What’s the Real Cause of Heart Attacks?
December 17, 2014
- Bypass surgery provides minimal benefit for most people, as sites that are over 90 percent blocked in almost all cases compensate for the blockage by developing collateral blood vessels
- Most heart attacks are likely caused by an imbalance in your central nervous system (CNS) and your autonomic (or unconscious) nervous system (ANS), which controls the function of our internal organs
By Thomas S. Cowan, MD
In a previous article in this journal (“What Causes Heart Attacks,” Fall 2007), I presented the case that the spectrum of heart disease, which includes angina, unstable angina, and myocardial infarction (heart attack), is better understood from the perspective of events happening in the myocardium (heart) as opposed to events happening in the coronary arteries (the arteries that supply the heart).
As we all know, the conventional view holds that the central event of heart disease occurs in the arteries, with the buildup of blockage called plaque.
In this follow-up article I will go into more detail about the conventional theory and why it is largely misleading; then I will describe the precise and well documented events that do lead to MIs (myocardial infarctions or heart attacks).
This understanding is crucial since during the last fifty years, the pursuit of the coronary artery theory has cost this nation billions of dollars in unnecessary surgical costs, billions in medications that cause as much harm as allow for any positive benefits, and, most seriously, has led many to adopt a low-fat diet, which only worsens the problem.
Newer twists on this theory only serve to further obscure the real cause. In contrast, by understanding the real patho-physiological events behind the evolution of MIs, we will be led to a proper nourishing traditional style of eating, the use of the safe and inexpensive heart tonic called g-strophanthin.
Most importantly, we will be forced to look at how heart disease is a true manifestation of the stresses of modern civilized life on the core of the human being.
To overcome the epidemic of heart disease, we literally need a new medical paradigm, a new economic system, a new ecological consciousness; in short, a new way of life. The coronary theory misses all of this, just as it misinterprets the actual pathological events.
In writing this article, I am indebted to the work of Dr. Knut Sroka and his website heartattacknew.com. For all interested in this important subject it is advised to read the entire website and watch the video on the website. The video above shows how the collateral circulation nourishes the heart even with a severe blockage of a coronary artery.
For health professionals and researchers, your understanding of this subject is incomplete without reading and studying the two articles found in the print version of the website.
The first is by G. Baroldi, “The Etiopathologies of Coronary Heart Disease: A Heretical Theory Based on Morphology,” and the second by K. Sroka, “On the Genesis of Myocardial Ischemia.” Both articles are reprinted in full on the website.
Rebuttal of Conventional Theory
Until recently I believed, along with most physicians, that most heart attacks were caused by the progressive blockage caused by plaque buildup in the four major coronary arteries leading to the heart.
These plaques were thought to be composed of cholesterol that built up in the arterial lumen (inside of the vessel), which eventually cut off blood supply to a certain area of the heart, resulting in oxygen deficiency in that area, causing first pain (angina), then progressing to ischemia (heart attack).
The simple solution was to unblock the stenosis (the blockages) with either an angioplasty or stent, or, if that was not possible, then bypass this area with coronary bypass grafting (CABG). Simple problem, simple solution.
The problems with this approach became apparent to me through a number of avenues. The first emerged in a story related by the head of cardiology during a northern California heart symposium at which I was a speaker. He told us that during his residency he was part of a trial conducted in rural Alabama on black men.
In this trial, they did angiograms (injecting dye into the coronary arteries to detect blockages) on all the men presenting with chest pains. For the ones who had a single artery blocked, they did no interventions, only noting which part of the heart would have a subsequent heart attack if one occurred.
Of course, they all predicted it would be in the part of the heart supplied by that particular coronary artery. Then they waited. Eventually, many did return and did have heart attacks, but to the researchers’ surprise less than ten percent had a heart attack in the area of the heart supplied by the original blocked artery.
