The Natural Heartbeat

References

Despite great efforts at preventing the progression of cardiovascular disease (CVD)reducing cholesterol, triglycerides and other lipid factors, and controlling blood pressureits pathological fervor can be formidable, and patients must begin to think about the many cardiac events that can happen as a result of the disease. Advanced atherosclerosis can lead to infarctions (heart attack and stroke) and fatal arrhythmias. Survive these, and heart failure could be in the future. However, much as they help in preventive measures against CVD, natural ingredients can be useful in avoiding or promoting survival from these cardiac events.

An American Heart Association (AHA) national opinion poll revealed more than two-thirds of consumers are worried they, or someone they love, will suffer from CVD; 20 percent were very concerned. And with good reason. The latest data from AHA and Circulation shows one in three Americansa total of 79.4 million peoplehave one or more types of CVD.¹ The nightmare does not end there. In every year since 1900 (save 1918), CVD accounted for more deaths than any other single cause or group of causes in the United States. Currently, 2,400 Americans die each day from CVD (one every 36 seconds), more than from cancer, diabetes, respiratory disease and accidents combined.

Staying alive requires keeping the heart supplied with blood and maintaining a healthy heartbeat. In humans, a four-chamber heart is responsible for drawing oxygen-rich blood from the pulmonary arteries and pumping it throughout the circulatory system. Then it must draw the old blood back through the veins to the lungs where it trades carbon dioxide for a new batch of oxygen. It all sounds simple, but the drawing, pumping and exchanging blood contents with a roster of organs and tissues is a well-timed, well-balanced hoedown.

The rhythm of this dance is the heartbeat. A node in the right atrium of the heart is the primary cardiac pacemaker, emitting electrical impulses that cause the various chambers of the heart to contract. The right atrium draws in blood that has already circulated the body and delivers it to the right ventricle below it, while the left atrium draws in blood from the lungs. The electrical pulse eventually passes through another node that controls the ventricles (the two bottom chambers). The right ventricle contracts and pumps blood out to the lungs to be re-oxygenated, while the left ventricle pumps the new oxygen-rich blood out of the heart for its journey around the body.

A normal resting heartbeat, or heart rate, is between 60 and 80 beats per minute (bpm). Anything significantly faster or slower is considered arrhythmic. More than 100 bpm is called tachycardia; slower than 60 bpm is called bradycardia. Worse than having two left feet, an arrhythmia experienced for a long period of time can have devastating effects, including rapidly decreased blood pressure and altered pumping action. The irregular heart muscle contractions that can mark arrhythmia can present as a rapid quivering, or fluttering, of various chambers of the heart. A dangerous form of arrhythmia is fibrillation, which can be either atrial or ventricular. Ventricular fibrillation (V-Fib) is imminently fatal, as it effectively stops the pumping action of the heart. This is why defibrillators are so crucial to survival in V-Fib, which is a form of cardiac arrest.

Affecting as many as 3 million Americans, atrial fibrillation (AFib) is more common and is often a hidden condition. While it is less immediately life-threatening, it can indicate an underlying condition requiring medical attention. Moreover, when the atria suffer irregular contractions, blood flow through these chambers can pool and clot. In fact, A-fib is a leading risk factor for stroke.

When a clot dislodges and blocks blood flow in an arterycalled an embolismit can cause an infarction, tissue death from oxygen starvation. When this occurs in a brain-feeding artery, a stroke, or cerebral infarction, ensues. If a clot clogs any of the small arteries that supply blood to the heart muscle (myocardium), a heart attack, or myocardial infarction, results.

The most recent AHA data indicates 5.6 million Americans suffer a stroke each year, with 15 percent of these caused by AFib. A clot causing a stroke can also come from thrombosis, the formation of a thrombus (clot) associated with atherosclerotic plaque build-up. These two kinds of blockages of brain arteries are called ischemic strokes. Another form of stroke can result when a blood vessel in the brain breaks, leaking into the surrounding tissue. This is a hemorrhagic stroke.

