Heartblog

At least 20 books have been authored on the subject of chelation therapy. The majority of these books were written by respected medical doctors. Though many medical doctors use this therapy in their private practices it has not gained widespread acceptance…yet. Using chelation therapy for the treatment of heart disease is still considered to be an experimental treatment. Chelation must be administered by a trained medical professional because it can affect kidney function. Currently the only certification course on EDTA chelation is offered by the American College for the Advancement of Medicine (ACAM).

What is EDTA chelation therapy?

In medicine, chelation is used to rid the body of toxic or excess metals/minerals such as lead or calcium. For example, a person who has lead poisoning may be given EDTA chelation therapy in order to bind and remove excess lead from the body before it can cause damage. EDTA (ethylene diamine tetra-acetic acid), is a synthetic, or man-made, amino acid that is delivered intravenously. EDTA was first used in the 1940s for the treatment of heavy metal poisoning. EDTA chelation removes heavy metals and minerals from the blood, such as lead, iron, copper, and calcium, and is approved by the U.S. Food and Drug Administration (FDA) for use in treating lead poisoning and toxicity from other heavy metals.

Although it is not approved by the FDA to treat heart disease, some physicians and alternative medicine practitioners use EDTA chelation as a way to treat this disorder. This is considered to be an “off label” use.

How does chelation therapy work?
There a numerous ways in which chelation may work. The effects on humans may be a sum of all the mechanisms of action or just one – we still do not know for sure just why chelation is so helpful in atherosclerosis. The following is a list of all the mechanism by which EDTA chelation may work:

1. EDTA chelation improves the elasticity of arteries by reducing the number of cross linkages in the connective tissue and elastic tissue comprising arterial walls. Cross linking accelerates aging is what causes skin to wrinkle, sag and loose its youthful elasticity. In the artery cross linking causes stiffness. EDTA decreases the cross linkages in the arterial wall allowing it to expand and contract as it was designed to do. As arteries become less stiff improved circulation and lower blood pressure is a result. Lower blood pressure reduces the work the heart must do thus improving symptoms of angina.

2. Chelation therapy can also reduce the non metallic cross linkages that occur between molecules such as sulfur to sulfur cross linkages. One of the metals EDTA removes in aluminum. Aluminum can cause cross linkages between collagen and elastic tissue, making soft tissue and arteries more rigid and speeding the aging process. This makes arteries more elastic or flexible, returning them to a more youthful state. Another benefit of this is a lower blood pressure.

3. EDTA chelation therapy is a potent antioxidant. This is the most important action of EDTA.

4. During the short time that EDTA circulates in the body it temporarily lowers blood calcium. This signals the parathyroid gland to step up production of parathyroid hormone to help bring calcium levels back up. This may be how EDTA chelation increases bone density.

5. EDTA help balance prostaglandin production. Prostaglandins are important hormones that control inflammation, clotting and blood pressure. The two most important prostaglandins for blood vessel health are thromboxane and prostacyclin. Prostacyclin reduces platelet “stickiness”, helps prevent arterial spasm and blood clots, counters plaque formation, and improves blood flow. Thromboxane causes platelets to stick together and also promotes arterial spasm, something we definitely do not want. Prostaglandins are produced from fats in the cell membrane. The oxidation of fats in cell membranes is called “lipid peroxidation” by scientists and is one of the main ways in which cells age. The production of prostaglandins is imbalanced by the presence of oxidized fats (also know as lipid peroxidation). EDTA inhibits oxidation of lipids in the cell membrane and restores optimal prostaglandin balance. Fatty acid oxidation (lipid peroxidation) inhibits prostacyclin production. EDTA is able to reduce oxidation of fats in cell membranes by chelating out the metallic ions that cause lipid peroxidation. Measuring and reducing lipid peroxidation is a foundational element in anti-aging medicine.

6. EDTA acts as an anticoagulant through its beneficial effect on platelets.

7. EDTA lowers blood calcium levels and helps normalize calcium metabolism by stimulating uptake of calcium in bones. Evidence demonstrates the chelation therapy may help improve bone density.

The way I describe chelation to patients is this: You are getting a safe intravenous antioxidant that removes toxic metals, makes your blood vessels more flexible and acts as an anticoagulant all at the same time.

Another study links blood viscosity to heart attacks and strokes. As many of you know I am big on blood viscosity. Following is a press release on the latest study sent to me by my friends at The Blood Clinic.

April 23, 2008 – Research published in the European Journal of Clinical Investigation suggests that elevated blood viscosity increases the risk for heart attacks and strokes by 342% in men with high blood pressure.