This means, of course, that had they performed the usual angioplasty, stent, or bypass on that artery, the patient would have received no benefit. The second occurrence that helped change my mind was the publication in 2003 of a large study conducted by the Mayo Clinic on the efficacy of bypass surgeries, stents, and angioplasty.1
The study concluded that bypass surgery does relieve symptoms of heart attack (chest pain); that bypass surgery does not prevent further heart attacks; and that only high risk patients benefit from bypass surgery with regard to a better chance of survival. In other words, the gold standard for treating arterial blockages provides at best only minimal benefits.
If you watch the video on http://www.heartattacknew.com and go to the FAQ called “The Riddle’s Solution,” it becomes clear why this is so. Large stable blockages, that is, sites that are over 90 percent blocked, in almost all cases compensate for the blockage by developing collateral or additional new blood vessels.
In fact, the view that the four coronary arteries supply all the blood to the heart is completely wrong. Starting soon after birth, the normal heart develops an extensive network of small blood vessels called collateral vessels that eventually compensate for the interruption of flow in any one (or more) of the major vessels.
As Sroka correctly points out in the above video, coronary angiograms fail to show the collateral circulation; furthermore the procedure creates spasms in the coronary arteries through the injection of heavy dye under high pressure. Thus, coronary angiograms are notoriously inaccurate at assessing the amount of stenosis in the vessels as well as the true blood flow in the heart.
To this day, most of the bypasses, stents, and angioplasties are performed on minimally symptomatic patients who show a greater than 90 percent blockage in one or more coronary artery. These arteries are almost always fully collateralized; it is not the surgery that restores blood flow, because the body has already done its own bypass.
If tests found a major coronary artery 90 percent blocked, with only 10 percent flow “squeezing through the bottleneck,” how could you possibly still be alive if you did not have collateral blood vessels? And are we really to believe that the decisive thing that will cause the eventual heart attack is when the stenosis goes from 93 percent to 98 percent?
This is an insignificant difference, and the premise that this small increase will cause a heart attack is completely nonsensical. Yet this is what most of the procedures are meant to accomplish, to unblock the stenosis, which as the video on heartattacknew.com shows, does not actually improve blood flow.
It is no wonder that in study after study, these procedures fail to provide any significant benefit to the patients. For these reasons, conventional cardiology is abandoning the stable plaque model in favor of a different model for the etiology of heart attacks one that, as it turns out, is equally invalid.
Meet the Unstable Plaque
We can now all agree that the entire focus of cardiology—upon the stable, progressing calcified plaque: the thing we bypassed and stented for years, the thing we do CT scans of arteries for, the thing they told us is created from cholesterol buildup in arteries, the thing “alternative cardiology” like the Ornish program focused on eliminating—all this is not so important after all.
Don’t worry, though, say the “experts,” we know it must be the arteries, so let’s introduce another concept—drum roll—that of unstable or friable plaque. This insidious scoundrel can attack at any time in any person, even when there is no large blockage. That’s because these soft, “foamy” plaques can, under certain situations (we don’t know which situations), rapidly evolve and abruptly close off the involved artery, creating an oxygen deficit downstream, with subsequent angina and then ischemia.
These soft plaques are thought to be the result of a combination of inflammatory “buildup” and LDL-cholesterol, the exact two components that are targeted by statin drugs. Therefore, since unstable plaque can come loose at any time, everyone should be on statin drugs to prevent this unfortunate occurrence. Some spokesmen have even suggested putting therapeutic doses of statins in the municipal water supplies.
Defendants of this theory point to angiogram studies that show the changes in these unstable plaques, claiming them as proof that unstable plaque is the true cause of the majority of MIs. As I will show, this acute thrombosis does happen in patients having heart attacks, but it is a consequence, not the cause of the MI. What can pathology reports—as opposed to angiography studies—tell us about the role of unstable plaque in heart attacks?