In either case, stroke prevents sufficient blood from reaching parts of the brain, causing various levels of temporary or permanent brain damage. Brain cells can die from lack of blood and nutrients, rendering the abilities managed by these areas lost as well. It is not uncommon for stroke victims to lose some memory, speech or motor skills. In fact, the American Stroke Foundation reported stroke is the leading cause of adult disability in the United States.

In myocardial infarction, coronary arteries branching off the aorta to the heart are the victims, as the heart muscle does not receive its nutrients from the blood passing through it. Thrombosis is the usual culprit. As in a stroke, the tissue not getting sufficient blood and oxygen can die. Unfortunately, so can the person suffering the infarction, as the loss of heart function can lead to fatal V-Fib. More than 1.3 million Americans will suffer a heart attack this year, and nearly 40 percent of them die from the attack, according to the AHA report.

A heart attack and/or arrhythmia can cause congestive heart failure (CHF), the progressive inability of the heart to pump blood through the body or prevent it from backing up. The key is the side of the heart that fails. If the left ventricle fails, blood can back up into the lungs, causing difficult breathing and fluid congestion. In right ventricle failure, pressure in the blood vessels rises dramatically, forcing fluid into the surrounding tissues, and resulting in swelling (most often in the legs and abdomen). AHA notes of the 500,000 people annually who suffer CHF, 75 percent had been previously diagnosed with hypertension.

Solving the Cardiac Conundrum

The cascade of events that mark progressive CVD are all linked to similar risk factors. Chief among these are atherosclerosis and hypertension. While genetics play a huge part in the risk of developing CVD and its assorted complications, most cases of CVD, heart attacks and strokes can be prevented. The keys to preventing such advanced heart disease include lifestyle changes such as smoking cessation, increased exercise, limited saturated and transfat intakes, decreased salt intake, reduced stress, and increased intake of vegetables and fruits. While dietary improvements can help, dietary supplementation can sometimes provide extra benefit, improving blood flow, reducing inflammation, decreasing the risk of developing and dying from heart attacks, arrhythmias and strokes, and improving recovery from these CVD events.

A large portion of advanced CVD complications involves blood flow, also called blood rheology. Atherosclerosis, thrombosis and hypertension all contribute to decreased blood flow that can cause infarctions. One method of keeping the vascular system open for blood travel is by limiting aspects of the arterial hardening and obstruction caused by advanced atherosclerosis. Part one of this CVD series addressed prevention and management of atherosclerosis. Another method of promoting blood flow is to dilate the vessels, creating more flow space.

Nitric oxide (NO) signals the smooth muscle cells in a blood vessel wall to relax, thereby dilating the artery and increasing blood flow. Nitric oxide synthase (NOS) enzymes manufacture NO from arginine and oxygen; NO levels decrease dramatically following infarctions. Thus, scientists have investigated supplemental arginine for benefits to survival and recovery from heart attacks and strokes.

On stroke, researchers from the University of Nottingham, United Kingdom (U.K.), who reviewed relevant trials in the Cochrane Database, reported arginine and NO reduced the total volume of stroke lesions in both permanent and transient ischemia attacks (TIA), but the window of opportunity for this intervention is unfortunately brief.² However, Japanese scientists showed arginine limited thrombosis in microvessels around the brain.³ In similar research, arginine produced favorable results in a model of induced forearm ischemia by improving blood flow.⁴

