension, with the researchers concluding Q-Gel® (from Tishcon) was the most well-studied and bioavailable of the CoQ10 supplements.¹¹⁵ Administration of 3 mg/kg/d of CoQ10 (as Q-Gel) for 24 weeks in rabbits with high trans fat levels resulted in reduced oxidative damage and atherosclerosis development.¹¹⁶ Further, a review conducted by UCLA researchers suggested CoQ10 as a potent tool in prevention of hypertension and hyperlipidemia.¹¹⁷ There is also evidence CoQ10 production and supply in the body are decreased in CVD patient taking statin drugs, a state that can be reversed by CoQ10 supplementation.¹¹⁸

CoQ10 appears to enjoy a heart health synergy with vitamin E, as CVD patients taking the coenzyme had increased plasma levels of both vitamin E and HDL cholesterol.¹¹⁹ while co-supplementation with the two antioxidants significantly reduced atherosclerosis at the aortic root and descending thoracic aorta, according to Australian scientists.¹²⁰

As a result of its antioxidant properties, lipoic acid can affect lipid peroxidation and endothelial function, thereby helping to control blood pressure and lipid metabolism. One study found alpha-lipoic acid improved endotheliumrelated blood vessel relaxation in diabetic subjects, but not in nondiabetic controls.¹²² However, additional research discovered lipoic acid could decrease hypertension due to both hyperglycemia¹²³ and high salt intake.¹²⁴ Subsequent study showed lipoic acid’s benefit to lipid metabolism helps protect against both hypertension and lipid peroxidation.¹²⁵ Annamalai University, India, scientists researching lipid metabolism found lipoic acid helps normalize lipid levels, in addition to its assistance in lipid metabolism.¹²⁶

Among heart-healthy antioxidant micronutrients is selenium, low levels of which have been associated with decreased HDL and increased prevalence of atherosclerosis.¹³⁰ According to Spanish researchers, low serum selenium levels are also linked to higher homocysteine levels, a risk factor for atherosclerosis and heart disease.¹³¹ However, a review of selenium research on CVD concluded more research is needed to better understand the mineral’s benefits to heart health.¹³²

Better understood is the mineral magnesium, which influences endothelial function and carotid IMT, key factors in hypertension.¹³³ Upon finding high levels of magnesium administered to hypertensive rats affected exchangeable cellular magnesium stores, French researchers suggested hypertension might involve a disturbance in magnesium metabolism.¹³⁴ Further research determined magnesium supplementation in hypertensive piglets improved circulation and heart function in cases of embolism (arterial blockage from a clot, cholesterol or tissue).¹³⁵

Still other minerals support vascular health. In one recently published study, calcium phosphate reduced serum cholesterol, possibly due to enhanced cholesterol metabolism and bile acid excretion.¹³⁶ Fellow mineral chromium may benefit both lipid health and hypertension. Creighton University, Omaha, Neb., research showed chromium polynicotinate (as ChromeMate®, from InterHealth Nutraceuticals), individually and combined with GSE (as Activin®, from San Joaquin Valley), reduced systolic blood pressure in healthy and hypertensive rats.¹³⁷ More recently, 12 weeks of supplementation with chromium picolinate with biotin (as Diachrome®, from Nutrition 21) decreased non-HDL cholesterol and triglycerides in type II diabetes patients.¹³⁸

Biotin is a member of the B vitamin complex, which includes niacin, pantothenic acid and folic acid. Although folic acid has been shown to reduce homocysteine levels and enhance NO synthesis,¹³⁹ scientists are still uncertain if folate supplementation helps prevent atherosclerosis.¹⁴⁰ In contrast, pantothenic acid supplementation has been proven effective in addressing hyperlipidemia, as its derivatives— including pantethine—lowered total cholesterol and triglycerides in obese mice, ¹⁴¹ and 600 mg/d of pantethine severely reduced fatty liver in 16 hypertriglyceridemic patients.¹⁴² A University of Minnesota trial further showed 600 mg/d to 900 mg/d of pantethine (as Pantesin®, from Daiichi Pharmaceutical) improved levels of LDL, VLDL and triglycerides and increased HDL.143

