Cardiovascular Health: The First Component of Healthy Aging

by Chris D. Meletis, ND 

This article addresses interrelated factors that play an equally important role in heart health: arterial calcification (atherosclerosis), thrombus (clot formation) and high fibrinogen and C-Reactive Protein levels.

Arterial Calcification
 
Atherosclerosis, otherwise known as hardening of the arteries or arterial calcification, is derived from the Greek words athero, meaning gruel or paste and sclerosis, which means hardness. The simple explanation of atherosclerosis is that it occurs due to a progressive buildup of plaque within the arterial wall and a loss of elasticity. The more in-depth explanation involves taking a look at the description of an artery.

The artery wall is a collection of three layers. There is a layer of connective tissue, a second layer comprised of smooth muscle cells and elastic connective tissue, and a third layer of endothelial cells. When the endothelial cell layer is damaged, normal blood flow is altered. In addition, the damaged area provides sites for the adhesion and aggregation of blood platelets, leading to the formation of blood clots (thrombi) in the arterial wall. Alterations of the endothelial layer causes white blood cells (macrophages) to become more easily attracted to this area, where they stick like glue.

Once the macrophages infiltrate the inner endothelial layer they begin to convert and accumulate modified LDL cholesterol, which results in the formation of what’s called foam cells. Foam cells congregate into lesions known as fatty streaks in the inner arterial layer (Fig. 1). Foam cell aggregation causes muscle cells from the medium arterial wall layer to replace the normal smooth endothelial cells. The muscle cells, in turn, convert into cells that produce connective tissue and that have a greater propensity to collect lipids. This begins a vicious cycle of inflammation and platelet aggregation in the damaged arteries, which results in additional platelet aggregation and adhesion. The result is the formation of thrombi (clots) in the arterial wall. As more fatty streaks build up, this continues to attract more blood cells to the arterial wall as well as cholesterol deposition, smooth muscle cell expansion and connective tissue formation, all processes that lead to more advanced lesions. As these lesions, called fibrous plaques, cling to the arterial wall, they increase in size, narrowing the arterial lumen and interfering with blood flow. Fibrous plaques are covered by a thick layer of connective tissue, which in turn covers a tangled mess of smooth muscle cells and an overlay of lipid and necrotic debris. Gradually, these plaques calcify and evolve, either partially or completely reducing arterial blood flow. These atherosclerotic changes can lead to myocardial infarctions (heart attacks), angina pectoris (severe chest pain), strokes, intermittent claudication, and even macular degeneration.

Fibrinogen’s Fatal Role 

Fibrinogen is a high molecular weight plasma protein that plays a key final role in the blood-clotting cascade. In simplistic terms, it acts like the needle that sews the fabric of a blood clot together. Elevated blood levels of fibrinogen have been identified in a number of studies to be a major risk factor for coronary heart disease (heart attacks) and cerebrovascular disease (strokes), which together account for about 60 percent of deaths in the elderly. Without fibrinogen, the atherosclerosis process described above could not occur.

In fact, fibrinogen may possibly be the major risk factor for heart disease, exceeding the risk posed by homocysteine, cholesterol and other lipid parameters.¹ 

In a recent study, men with a high coronary heart disease risk score had higher fibrinogen levels than men with a lower risk of coronary heart disease. Men with a high stroke risk score also had significantly higher levels of fibrinogen.² 

Strengthening Arterial Health 

One of the most effective ways to strengthen arterial health is through a combination of oral and IV chelation. In oral chelation, agents are used to strengthen the health of the arteries. The most effective combination of chelators includes the synthetic amino acid, ethylene diamine tetraacetic acid (EDTA) (Fig. 2) along with garlic, chlorella, and malic acid.

EDTA is thought to help support cardiovascular health through removal of heavy metals. The Food and Drug Administration has approved EDTA as a pharmaceutical agent for the treatment of lead and other heavy metal poisoning or exposure. In older literature, the FDA also approved EDTA as being “possibly effective in occlusive vascular disorders…arrhythmias and atrioventricular induction defects…and in the treatment of pathologic conditions to which calcium tissue deposits or hypercalcemia may contribute other than those listed above.”³ 