L-arginines effect on the course of infarction, including mortality, re-infarction, edema or recurrent ischemia, was studied in 792 heart attack patients in a randomized, double blind, placebo-controlled trial conducted in Grochawski Hospital, Warsaw, Poland.⁵ Researchers observed a trend toward reduced major CVD events during arginine supplementation, but the benefit did not reach clinical significance. Providing more concrete evidence, a Russian team found L-arginine treatment in mice following a heart attack stabilized parameters associated with post-attack NO decline, including heart rate, stroke volume, cardiac output and blood pressure.⁶ They noted survival after arginine supplementation was 80 percent, compared to 33-percent survival in the control group. Further clouding arginines use in heart attack cases, Johns Hopkins University researchers published results showing arginine supplementation in conjunction with standard post-infarction therapies failed to improve vascular stiffness or cardiac output; they suggested arginine might actually be associated with increased post-infarction mortality.⁷ Possibly shedding light on the barriers to arginine benefits in infarction, University of Antwerp, Belgium, scientists concluded NO-mediated vasodilation following a heart attack might be restricted by a concurrent increase in superoxide.⁸

Activity of the cardiac sympathetic nerve is increased in CHF patients and can contribute to sudden cardiac death.⁹ Citing a possible connection between decreased NO in the brain stem, Japanese scientists investigated the role of increased NO production on nerve activity central to development of CHF.¹⁰ They found increased NO via endothelium NOS (eNOS) expression limits activity of sympathetic nerve activity. Further, exercise by CHF patients has been shown to reduce sympathetic activity.¹¹ Thus, arginine presents two possible benefits to CHF sufferers, based on its increase of NO and its ability to improve exercise in CHF patients. A recent study from the Institut de Physiologie in France found arginine supplementation might improve the physical fitness of CHF patients by increasing their endurance to exercise.¹² Patients taking L-arginine had a significant decrease in average heart rate during exercise and recovery period; researchers suggested arginines increase of NO and blood flow as a possible mechanism behind the results.

Arginine and NOS work with neurotransmitter acetylcholine to control vasodilation via the NO-pathway. There are, however, both beneficial and harmful levels of NO relative to health, and the devil is in the details of where NO is made. Inducible NOS expression creates large amounts of NO in the immune system during infection and inflammation; eNOS, as well as neuronal NOS (nNOS), is expressed in the endothelium, including the myocardium.¹³ Two flavone compounds from bamboo leaf (as UniBEX from Unigen Pharmaceuticals) might limit harmful NO production by iNOS, while increasing eNOS expression of NO. Corroborating this mechanism by bamboo leaf, Chinese researchers found one of the herbs flavonoids, orientin, caused vasorelaxation in animal aortic rings via eNOS manipulation.¹⁴ Additional research by these researchers showed bamboo leaf extract reduced blood viscosity in an animal model.¹⁵ Bamboo leaf (as Unibex) has further demonstrated an ability to manage atherosclerotic plaques in addition to curbing inflammation by suppressing vascular adhesion molecule (VCAM) expression and IL-6 in endothelial cells.¹⁶

Fellow Chinese herb Ginkgo biloba also promotes vasodilation along the NO pathway. Ginkgo may offer strong anti-thrombotic and antioxidant benefits in cerebral thrombosis, according to Japanese-British research, which found ginkgo extract administered to hypertensive rats decreased blood pressure.¹⁷ A more recent study from Mukogawa University in Japan confirmed ginkgo extract enhanced endothelium-dependent vasodilation and tamed hypertension.¹⁸ Offering further benefit to ischemic events, a French trial reported ginkgo can limit myocardial stunningbrief, reversible ischemia that can occur in cardiac surgery, myocardial infarction and unstable angina.¹⁹ Researchers noted the extract (EGb761) decreased free radicals in the animal heart model of myocardial stunning; the effect was not directly linked to ginkgolide B (an antioxidant), but may be a synergistic action of both ginkgolide and non-ginkgolide constituents. While research review has supported ginkgos benefit in ischemia,²⁰ a number of recent trials have found no evidence of benefit from ginkgo in recovery from stroke.^21,22 However, a 2007 Texas Tech University study found a bilobalide extract of ginkgo strongly reduced edema formation in models of brain ischemia in vitro and in vivo.²³