The findings are based on a study of 331 men between 40 and 64 years of age who were newly diagnosed with essential hypertension, then followed for up to 12 years. Researchers grouped patients into three categories by their diastolic whole blood viscosity (“WBV”) levels: top-tertile diastolic blood viscosity (WBV > 243), middle tertile (228 < WBV < 243), and bottom tertile (WBV < 228), (all units in millipoise [mP]). The highest blood viscosity group had more than a threefold risk of cardiovascular events than the lowest blood viscosity group (hazard ratio = 3.42, 95% confidence interval = 1.40-8.38, p-value = 0.006).

In the 331 men with high blood pressure who were studied, there were 42 first cardiovascular events, specifically, 9 subjects with myocardial infarction, 14 with unstable angina, and 19 with acute stroke.

The study authors wrote: “Whole blood viscosity, an overall measure of flow resistance of bulk blood, depends on several factors, including cell concentration, cell aggregation, cell deformability and plasma viscosity. In our data, both WBV and hematocrit were univariate predictors of cardiovascular morbidity but only the former came out as an independent risk factor in a multivariate analysis, thus supporting the perspective that low-shear-rate (diastolic) WBV as a global marker of the whole-blood rheological properties may be a better discriminant of cardiovascular risk in hypertensive men.”

The researchers concluded that their findings highlighted the role of blood viscosity in impairing microcirculation and that a “vicious cycle” may exist in which impaired microcirculation maintains, or even amplifies, an initial increase in blood pressure.

The report states: “This study has documented the powerful independent associations between WBV at low shear rate (diastolic)and cardiovascular events.” (Ed. note. parentheses added)

SOURCES:

G. Ciuffetti, et al. Prognostic Impact of Low-Shear Whole Blood Viscosity in Hypertensive Men. European Journal of Clinical Investigation, 2005:35(2), 93-98.

Myth number one

The thought of having a sudden heart attack is so disturbing that many people don’t even consider that it could happen to them. I call this the “it can’t happen to me scenario”. Other people may say things like “my cholesterol is normal and I exercise, eat well and don’t have too much stress so I will not get a heart attack.” Well I’m here to tell you from personal experience that this is a very poor way to gauge your risk of an unexpected heart attack. I call this myth number one. While getting regular exercise and following a heart healthy diet reduce risk of heart disease these elements alone do not completely prevent it and if you have plaque, I assure you that diet and exercise are not enough to reverse it.

When I speak about unexpected heart attacks, I am referring to heart attacks in otherwise healthy people between 30 and 70. At over 70 years of age many of us already have extensive coronary plaque, and though still somewhat preventable, a heart attack would not be that unexpected. In clinical practice my focus on modifiable causes of heart attacks: arteriosclerosis, atherosclerosis and coronary heart disease. Many other non-reversible cardiac and vascular conditions exist (valve problems, aneurysms, conduction abnormalities), and these may need to be corrected with surgery.

In the Boulder area in particular there are people who get much more exercise than the average American. They think that because they train 6-12 hours a week their heart must be very healthy. This simply is not true. In fact, athletes may even be at increased risk for coronary artery disease. Here’s why. It’s because of phenomenon called shear stress. Shear stress is cause by a combination of pressure, velocity and high blood viscosity (thick blood). If your blood is very thick and the pressure is high stress on the wall of the artery is the highest. High pressure and thick blood can also occur separately. Shear stress causes damage to the blood vessel lining, causing the vessel wall to thicken, become stiffer and develop plaque.

Athletes, especially those who live at higher elevation, tend to have high red blood cell counts which are a major cause of thick blood. Also, the higher work demands that they put their vascular systems through can exacerbate this effect. I’m not saying exercise is bad, but if you have a high blood viscosity exercising at high intensity may be like taking three steps forward and two back. The incidence of sudden death during athletic activity is still very low, ranging from 1 per 13,000 man-hours of activity in cross-country skiing, to 1 in 396,000 man-hours of activity in jogging. [1]

Blood viscosity

Blood is a non Newtonian fluid and behaves much like catsup coming out of a bottle. Once you get it moving is really moves fast. Non Newtonian fluids do not behave in a linear fashion. An example of a Newtonian fluid is water. Blood, on the other hand, moves sluggishly is low speeds and is more liquid at fast speeds. When the heart is resting between beats (called diastole) it becomes more viscous and then when the heart forces blood out (called systole) blood becomes less viscous. The main determinant of blood viscosity is red blood cell mass (also known as hematocrit). Though there are other factors that affect blood viscosity, they go beyond the scope of this discussion.