In addition to EDTA’s intravenous benefits are its clinical uses when administered orally. Early clinical studies with EDTA reported loss of fat in rats, reduction of cholesterol in rabbits, and reduced blood pressure in humans. Consequently, a study of the effects of oral EDTA on patients with atherosclerosis and/or hypertension was conducted on 10 patients. Four of these patients had hypertension, four had angina pectoris, one had peripheral vascular disease (intermittent claudication), and one was recovering from a heart attack. All were treated with one gram of oral EDTA daily for three months. Seven of the ten patients experienced significant reductions in their cholesterol levels, and blood pressure was reduced in all ten. The most marked change occurred in the patient with intermittent claudication, whose cholesterol dropped from 278 mg per 100 ml to 128. This patient also reported improved exercise tolerance, and the researchers found improved pulsations in the extremities. The four patients with angina pectoris also all reported improvement.⁴ 

Scientists at Wayne State University also quantified reversal in atherosclerotic plaque in rabbits that were treated with daily subcutaneous EDTA injections.⁵ 

Garlic is another chelating agent that supports arterial health and healthy cholesterol levels, reduces the risk of thrombosis (the ability of clots to break away from the arterial wall and move through the blood stream), and promotes healthy blood pressure levels.⁶ Garlic’s effects are attributed to allicin, ajoene, and other organosulfur constituents in the herb.⁷ 

Garlic shows promise for improving platelet-function discrepancies related to cardiovascular disease. In one study, garlic extract inhibited platelet aggregation and adhesion to fibrinogen at all levels of supplementation.⁸ In another study of the effects of garlic on human blood, platelet adhesion to fibrinogen was decreased by approximately 30 percent compared to placebo.⁹ A new study on garlic confirms that it exhibits powerful fibrinolytic activity both in vitro and in vivo. In this study, it acted as an anticoagulant by downregulating thrombin formation.¹⁰ Thrombin is an enzyme formed in blood from prothrombin, which reacts with fibrinogen to convert it to fibrin, the primary material that holds together a blood clot. Garlic’s thrombin-reducing mechanism of action led the researchers to state that garlic may have “a beneficial role in preventing pathological thrombus formation” in cardiovascular disorders that involve blood clotting.

Using chlorella to complement the chelating effects of EDTA and garlic can serve as a highly effective way to improve heart health. In a pilot study on chlorella’s role in blood pressure health in 24 hypertensive subjects, 25 percent of the patients (6 of 24) experienced a reduction in the blood pressure. In the remaining subjects, the blood pressure stabilized after chlorella supplementation. Quality-of-life questionnaires indicated an overall perception that health had significantly improved in conjunction with chlorella consumption.¹¹ 

In animals, chlorella also has been shown to have anti-atherosclerosis actions and to protect the arteries against the damaging effects of a high-fat diet.¹² 

Malic acid works with EDTA, garlic, and chlorella to help improve vascular health. This organic acid is important for overall heart health and protects human vascular endothelial cells from the effects of oxidized cholesterol.¹³ 

Weakening Fibrinogen 

One of the most effective natural agents for lowering fibrinogen levels is nattokinase, an enzyme derived from the traditional fermented Japanese soy food known as natto. In vitro and in vivo studies have consistently demonstrated the potent fibrinolytic (fibrinogen-destroying) effect of this enzyme. In one in vitro study, nattokinase significantly reduced red blood cell aggregation and blood viscosity, with these beneficial effects evident at concentrations similar to those achieved in previous in vivo animal trials.14 

In another study, nattokinase demonstrated some impressive effects in rats. Three weeks before the researchers triggered endothelial damage in the arteries of the animals, they began feeding the animals nattokinase. Intimal thickening in animals fed nattokinase was significantly suppressed compared with controls. In the control group, after arterial injury was induced, although the center of vessel lumen was reopened, thrombi were attached on the surface of vessel walls. In contrast, in nattokinase-treated groups, thrombi near the vessel wall split apart. In addition, after breaking apart, most of the thrombi detached from the surface of vessel walls.¹⁵ 

“In conclusion,” the researchers wrote, “dietary natto-extracts supplementation suppressed intimal thickening produced by endothelial injury in rat femoral artery.”

Scientists have found that nattokinase has four times greater fibrinolytic activity than plasmin, an clot-destroying enzyme found naturally in the human body that is produced from the protein plasminogen.¹⁶ 

Human studies have produced similar results. In one study, 12 volunteers (six men and six women) were fed 200 grams (seven ounces) of natto, and two methods of measuring their blood’s fibrinolytic activity were used. In the euglobulin clot lysis test, a blood sample was taken and the formation of a thrombus (clot) was then artificially stimulated. The time required for the blood to completely dissolve the clot was then measured. In the natto group, the time needed to completely dissolve the clot was cut in half compared to those in the control group.
The fibrin plate method was then used on other blood samples. In this test blood was added to a plate with a special polymerized fibrinogen to see how much it would dissolve in four hours. The control group’s blood had no effect in this test, but the natto group’s blood dissolved 15 mm2 of fibrinogen.¹⁷ 