Perhaps the most potent heart health B vitamin is niacin, which was used for treatment of dyslipidemia as early as the 1950s due to its favorable impact on HDL levels. In fact, a research review revealed niacin can increased HDL cholesterol and decrease LDL to its less atherogenic large particle size.¹⁴⁴ Niacin supplementation added to statin therapy has been shown to impede IMT progression,¹⁴⁵ and optimize lipid levels, including LDL, HDL and triglycerides.¹⁴⁶

Cholesterol found in humans has similar structure to plant sterols, which can lower cholesterol levels by competing for absorption. In one trial, plant sterols lowered serum levels of low-density lipoprotein (LDL) cholesterol levels and non-high-density lipoprotein (non-HDL) cholesterol in both diabetic and non-diabetic subjects.¹⁴⁷ Likewise, 2.4 g of sterol esters (as Vegapure®, from Cognis Nutrition & Health) lowered LDL cholesterol, without affecting plasma carotenoid or tocopherol levels,¹⁴⁸ while 2.7 g of sterols (as Vegapure) lowered total and LDL cholesterol.¹⁴⁹ Similarly, orange juice containing 2 g/d of plant sterols (as CoroWise™, from Cargill Health & Food Technologies) was shown to reduce levels of total cholesterol, LDL, HDL and apoB.¹⁵⁰ Another study, conducted at McGill University, Canada, concluded a proprietary delivery platform of DHA and plant sterols (as cardiaBeat™, from Enzymotec) decreased levels of total cholesterol, LDL and triglycerides in overweight patients with elevated lipid levels.¹⁵¹

Most recently, University of Nebraska, Lincoln, scientists studying grain sorghum suggested its sterols content reduced cholesterol absorption, while its policosanol content appeared to inhibit cholesterol production in the body.¹⁵²

Policosanol, a mixture of cyclic alcohols derived from sugar cane wax and beeswax, has demonstrated cholesterol-lowering abilities equal to statin drugs, and a McGill University review noted the supplement may reduce platelet aggregation, endothelial damage and foam cell formation, as well as lower total and LDL cholesterol.¹⁵³ Numerous policosanol studies conducted at the National Center for Scientific Research, Cuba, have shown short- and long-term supplementation of 5 mg/d and 10 mg/d of policosanol can significantly lower total and LDL and increase HDL in hypercholesterolemic patients.^154,155,156

Lipid control is also a feature of botanical ingredients, including garlic and guggul. Garlic (Allium sativum) has been shown to reduce total cholesterol and platelet aggregation,¹⁵⁷ as well as protect LDL from oxidation and glycation—which causes tissue stiffening—possibly due to its organosulfuric content.¹⁵⁸ Additional garlic studies have found aged garlic extract (AGE) can improve endothelial function by increasing NO production,¹⁵⁹ in addition to improving the ratio of LDL-to-HDL and lowering homocysteine levels.¹⁶⁰

Made from the oleogum resin of the Cammiphora mukul tree, native to India, guggul has been credited with impacting lipid profile, possibly due to its guggulsterone content. Preclinical and clinical studies conducted in India, where the pharmacopoeia lists guggul for use in dislipidemia, have shown a standardized extract of guggul (as Gugulipid®, from Sabinsa) can lower total, VLDL and triglycerides, as well as raise HDL in both healthy and hyperlipidemic subjects. Proprietary studies have further shown guggul (as Gugulipid) can also decrease platelet adhesion and increase fibrinolytic activity, the breaking of fibrin traps that can lead to atheromas. Recently published research has confirmed gugul’s lipid-lowering effect, adding the supplement can also inhibit LDL oxidation.¹⁶¹ A Baylor College of Medicine, Houston, review suggested guggulsterones act as atagonist ligands for a key bile receptor in the regulation of cholesterol homeostasis.¹⁶²

Controlling lipid, blood vessel integrity and oxidative damage is crucial to impeding atherosclerosis and the dangers it can cause. Despite genetic factors, natural health ingredients have proven exceptionally useful in mediating manageable CVD risk factors.

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