After all, pathology reports are the only accurate way of determining what actually happened during a heart attack, as opposed to angiograms, which are misleading and difficult to read. The first major autopsy study of patients dying of heart attack was carried out in Heidelberg in the 1970s.2 The study found that sufficient thrombosis to cause the heart attack was found in only twenty percent of cases.
The largest such study found sufficient thrombosis in only 41 percent of cases.3 The author, Baroldi, also found that the larger the area of the heart attack, the more often the pathology report found stenosis; in addition, the longer the time between heart attack and the death of the patient, the higher the percentage of stenosis. Some researchers have used these two facts to “cherry-pick” the numbers and make the stenosis rate seem high by studying only those with large MIs and those who live the longest after the heart attack event.
Another observation that puts into doubt the relevance of the coronary artery theory of heart attack is the fact that the proposed etiological mechanism of how thrombosed arteries cause ischemia is through cutting off the blood supply and thereby the oxygen supply to the tissues. To the enormous surprise of many investigators, the reality is that when careful measurements are done assessing the oxygen level of the myocardial cells, there is no oxygen deficit ever shown in an evolving heart attack I.4 The oxygen levels (measured as pO2) do not change at all throughout the entire event. I will come back to this fact later when I describe what does change in every evolving MI ever studied.
Again, the question must be asked: if this theory is predicated on the lowering of the oxygen levels in the myocardial cells when in fact the oxygen levels don’t change, then what exactly does happen? The conclusion is that while thrombosis associated with MI is a real phenomenon, it does not occur in more than 50 percent of cases—which leads to the question: why do the other 50 percent, those without an occlusion in the coronary arteries, even have an heart attack?
Second, it is clear from all pathology studies that thromboses of significant degrees evolve after the heart attack occurs, again leading to the question: what causes the heart attack in the first place? The fact that thrombosis does occur after a heart attack also explains why emergency procedures—remember, the only patients who benefit from bypass and stents are critical, acute patients—can be helpful immediately post-heart attack I to restore flow in those patients who do not have adequate collateral circulation to that part of their heart. So again, all the existing theories as to the relevance of the coronary arteries in the evolution of the heart attack are fraught with inconsistencies. If this is so, what then does cause heart attacks?
The Etiology of Myocardial Ischemia
Any theory as to what causes myocardial ischemia must account for some consistent observations over the past fifty years. The most consistent risk factors for a person having heart disease are male sex, diabetes, cigarette use and psychological or emotional stress. Interestingly, in none of these is there a direct link to pathology of the coronary arteries—diabetes and cigarette use cause disease in the capillaries, not, as far as we know, in the large arteries. Also, we have learned over the past decades that the four main medicines of modern cardiology—beta-blockers, nitrates, aspirin, and statin drugs—all provide some benefits for heart patients (albeit all with serious drawbacks as well) and this observation must be accounted for in any comprehensive theory of myocardial ischemia.
Heart Rate Variability
The real revolution in the prevention and treatment of heart disease will come with increased understanding of the role played by the autonomic nervous system in the genesis of ischemia and its measurement through the tool of heart rate variability (HRV). We have two distinct nervous systems: the first, the central nervous system (CNS), controls conscious functions such as muscle and nerve function; the second nervous system, the autonomic (or unconscious) nervous system (ANS), controls the function of our internal organs.
The autonomic nervous system is divided into two branches, which in a healthy person are always in a balanced yet ready state. The sympathetic or “fight-or-flight” system is centered in our adrenal medulla; it uses the chemical adrenaline as its chemical transmission device and tells our bodies there is danger afoot; time to activate and run. It does so by activating a series of biochemical responses, the centerpiece of which are the glycolytic pathways, which accelerate the breakdown of glucose to be used as quick energy as we make our escape from the bear chasing us.