L-carnitine, derived from the amino acid lysine, also promotes heart health via NO-mechanisms. In a Canadian trial, administration of propionyl-L-carnitine, a carnitine derivative, improved left ventricle function in rats with induced heart attack and failure.²⁴ Similarly, L-carnitine and acetyl-L-carnitine improved heart function recovery in an animal ischemic infarction model, reducing the amount of heart damage and lowering mortality rate.²⁵ In patients who suffered recent heart attack, angina or CHF, carnitine reduced post-infarction death and recurrent failure, in addition to showing some potential ability to improve exercise tolerance and oxygen consumption in cases of moderate to severe CHF.²⁶

In 2002, a University of Sevilla, Spain, trial found carnitine supplementation in rats led to endothelial-dependent relaxation in the aorta, but they cited two possible mechanisms, the NO pathway or cyclooxygenase (COX) pathway.²⁷ However, in late 2006, a subsequent team from the same university published similar results, with reduced blood pressure in hypertensive rats; they were able to pinpoint a mechanism involving antioxidant action and NO.²⁸ They reported carnitine can increase cardiac antioxidant defense and reduce the systemic oxidative process in hypertension; by this, carnitine can increase NO availability in the hypertensive aorta by reducing superoxideone of the enemies of NO-mediated vasorelaxation following heart attacks.

A similar combination antioxidant-NO vasodilation effect is credited to French maritime pine bark extract (as Pycnogenol, from Natural Health Science). A 2002 review noted, among its many mechanisms, Pycnogenol fights vasorestriction caused by neurotransmitters (activated during stress by the sympathetic nervous system) by increasing eNOS expression.²⁹ It further noted the extract has exhibited the ability to dilate small blood vessels in patients with CVD, as well as reduce platelet aggregation and thromboxane concentration. Explaining the antioxidant aspect, the review noted Pycnogenol protects against oxidative stress in various cardiovascular cells by increasing intercellular antioxidant enzyme production and by scavenging free radicals.

A placebo-controlled, double blind study from the Chinese Medical Science Research Institute, Beijing, discovered 100 mg/d Pycnogenol for 12 weeks by 58 hypertensive patients decreased the need for hypertension medications by decreasing concentrations of vasorestrictive enzyme endotheiln-1, while also slightly increasing NO in plasma.³⁰ Other research on the extract has shown it is effective in controlling edema, particularly in the legs and in hypertensive patients with chronic venous angiopathy;^31,32,33 and studies have also confirmed Pycnogenol effectively inhibits deep vein thrombosis (DVT) in the legs.^34,35

Antioxidant Prowess

A slew of antioxidant compounds are making strides on advanced CVD and the damaging events that can befall patients. As with ginkgo and pine bark extract, many botanicals contain a wealth of phytochemicals with antioxidant properties. Flavanoids in tea have antioxidant properties and have generated some positive epidemiological results. A Dutch National Institute of Public Health review found increased intake of catechin flavanols from tea may decrease the risk of ischemic heart disease mortality, but not necessarily of heart attack or stroke.³⁶ Other Dutch research reported an inverse relationship between tea consumption and heart attack risk.³⁷ Despite the growing body of research on tea catechins and CVD risk, the Food and Drug Administration (FDA) rejected a health claim petition in mid-2006 for green tea and CVD risk, citing lack of credible evidence. However, shortly after this rejection, JAMA published results from a Japanese study that showed increased green tea intake led to decreased all-cause and CVD mortality.³⁸ Specifically, drinking five or more cups of green tea daily decreased CVD death risk by 31 percent in women and 22 percent in men, compared to their counterparts who drank less than one cup daily. Five cups daily also dropped the risk of death from stroke by 62 percent in women and 42 percent in men.