Next, the researchers had volunteers consume nattokinase tablets for eight days, using the same two tests plus the fibrin degradation product test. They also measured tissue plasminogen activator (TPA) blood levels. These tests further confirmed nattokinase’s clot-dissolving power, with the men showing an increase in TPA activity as well. While the researchers had previously shown that nattokinase had direct fibrinolytic activity, the finding of increased TPA activity (which increases plasmin) showed nattokinase to augment the body’s own fibrinolytic activity.¹⁷ 

Nattokinase can be especially effective when combined with serrapeptase, an enzyme derived from the Serratia bacteria, which lives in the intestinal tract of silkworms. Hans Nieper, a pioneering medical doctor in Germany, became one of the first clinicians to use serrapeptase to gradually reduce atherosclerotic plaque buildup. Other researchers have observed that serrapeptase “has been shown to induce intense fibrinolytic, anti-inflammatory, and anti-edemic activity….”¹⁸ Because inflammation elevates fibrinogen, and elevated fibrinogen increases clotting risk, serrapeptase’s anti-inflammatory activity complements its fibrinolytic activity.

Turmeric (Curcuma longa) has exhibited equally powerful fibrinogen-destroying properties. Scientists in Spain treated eight subjects with elevated fibrinogen levels with 20 mg of turmeric extract per day. After only 15 days, previously elevated levels of fibrinogen dropped in all eight subjects.^19 20 A more recent review of turmeric’s effects by the same researchers indicated that in human healthy subjects, a daily intake of 200 mg results not only in a decrease in lipid peroxidation, but also an antioxidant-induced normalization of the plasma fibrinogen levels.²¹ 

In addition to lowering fibrinogen levels, turmeric is emerging as one of the most effective natural substances for lowering C-Reactive Protein, a risk factor for heart disease that becomes elevated in response to inflammation. When researchers induced inflammation in rodents, the level of C-Reactive Protein increased to 200 percent on day 21 and then fell to 50 percent on day 35 compared to controls not exposed to the inflammatory treatment. Curcumin, the pigment in turmeric responsible for its yellow color, further reduced the increased levels of CRP at both the time intervals.²² 

Bacterial Origin of Heart Disease 

Because a lot of the medical literature is now pointing to a possible infectious origin of heart disease, I wanted to briefly touch upon heart disease risk in patients whose cardiovascular concerns may be bacterial related. One of the agents shown to help in this group of patients is EDTA, the chelator I mentioned above. An interesting recent study indicates that EDTA, when combined with antibiotics and natural heart-supportive nutrients, can reverse calcification in coronary arteries in patients whose calcification may be pathogen triggered.

Recent reports in the medical literature suggest that infectious blood nanobacteria may serve as a trigger to begin the process of arterial calcification. Consequently, researchers enrolled 100 patients with stable coronary artery disease into a four-month study. The patients consumed a variety of substances, including vitamin C, niacin, folic acid, arginine, CoQ10, EDTA and hawthorn taken orally every evening. They also received an antibiotic every evening and rectal EDTA in addition to oral EDTA. Seventy-seven patients completed the study and all patients were positive for nanobacteria. In 44 of the subjects (57 percent), there was a significant decrease in total coronary artery calcium scores, the average decrease being 14 percent. Angina was decreased or ablated in 16 of 19 patients (84 percent). Lipid profiles significantly improved to non-atherogenic levels, a remarkable finding in a patient group where 86 percent were on continuous statin medication before the trial. No adverse physiologic effects were seen. The researchers concluded that their results inferred that the combination of EDTA, the nutritional supplements listed above and antibiotics regressed the calcified coronary artery plaque volume.²³ 

It would be interesting to take this study one step farther and to research whether the EDTA and additional nutrients were able to achieve the same effects independently of the antibiotics. However, this study indicates that EDTA combined with the nutrients mentioned above as well as natural anti-infectious substances, may prove to be an additional modality to support arterial health.

Conclusion 

Nourishing the health of the heart entails focusing on a number of factors including cholesterol, homocysteine, arterial calcification and blood clots, fibrinogen and C-Reactive Protein levels. Using a combination of the supplements mentioned above, along with omega-3 fatty acids and connective tissue nutrients such as vitamin C and bioflavonoids, will help address all these factors to ensure that as we age our cardiovascular systems remain as strong and healthy as possible.

Dr. Chris D. Meletis , Executive Director, The Institute for Healthy Aging, article reprint via an educational grant from Complementary Prescriptions  

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