In contrast, the parasympathetic branch, centered in the adrenal cortex, uses the neurotransmitters acetylcholine (ACh), nitric oxide (NO), and cyclic guanosine monophosphate (cGMP) as its chemical mediators; this is the “rest-and-digest” arm of the autonomic nervous system. The particular nerve of the parasympathetic chain that supplies the heart with nervous activity is called the vagus nerve; it slows and relaxes the heart, whereas the sympathetic branches accelerate and constrict the heart. I believe it can be shown that an imbalance in these two branches is responsible for the vast majority of heart disease.
Using the techniques of heart rate variability (HRV) monitoring, which gives a real time accurate depiction of autonomic nervous system status, researchers have shown in multiple studies5 that patients with ischemic heart disease have on average a reduction of parasympathetic activity of over one-third. Typically, the worse the ischemia, the lower the parasympathetic activity.6 Furthermore about 80 percent of ischemic events are preceded by a significant, often drastic, reduction in parasympathetic activity.7
By contrast, those with normal parasympathetic activity, who experience an abrupt increase in sympathetic activity (such as physical activity or an emotional shock), never suffer from ischemia.
In other words, without a preceding decrease in parasympathetic activity, activation of the sympathetic nervous system does not lead to MI.8 Presumably we are meant to experience times of excess sympathetic activity; this is normal life, with its challenges and disappointments. These shocks only become dangerous to our health in the face of an ongoing, persistent decrease in our parasympathetic, or life-restoring, activity. The decrease in parasympathetic activity is mediated by the three chemical transmitters of the parasympathetic nervous system: acetylcholine, NO, and cGMP. It is fascinating to note that women have stronger vagal activity than men, probably accounting for the sex difference in the incidence of MI.9
Hypertension causes a decrease in vagal activity,10 smoking causes a decrease in vagal activity,11 diabetes causes a decrease in vagal activity,12 and physical and emotional stress cause a decrease in parasympathetic activity.13 Thus, all the significant risk factors suppress the regenerative nervous system activity in our heart. On the other hand, the main drugs used in cardiology upregulate the parasympathetic nervous system.
Nitrates stimulate NO production while aspirin and statin drugs also stimulate the production of ACh along with NO—that is, until they cause a rebound decrease in these substances which then makes the parasympathetic activity even worse. Beta-blockers work by blocking the activity of the sympathetic nervous system, the increase of which is a central factor in the etiology of MI. The bottom line: the risk factors for heart disease and the interventions used all affect the balance in our ANS; whatever effects they may have on plaque and stenosis is of minor relevance.
How Heart Attacks Occur
So what is the sequence of events that leads to a heart attack? First comes a decrease in the tonic, healing activity of the parasympathetic nervous system—in the vast majority of cases the pathology for heart attack will not proceed unless this condition is met. Think of the person who is always pushing himself, who never takes time out, who has no hobbies, who constantly stimulates the adrenal cortex with caffeine or sugar, who does not nourish himself with real food and good fats, and who does not incorporate a regular pattern of eating and sleeping into his daily life.
Then comes an increase in the sympathetic nervous system activity, usually a physical or emotional stressor. This increase in sympathetic activity cannot be balanced because of chronic parasympathetic suppression. The result is an uncontrolled increase of adrenaline, which directs the myocardial cells to break down glucose using aerobic glycolysis. Remember that in a heart attack, there is no change in blood flow as measured by the p02 in the cells. This step shunts the metabolism of the heart away from its preferred and most efficient fuel sources, which are ketones and fatty acids.
This explains why heart patients often feel tired before their events. This also explains why a diet liberal in fat and low in sugar is crucial for heart health. As a result of the sympathetic increase and resulting glycolysis, a dramatic increase in lactic acid production occurs in the myocardial cells; this happens in virtually one hundred percent of heart attacks, with no coronary artery mechanism required.14, 15 As a result of the increase in lactic acid in the myocardial cells, a localized acidosis occurs. This acidosis prevents calcium from entering the cells,16 making the cells less able to contract.