Why is blood viscosity important? 1) High blood viscosity increases the amount of work the heart must do to perfuse the tissues and deliver oxygen. This makes for an inefficient circulatory system and can cause the heart to enlarge to compensate for the extra work. An enlarged heart requires more oxygen and can lead to other problems. Enlarged hearts are common in athletes but become a health risk if the enlargement becomes too great.

An analogy is the car engine. Motor oil comes in different viscosities…thicker for summer and thinner for winter. High blood viscosity is analogous to putting summer oil in your car in the winter and the result is poor gas mileage as the engine’s efficiency is decreased.

1) A surplus of red blood cells (the most common cause of elevated blood viscosity) can cause damage to the inner lining of the blood vessel as they constantly bump against the surface

2) The damage eventually leads to plaque formation (also called a callus). This is an adaptive response to the injury and acts to protect the artery wall in the short term at the expense of long term function. An analogy here is the calluses we get in response to friction on the skin.

4) High blood viscosity also creates something called low shear stress. The easiest way to think about this is that in between heart beats the blood thickens and swirls around, causing eddies and turbulence. Turbulent blood flow also causes damage to the cells that line your arteries. A good analogy here is the sandbars that form in rivers and streams from eddies and back currents. Plaque tends to deposit most heavily in the low shear regions of arteries, like a sandbar. As plaque continues to deposit blood flow is further disturbed leading to more turbulence and plaque deposition.

5) High blood viscosity also contributes to something called injurious pulsatile blood flow. Think of this as a pressure wave with a high peak. Injurious pulsatile blood flow damages the lining of the blood vessel.

Why thinner blood might make you faster

As long ago as the early 1970 researchers began study the question of what is the hematocrit level that allows for optimal oxygen delivery to the body. Recently, in 2000 an Oxygen Delivery Index (ODI) was created by Kamenva et al. The highest oxygen delivery occurred in subjects with hematocrits between 25-30%. Higher hematocrits and elevated blood viscosity were also associated with higher risk of coronary artery disease in these studies.The workload of the heart is also reduced by having thinner blood. Also by donating blood younger red cell blood (RBCs) will predominate. Younger RBCs carry and deliver oxygen better than older cells.

How do you get tested?

I run this test though a special lab dedicated to blood viscosity testing called The Blood Clinic. This is NOT a standard test any doctor can do.

What is the treatment for elevated blood viscosity?

Often the best treatment is to donate blood. Elevated red blood cells are the main cause of thick blood and donating blood lowers your red blood cell count. In the Boulder/ Denver area I shoot for a hematocrit of 40-45 in men and 35-40 in women. How often you should donate will depend on your profile. Some people should not donate at all. Occasionally there are other causes of elevated blood viscosity.

Other effective treatments include fish oil and nattokinase.

Why have you not heard of blood viscosity before?

The science of hemodynamics and blood rheology is not new, but the testing is, thus it has not entered the mainstream yet. Also since drugs do not treat this problem pharmaceutical companies are not interested.

Cholesterol and Lipoproteins

Where does cholesterol come in? Think of cholesterol as a mediator of plaque formation. Cholesterol has received overemphasis by the media and drug companies because there are profitable drugs to treat it but cholesterol by itself is not really the problem. We should be focusing on particles called lipoproteins. Cholesterol is packaged in a protein shell called a lipoprotein. It’s the nature of the lipoprotein that determines how damaging a given level of cholesterol is. Lipoproteins also affect blood viscosity.

Lipoproteins that are small and dense are more damaging than those that are large and non-dense. Some types of cholesterol are worse than others, and some types, such as large HDL are actually protective. Only treating cholesterol in a patient with evidence of coronary artery disease is like fighting forest fires but neglecting to deal with the problem of too much underbrush and dry wood in the forest. Cholesterol is an important risk factor but to get the best results it’s the lipoproteins we should be targeting, along with other risk factors.

Myth number two

Many of you reading this will have asked your doctor about heart disease. Most doctors respond by giving you an electrocardiogram (ECG) or a stress test (also known as a treadmill test). If you fail the treadmill test you will need further work up by your cardiologist (angiogram etc). But if you pass these tests, are you free of heart disease? The answer is no. You can have extensive plaque and still pass a treadmill test. There usually has to be blood flow limitation to the heart muscle to cause you to fail this test.