Other work on flavonoid-rich plant products includes research from the University of South Florida, College of Medicine, Tampa, and the National Institute on Drug Abuse, Baltimore, showing treatment with antioxidant-rich blueberries, spinach and spirulina reduced ischemia/reperfusion-induced apoptosis and stroke.³⁹

Plants also contain a host of vitamins and minerals indicated in CVD events. Low serum levels of selenium, an antioxidant trace mineral, have been linked to increased homocysteine levels and risk of cardiac death.⁴⁰ In a combination antioxidant trial, 50 mcg/d of selenium, 100 mg/d of vitamin C, 100 mg/d of vitamin E and 6 mg/d beta-carotene administered to 28 heart attack survivors for three months inhibited genetic-level damage compared to controls.41 Individually, vitamin C has been deemed a promising antioxidant inhibitor of oxidative damage in heart failure,⁴² while vitamin E has a more jumbled past on cardiac mortality, with one trial even suggesting vitamin E may increase the risk of heart failure.^43,44

However, a series of trials conducted at Ohio State University, Columbus, showed vitamin E and alpha-tocotrienols are neuroprotective, especially following a stroke. In fact, palm tocotrienol complex (as Tocomin®, from Carotech) is more potent than tocopherols in protecting brain cells from glutamate-induced degeneration and toxicity, which contributes to cell death and is central to stroke.^45,46 A 2005 Stroke journal article confirmed Tocomin protected against stroke-induced injury by acting on key molecular checkpoints (c-Src and 12-Lipoxygenase) in inhibiting glutamate- and stroke-induced neurodegeneration.⁴⁷ Similar results were reported in late 2006, as published results noted neuroprotection by Tocomin might be a synergy of both antioxidant and non-antioxidant mechanisms.⁴⁸

One rich source of tocotrienols is red palm oil. According to South African scientists, hearts administered red palm oil showed increased total myocardial polyunsaturated fat (PUFA) content, possibly improving reperfusion function (restoration of blood flow), possibly via the NO-cGMP pathway.⁴⁹ In addition to tocotrienols, red palm oil also contains an abundant supply of antioxidant carotenoids, including vitamin A precursor beta-carotene.

Plasma carotenoid levels have been inversely linked to risk of ischemic stroke.⁵⁰ In fact, Taiwanese researchers showed plasma concentrations of alpha- and beta-carotene are depressed following acute ischemic stroke and are negatively correlated with C-reactive protein and neurodegeneration.⁵¹ Increased beta-carotene intake also decreases risk of heart attack.⁵²

The non-provitamin A carotenoid lycopene is also useful in heart attack and stroke cases. Lycopene-rich tomatoes possess anti-thrombotic effects both in vitro and in vivo.⁵³ The Kuopio Ischaemic Heart Disease Risk Factor Study, conducted in Finland, demonstrated men with the lowest serum lycopene levels had a 3.3-fold risk of acute coronary events, including stroke.⁵⁴ And increased adipose lycopene levels may also correlate to decreased risk of heart attack.⁵⁵

Fellow non-provitamin A carotenoid astaxanthin has proven its own potential benefits to heart attack and stroke patients. According to study results from Medical College of Wisconsin, Milwaukee, astaxanthin supplementation inhibits stroke, possibly via antioxidant protection of neurons, in ischemic mice.⁵⁶ The carotenoid may also protect the heart from oxidative damge;⁵⁷ a Japanese trial showed rats given astaxanthin prior to induced heart attack had reduced infarction or damage area.⁵⁸

Vitamin-like coenzyme Q10 (CoQ10) also confers antioxidant benefits to later stage CVD. Research has confirmed CoQ10 is taken up in the heart,⁵⁹ where it might curb oxidative damage and restore CoQ10 levels depressed by heart failure.^60,61 Researchers noted CoQ10 improved left ventricular ejection fraction (systolic) and diastolic volume, and systolic function decreased three months after supplementation stopped. In addition to increasing cardiac output, CoQ10 has been shown to reduce stroke volume and improve exercise tolerance.⁶²