This inability to contract causes localized edema (swelling), dysfunction of the walls of the heart (hypokinesis, which is the hallmark of ischemic disease as seen on stress echoes and nuclear thallium stress tests), and eventually necrosis of the tissue—in other words, a heart attack. The localized tissue edema also alters the hemo-dynamics of the arteries embedded in that section of the heart, resulting in shear pressure, which causes the unstable plaques to rupture, further block the artery, and worsen the hemodynamics in that area of the heart.
Please note that this explanation alone explains why plaques rupture, what their role in the heart attack process is, and why they should indeed be addressed. Notice also that this explanation accounts for all the observable phenomena associated with heart disease and is substantiated by years of research. It could not be clearer as to the true origin of this epidemic of heart disease.
Nourishing the Parasympathetic Nervous System
If heart disease is fundamentally caused by a deficiency in the parasympathetic nervous system, then the solution is obviously to nurture and protect that system, which is the same as saying we should nurture and protect ourselves. Nourishing our parasympathetic nervous system is basically the same as dismantling a way of life for which humans are ill-suited. This means avoiding the excesses of industrial civilization. The known things that nourish our parasympathetic nervous system are contact with nature, loving relations, trust, economic security (a hallmark of indigenous peoples the world over) and sex—this is a whole new world of therapy for ailing hearts.
The medicine that supports all aspects of the parasympathetic nervous system is an extract from the strophanthus plant called ouabain or g-strophanthin. G-strophanthin is an endogenous (made within us) hormone manufactured in our adrenal cortex from cholesterol and therefore inhibited by statin drugs.
G-strophanthin does two things that are crucial in this process—two actions provided by no other known medicine. First, it stimulates the production and liberation of ACh, the main neurotransmitter of the parasympathetic nervous system; secondly, and crucially, it converts lactic acid—the main metabolic culprit in this process—into pyruvate, one of the main and preferred fuels of the myocardial cells. In other words, it converts the central poison in this process into a nutrient.
This may be what is meant in Chinese medicine when they say that the kidneys (that is, the adrenal glands, where ouabain is made) nourish the heart. In my many years of using ouabain, I have not had a single patient have an MI while taking it. It is truly a gift to the heart. Of course, I put all my patients on a WAPF-style heart-healthy diet, loaded with healthy fats and fat-soluble nutrients, and low in the processed carbs and sugars that are the hallmark of industrial, civilized life. There are homeopathic versions of strophanthus available, which could be used. Another option that is effective but not ideal is an extract of the plant. The drawback is that the amount of ouabain is unknown.
Reprinted with kind permission of the Townsend Letter, http://www.townsendletter.com.
About the Author
Dr. Cowan has served as vice president of the Physicians Association for Anthroposophical Medicine and is a founding board member of the Weston A. Price Foundation. He is the principal author of The Fourfold Path to Healing and is co-author of The Nourishing Traditions Book of Baby and Child Care. Dr. Cowan lectures throughout the United States and Canada. Dr. Cowan is completing a book on the human heart that will be published by Chelsea Green Publishing in 2015.
A New Way of Looking at Heart Disease and Novel Treatment Options
December 18, 2016
- Conventional wisdom says heart attacks are caused by arterial plaque formation. However, you have enormous numbers of capillaries feeding your heart, which can easily bypass blocked large vessels
- Compelling evidence suggests the real cause of heart attacks is decreased parasympathetic tone followed by sympathetic nervous system activation, and/or collateral circulation failure, which are easily prevented and treated
- In Germany, g-strophanthin (ouabain) has a long history of clinical use for heart attack prevention and treatment of angina. Enhanced External Counterpulsation (EECP) is a safe and effective alternative to bypass
By Dr. Mercola
We have an epidemic of heart disease in this country and the conventional treatments, such as the use of statin drugs and surgeries involving artery bypasses and stents, typically do not work well. So, what does?
Dr. Thomas Cowan is a family physician and a founding member of the Weston A. Price Foundation.