It’s a good idea to have an ECG to rule out an abnormal electrical heart pattern called “diffusely distributed and deeply inverted T waves.” This pattern has been linked to sudden death in young athletes. But what about older athletes? In addition to plaque rupture chronic exercise conditioning may cause a condition called hypertropic cardiomyopathy. An echocardiogram can rule this out and I occasionally recommend these to older athletes. The main concerns in older athletes are plaque rupture.

The single best way to determine the level of plaque in your coronary arteries is to get a heart scan. I like to send my patients to Front Range Preventive Imaging in Boulder for this test. They use a special low radiation CT scan machine that can accurately give you a “plaque score.” This score is based on the fact that 20% of well established hard plaque is calcium. The machine is able to detect this calcium and even show which arteries are affected. I recommend that everyone over 40 get this test. Occasionally I recommend it for people under 40 who have more risk factors. I can track plaque progression (or reversal) by repeating the heart scan every few years. This is one of the best anti-aging and heart disease prevention tools that we have. Blood viscosity testing coupled with plaque scoring, blood chemistries and lipoprotein analysis provides an unsurpassed method for preventing heart attacks.

[1] R. Virmani Cardiology clinics Volume 15, Issue 3, 1 August 1997, Pages 439-466

Low-density lipoprotein cholesterol (LDL) is well established as a major cause of CHD and your risk of getting CHD can be reduced by 20% to 40% if you can get your LDL down to optimal range. This sounds good until your realize that we still have 60% to 80% available for further risk reduction. This is where raising HDL comes in. Cardiac risk is thought to drop by two to three percent for each 1 mg/dL increase in HDL.

Increased reductions in plaque formation can progressively occur the lower your LDL goes down (to a level of 40 mg/dL). Going lower than 40 mg/dL does not provide any additional benefit.  By raising your HDL to greater than 60 mg/dl even greater protection and reductions in plaque may be seen. How much plaque regression you can achieve will depend on your lipoprotein pattern and other risk factors.

The Framingham Heart Study was one of the first studies to demonstrate that low HDL is associated with increased coronary heart disease (CHD). The prevalence of CHD increases by 25% to 30% for every 10-mg/dL decrease in HDL ( below 45 mg/dL).
 
Statistics show that individuals with HDL of less than 45 mg/dL, have 2- to 7 times more occurrence of CHD compared to people  with HDL greater or equal to 65 mg/dL. [Castelli WP, Garrison RJ, Wilson PW, Abbott RD, Kalousdian S, Kannel WB. Incidence of coronary heart disease and lipoprotein cholesterol levels: The Framingham Study. JAMA. 1986;256:2835-2838.]

In addition, the risk of cardiovascular events increases markedly with decreasing HDL concentration at every level of LDL concentration. [Kannel WB. Status of risk factors and their consideration in antihypertensive therapy. Am J Cardiol. 1987;59:80A-90A]

This means that even in people whose LDL is <100 mg/dL, as HDL-C declines, the risk of developing atherosclerosis continuously increases. [ Kannel WB. Status of risk factors and their consideration in antihypertensive therapy. Am J Cardiol. 1987;59:80A-90A]

Conversely, as LDL increases you have a higher risk of getting CHD with HDL between 25 mg/dL and 45 mg/dL than if it is higher.

This is why I look at your total cholesterol to HDL ratio and your LDL/HDL ratio.
Even among individuals with LDL below 70 mg/dL, those with HDL-C in the top 25%  have a reduced risk of major cardiovascular events compared with those in the lowest 25%.[HDL promotes endothelial proliferation and prevents and corrects endothelial dysfunction. [ Norata GD, Catapano AL. Molecular mechanisms responsible for the antiinflammatory and protective effect of HDL on the endothelium. Vasc Health Risk Manag. 2005;1:119-129.]

HDL has also been shown to help arteries relax, as well as inhibit white blood cells from entering plaques, these are all (vaso) protective effects. [Shah PK, Kaul S, Nilsson J, Cercek B. Exploiting the vascular protective effects of high-density lipoprotein and its apolipoproteins: an idea whose time for testing is coming, part I. Circulation. 2001;104:2376-2383, Norata GD, Catapano AL. Molecular mechanisms responsible for the antiinflammatory and protective effect of HDL on the endothelium. Vasc Health Risk Manag. 2005;1:119-129.]

The antioxidant properties of HDL inhibit the oxidation of LDL to oxidized LDL (ox-LDL); ox-LDL is associated with an increased damage to the endothelium and continues to be investigated as player in heart disease. [Norata GD, Catapano AL. Molecular mechanisms responsible for the anti-inflammatory and protective effect of HDL on the endothelium. Vasc Health Risk Manag. 2005;1:119-129., Libby P. Inflammation in atherosclerosis. Nature. 2002;420:868-874.]