A crucial link in the electron transfer chain in the mitochondria, CoQ10 is important for ATP synthesis. One of the components of ATP is ribose, a naturally-occurring pentose carbohydrate. Like CoQ10, ribose offers CHF patients numerous scientifically validated benefits, including increased high-energy phosphates and improved diastolic dysfunction following myocardial ischemia. The University of Utah, Salt Lake City, conducted a series of studies on ribose (as CORvalen, from Bioenergy) in CHF patients. In one trial, patients with advanced CHF who took 5 g/d ribose for eight weeks experienced increased ventilatory efficiency and oxygen uptake, which helps improve exercise ability.⁶³ The facilitys subsequent studies showed CORvalen improves survival rates among CHF patients, boosting myocardial performance scores and helping to maintain maximum exercise capacity.^64,65

The most recently reported work in this area was presented at Heart Failure Society of Americas 10th Annual Scientific Meeting in Seattle, in late 2006. In the study, researchers from Aurora Denver Cardiology Associates, Denver, administered ribose daily to 16 CHF patients for eight weeks and charted a significant improvement in submaximal exercise performance among the patients. The scientists noted seven of the patients on ribose showed improvement in Weber Functional Class scores, which means those patients may experience a better quality of life and be able to function more effectively in performing their day-to-day activities.

Recovery from heart attack is another hot research area for ribose, which is considered a useful adjunct in coronary bypass surgery; it helps reduce time between the attack and the surgery. A study on 24 heart attack patients at Saddleback Memorial Medical Center, Orange, Calif., revealed post-op cardiac index scores were 49-percent greater in those taking ribose supplements than in the control group.66 The researchers explained ribose preloading in conjunction with revascularization and off-pump bypass surgery improved cardiac function to a greater degree than traditional techniques.

Exercise helps CHF patients breathe easier without damaging their hearts. In addition to the ATP-level natural solutions, the herb hawthorn helps CHF patients exercise more and tire less. A review of hawthorn research literature revealed hawthorn treatment in CHF patients from eight different trials was more effective than placebo in decreasing pressure heart rate product and improving maximum workload.⁶⁷ Among the existing trials, exercise tolerance and maximum cardiac load were improved in 143 CHF patients taking a standardized fresh hawthorn extract;⁶⁸ and clinical progression of fatigue, stress dyspnea (shortness of breath) and palpitations were reduced in 952 patients taking the WS 1442 hawthorn extract.⁶⁹ A University of Chicago review reported hawthorns cardiac benefits, including antiischemic, anti-arrhythmic, hyolipidemic and hypotensive actions, may be partially due to its antioxidant flavonoids.⁷⁰ Most recently, a late-2006 in vitro test of hawthorn extract showed anti-arrhythmic actions via induction of rhythmicity in cardiac muscle cells.⁷¹

The rhythm of the heart is a particular focus of essential fatty acid (EFA) supplementation, which has been linked to decreased risk of heart attack, stroke, cardiac arrest and reduced CVD mortalityespecially sudden cardiac death.^72,73,74 In matters of the heart, fish oil leads the EFA charge. While some research has discovered a link between long-term intake of fish and reduced incidence of atrial fibrillation,⁷⁵ trials on fish oil and arrhythmia have delivered debatable results. A six-center, randomized, double blind, placebo-controlled trial conducted at Oregon Health and Sciences University, Portland, found fish oil supplementation did not reduce risk of either ventricular tachycardia (VT) or V-Fib.⁷⁶ Harvard Medical School scientists delivered contradictory results, as regular fish oil consumption in people at high risk of ventricular arrhythmias seemed to decrease potentially fatal ventricular arrhythmias.⁷⁷ However, results from the Study on Omega-3 Fatty acids and ventricular Arrhythmia (SOFA), published in JAMA in mid-2006, showed omega-3 EFAs from fish oil did not have a strong protective effect against ventricular arrhythmia.⁷⁸

The randomized, parallel, placebo-controlled, double blind trial was conducted at 26 cardiology clinics across Europe and involved 546 patients with implantable cardioverter-defibrillators (ICDs) and prior documented VT or V-Fib, who received either 2 g/d of fish oil or placebo for one year. According to the report, event-free survival did not substantially improve in the patients taking fish oil;⁷⁹ 75 patients (27 percent) in the fish oil group and 81 patients (30 percent) in the placebo group needed ICD intervention for VT or V-Fib.