In his book, “Human Heart, Cosmic Heart: A Doctor’s Quest to Understand, Treat, and Prevent Cardiovascular Disease,” which is also available as an audiobook from Audible, he helps answer that question.
It’s a fascinating book, and not overly technical, making it an excellent addition to any layman’s health library.
“Basically, the book has three parts,” Cowan says. “For whatever reason, my destiny in my career is that I take on some of the biggest accepted wisdoms … [and] I try to figure out whether they’re actually true or not.
The first part is my [personal] story … [In] the second part, I examine the theory that the heart is a pump. I say that the heart is not a pump. Then I explain why the blood moves and what the heart is doing, and the interesting ramifications of that.
The third part is … [about] what causes heart attacks … Here is an interesting point: I learned in medical school there were four major coronary arteries. In some places, it says three. In some places, it says two.
Even the basics of how many major coronary arteries we have is actually in dispute. It’s a matter of semantics.”
Questioning the Role of Arterial Plaque in Heart Attacks
Regardless of the exact number, conventional wisdom states that the coronary arteries, i.e., major blood vessels, supply all of the blood flow to the heart. If one or more of them gets blocked with plaque, a bottleneck forms that prevents blood from getting through.
The area downstream from that blockage doesn’t get any blood, and hence no oxygen or nutrients. The first indication that this is occurring is pain, which we call angina. As the problem progresses, the pain worsens, which is called unstable angina. Eventually, if left untreated, you end up with a heart attack.
The field of cardiology is primarily focused on getting rid of the plaque, whether by using stents, doing bypasses, angioplasties, lowering cholesterol (since the plaque is supposedly caused by excess cholesterol) or putting the patient on a low-fat diet.
“[Conventionally], it’s all about the plaque,” Cowan says. “My point in the book is that it’s NOT about the plaque.”
The Problem With Viewing the Heart as a Pump
Cardiologists and doctors in general are taught that the walls of the heart create pressure, which causes propulsion of the blood through the body. In essence, the heart is viewed as a pump — a pressure propulsion system caused by the muscular contraction of the ventricles.
However, your body actually contains an enormous amount of blood vessels. Most of the blood vessels in your heart and body are capillaries, which are very thin-walled, very narrow tubes.
If you were to spread these blood vessels out, they would cover three football fields. If you were to place the blood vessels end to end, in a series, they would encircle the Earth between one and three times.
“The pump theory is you have a 1-pound, somewhat thin-walled organ, and it’s going to pump [blood] around the Earth every single day for 70 years; 60 to 70 times a minute. That 1-pound, thin-walled organ can [supposedly] generate enough pressure [to do that] by squeezing …
Frankly, that’s ridiculous. But it actually gets worse than that. If you do a flow velocity diagram, it turns out that the blood is moving the fastest at the heart, both before and after the heart.
As it goes into the arterioles and then the smaller arteries, it gets to the capillaries … [where] it actually stops and does a little shimmy, or it goes very slow, depending on who you believe … The analogy is, a narrow river goes fast and when it goes out into a wetland, it goes very slow.
It has to go slow — it has to stop almost — to exchange the gasses and the food. So not only are we pushing all the way around the Earth, but halfway around our travel, we stop and then we get going again. You’re expecting that to be all from the push from behind …
It even gets worse than that because we have an outflow tube of the left ventricle called the aortic arch … which is shaped like McDonald’s arch. The blood goes from the left ventricle, out the aortic valve, through the arch, then down to the body.
The analogy here is if you stick a similarly shaped arched garden hose off your spigot outside your house, and then turn it on really hard, which recreates the pumping … you would expect the garden hose to straighten out because if you put pressure, the arch would straighten.
In fact, you can look on any angiogram and catheterization and you can see that arch actually bends in a little bit during systole, which from a pressure propulsion model makes absolutely no sense at all.”