Raising your HDL to >60 may also reduce coagulation (clot formation) and platelet adhesion (clot formation) and help promote the body’ ability to break down clots.[ Griffin JH, Kojima K, Banka CL, Curtiss LK, Fernández JA. High-density lipoprotein enhancement of anticoagulant activities of plasma protein S and activated protein C. J Clin Invest. 1999;103:219-227., Sugatani J, Miwa M, Komiyama Y, Ito S. High-density lipoprotein inhibits the synthesis of platelet-activating factor in human vascular endothelial cells. J Lipid Mediat Cell Signal. 1996;13:73-88.]

Niacin to the rescue - Niacin is the most effective agent in raising HDL [Castelli WP, Garrison RJ, Wilson PWF et al. Incidence of coronary heart disease and lipoprotein cholesterol levels: the Framingham Study. JAMA 1986; 256: 2835–8.]
Recent information also suggests that niacin may have positive effects on inflammation and endothelial function especially when added to statin therapy.

Results of the Coronary Drug Project showed that niacin significantly reduced cardiovascular events compared with placebo. The Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 2 (ARBITER 2) study measured carotid intima-media thickness (CIMT) in men with cardiovascular disease (CVD). Patients who had achieved an average LDL value of 100 mg/dL on statins alone had atherosclerosis that continued to progress. However, in patients treated with the combination of a statin plus niacin, HDL increased by 21% and the progression of atherosclerosis halted within the first year.

You should understand by now that HDL is highly protective and that a low HDL must be increased if you are to beat CHD. Niacin must only be taken under medical supervision because it can cause hepatitis certain individuals.  If you haven’t been paying attention to your HDL now is the time to start.  Other factors under your control that effect HDL are exercise, alcohol and insulin resistance.

Regular aerobic exercise (such as walking, jogging or bike riding that raises your heart rate for 20 to 30 minutes at a time) is an effective way to increase HDL levels. In the May 28 issue of the Archives of Internal Medicine investigators reported that the duration of exercise rather than the intensity, is the more important factor in raising HDL cholesterol. In individuals who exercised for at least 20 minutes, each additional 10-minute increase in exercise duration increased HDL levels by an additional 1.4 mg/dL. [Kodama S, Tanaka S, Saito K, et al. Effect of aerobic exercise training on serum levels of high-density lipoprotein cholesterol. Arch Intern Med 2007; 167:999-1008.]

The study called ENHANCE involved 720 patients with very high cholesterol levels and showed no significant difference between patients treated with ezetimibe and simvastatin versus patients treated with simvastatin alone over a two-year period.

Baseline levels on LDL were greater than 300 mg/dl, yes I said 300. This is three times the level that is considered optimal and means they have severe cholesterol disorder. These folks are at high risk for heart disease. In fact, even while on statins bad colesterol was still high in the patients in this study.

The study was designed to prove that Vytorin could slow the growth of plaque in carotid arteries supplying the brain more than simvastatin alone. Results of the trial showed no benefit from the combination of ezetimibe (Zetia) and simvastatin (sold together as Vytorin) over simvastatin alone. Zetia works in the small intestine to block the absorption of cholesterol thus reducing overall levels.

The overall incidence rates of cardiac events were nearly identical between both treatment groups. There should no be reason for patients to panic. If you are on Vytorin stay on it or try a natural alternative.

A natural alternative to Vytorin is Red Yeast Rice (RYR) with plant sterols (hypochol) and is available at my clinic. The RYR contains the naturally occurring statin lovastatin from the yeast Monascus purpureus. Plant sterols inhibit the absorption of cholesterol in the small intestine.  Lovastatin was first isolated from a strain of Aspergillus terreusand it was the first statin approved by the FDA (August 1987). As usual, nature serves as the inspiration for mankind’s inventions.

The ENHANCE trial was an imaging study and not a clinical-outcome study. Conclusions should not be made until the three large clinical-outcome trials are presented within the next two to three years.

Since Vytorin is an expensive drug it makes sense to see if its worth the money. I don’t think patients should stop Vytorin on the basis of the ENHANCE study alone.

Steve Parcell, ND

Hi everyone,

This blog will serve as an extension to my book on reversing coronary artery disease and will allow me to post answers to common questions I get from patients. Please refer friends to it. Also the blog is search-able.

Steve Parcell, ND