On a more positive note, a Dutch study showed fish oil supplementation (1.5 g/d) in patients with recurrent premature ventricular complexes (PVC)common arrhythmias that can lead to more dangerous arrhythmiasdid not curtail recurrent PVCs;⁸⁰ they did report the intervention significantly decreased decrease heart rate, indicating a lower risk of sudden cardiac death.

An Emory University School of Medicine, Atlanta, trial confirmed this benefit to heart rate, as 58 elderly patients randomized to receive either 2 g/d fish oil or 2 g/d soy oil for six months experienced improved heart rate variability, with more pronounced benefit in the fish oil group.⁸¹

Heart rate variability was an outcome in a trial on fungal proteases (Aminogen®, from Triarco) combined with whey protein.⁸² Researchers from University of Yaounde, Cameroon, 52 healthy, lean males (ages 19 to 35 with a body mass index [BMI] of 20 to 24) were given 50 g/d of whey protein concentrate for 10 days; then they were divided into two groups, one receiving the whey plus 2.5 g/d Aminogen and the other whey plus 5 g/d Aminogen. Results showed whey alone reduced heart rate and blood pressure, but the reductions were less pronounced with the addition of either Aminogen dose. Researchers theorized Aminogen, a digestive aid, may hydrolyze the whey in such a way to limit production of the peptides in whey responsible for lowering systolic blood pressure and heart rate.

Protein intake was linked to risk of ischemic disease in a collaborative cohort study from Harvard School of Public Health, Harvard Medical School, the Channing Laboratory and Brigham and Womens Hospital.⁸³ Researchers found decreased risk of ischemic heart disease in women correlated to increased protein intake. While both animal and vegetable protein proved beneficial, the authors acknowledged diets rich in animal protein might contribute an unhealthy amount of saturated fat and cholesterol.

Risk of advanced heart disease is further impeded by another dietary staple, fiber. Increased intakes of soluble fiber can significantly reduce risk of not only CVD, but also cardiac events.⁸⁴ In a University of Washington, Seattle, prospective cohort study, 3,588 CVD-free men and women aged 65 or older were monitored from 1989 to 2000 for fiber intake from cereal, fruit and vegetables, as well as for incident CVD.⁸⁵ Those with the highest fiber intakes experienced a 21-percent reduction in cardiac events, especially stroke and other cardiac ischemia. A review of existing cohort studies on the fiber and reduced cardiac eventsinvolving a combined 336,244 men and womenfound each 10 g/d incremental increase in total dietary fiber intake correlated to a 14-percent decrease in risk of all coronary events and a 27-percent reduction in risk of coronary death.⁸⁶

The heart presents a complicated conundrum. It beats 100,000 times a day, pumping blood through an intricate network of arteries and veins 60,000 miles long. This cardiovascular system runs well even in the face of poor diets, unfortunate genetics and sedentary lifestyles. But numerous biological villains can cause substantial and progressive damage to the heart and its vessels. The factors that threaten heart health, including high cholesterol and triglycerides, inflammation, hypertension and other atherosclerotic rogues can all be addressed with dietary intervention. When these factors are not sufficiently controlled, advanced CVD takes over with its roster of evildoers, including heart attack, stroke, arrhythmia and heart failure. Research shows these, too, can be impacted by dietary supplementation, either in preventing initial and recurrent cardiac events or in promoting recovery and long-term survival.

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