The Hydraulic Ram Model of the Heart
Clearly, if your heart stops beating, you won’t live very long, but if the heart isn’t actually pumping the blood, how does it work? In his book, Cowan describes the heart as a hydraulic ram, which he explains thus:
“What does the heart do? The blood is moving fast. It comes into the heart. The heart stops the blood, and like a hydraulic ram, it holds it back. The walls expand. The pressure differential happens, and then it opens the gate and comes out.
More so when the blood is in the heart, because of the unique shape of the heart … The heart is a vortex-creating machine … [I]t has these trabeculae (fibers) inside the heart. Each area of the trabeculae is connected with a certain part of the body.
[One] area of the heart is connected with the spleen, another area of the inner part of the heart is connected with the foot, and so on.
The blood comes in and these areas of the heart create their individual spirals, and package up certain parts of the blood, like the old red blood cells, into a vortex and send it to the spleen, whereas another part sends the fresh new red blood cells up to the brain.
If there’s a cut on your leg, it dissolves some of the inner fibers, puts that in a vortex and sends that to the cut on your leg. It’s so wild. Again, there’s an article about this on my website, as hard as it is to believe, that actually documents that in very clear terminology how this happens.”
What’s Water Got to Do With It?
Interestingly, the work of Gerald Pollack, author of “The Fourth Phase of Water,” was instrumental in helping Cowan understand the function of the heart and how blood flows if it isn’t being pushed or pumped by the heart.
First off, if any pumping action were to be involved, it would actually have to occur at the capillaries because that’s where the blood stops and needs to get moving again. However, the solution nature came up with is far simpler. As the blood moves up the venous tree, the blood vessels narrow and eventually coalesce to come back to the heart.
This narrowing of the vessels makes the blood flow faster, in and of itself. Valves and muscular contractions also play a role. However, the primary way blood moves has to do with water. As Pollack has described, water can exist in four phases, not just three. The fourth phase of water is formed by the interaction of water and a hydrophilic surface.
“What happens with that is you form a gel layer, or protective layer, on that hydrophilic surface, which is negatively charged. Therefore, the opposite of positive charge is dissolved into the bulk water in the middle of the tube (capillary or blood vessel) … All you need is a hydrophilic tube, which forms a gel layer, which is negatively charged, and then the bulk water is positively charged. The positive charges repel each other and that starts the flow going up the hill,” Cowan explains.
Sun, Earth and the Human Touch — 3 Key Principles for Healthy Blood Flow
Pollack has also clearly demonstrated there are three natural energies that result in separation of charges that create flow:
1. Sunlight charges up your blood vessels, which increases the flow of blood. When the sun’s rays penetrate your skin, it causes a massive increase of nitric oxide that acts as a vasodilator. As much as 60 percent of your blood can be shunted to the surface of your skin through the action of nitric oxide. This helps absorb solar radiation, which then causes the water in your blood to capture the energy and become structured.
2. Negative ions from the Earth, also known as earthing or grounding. This also charges up your blood vessels, creates a separation of charges, creates more positive ions and allows the blood to flow upward, against gravity.
3. The field effect or touch from another living being, such as laying on of hands.
As noted by Cowan, “The best thing is to be, more or less, with shorts or naked on the beach, with the saltwater, which acts as an electrical conductor, holding hands with somebody you love. That’s how you structure the water.” Sun exposure, grounding and skin-to-skin contact are three prevention strategies that, ideally, everyone should be doing. It doesn’t get a whole lot easier or less expensive than that.
“The water is a battery. Those inputs separate the charges, charge the battery, the battery does work and it starts flow. That flow, just through Bernoulli’s principle, which is the wider it is, the slower it goes, [when it] narrows, it goes faster. That is the reason the blood moves, in a nutshell.”
Does Plaque Really Cause Heart Attacks?
As mentioned, Cowan does not ascribe to the plaque theory of heart disease. Instead, he makes a strong case for heart disease being a problem rooted in mitochondrial dysfunction. What’s wrong with the plaque theory? For starters, if plaque were responsible, there would have to be something in the blood or blood vessels causing the plaque, such as cholesterol or inflammation.
And, since all blood vessels are identical — there’s no difference between the splenic artery, the femoral artery or the coronary artery, for example — if there’s plaque in one artery, there should be plaque everywhere, and an attack should theoretically occur just about anywhere in the body, depending on where the blockage is. Yet people do not have “spleen attacks,” or “foot attacks,” which would be the result of a bottleneck of plaque forming near these organs.
“There is such a thing as renal artery ischemia. But basically, there are only two organs that have attacks. The brain, we call that a stroke, and the heart, we call that a myocardial infraction (MI) or a heart attack,” Cowan says.
“Why not the other organs? Because that suggests there’s something different about those organs. It’s not the blood vessels because the blood vessels, they’re the same. There’s something different about the heart and the brain that’s causing the attacks. It’s not the blood flow.”
In the ’40s and ’50s when the plaque theory began to emerge, most cardiologists rejected it, noting there’s massive collateral circulation between the coronary arteries and this massive network of fine blood vessels. It doesn’t really matter whether one area gets blocked or not, because the whole thing is like the wetlands; it will simply compensate for a blockage in one area by increasing blood flow elsewhere.
What’s Wrong With the Plaque Theory?
Post-mortem autopsy studies — which are available on Cowan’s website, humanheartcosmicheart.com — looking at arterial blockages in the area leading to the part that had an attack showed that only 18 percent were actually blocked. That means that in 82 percent of cases, a blocked artery was NOT the cause of the heart attack.
So, what caused it? In another study, 66 percent of normal 50-year-olds who died in car accidents were found to have a one or more, greater than 90 percent stenosis or blockage of a coronary artery! Yet none of them had any symptoms.
“I’m not saying blockages are good. I’m not saying plaque is good. What I am saying is it’s nowhere near sufficient to explain why people have heart attacks,” Cowan says.
“Every week somebody comes in and says ‘I’m not feeling as well as I used to. I have some chest pain, a little shortness of breath walking up the hills. I went on a 5-mile walk yesterday and I’m not doing as well as I used to. I went to the cardiologist. He did tests and found I have a 95 percent blockage in one of my coronary arteries. He said if it blocks any more, I’ll have a heart attack and die… [and that I] better have a stent or an angioplasty.’
I think to myself, No. 1, if all of the blood flow comes through these coronary arteries and he’s got 95 percent blockage of this major vessel, how did he walk up this 5-mile hill? In fact, how is he even standing upright if he’s got less than 5 percent blood flow to a major part of his heart?
So, you mean to tell me if he blocks from 5 percent to 2 percent, that’s it? Curtains in, you die? The reality is 5 percent is 0 percent, and blocking to 2 percent is the same as 0 percent. It’s very clear that the theory that the blood squeezes through the bottle neck in the vessel is complete nonsense.
The blood does not squeeze through the bottleneck. It bypasses it. It goes through these collateral vessels and the flow is more or less normal, although there is some problem in the heart, but it’s not because of that blockage. That’s why the Mayo Clinic and other studies, when they unblock the blockage, it doesn’t do any good for the patient.”
In Cowan’s view, there is only a small subset of patients that might benefit from bypass intervention, specifically if you have a greater than 90 percent stenosis (blockage) of the proximal part (the early part) of the left anterior descending (the primary artery that supplies blood to your heart).
The Real Cause of Heart Attacks
If a blockage isn’t the cause of the heart attack, then what is? Cowan makes a strong case for three basic causes of heart attacks, in the following order of importance or likelihood:
1. Decreased parasympathetic tone followed by sympathetic nervous system activation. You have two nervous systems, a central and an autonomic. Your autonomic nervous system has two arms: the sympathetic fight-or-flight, and the parasympathetic, which governs rest and digestion.
Decreased parasympathetic tone results from stress, diabetes, high blood pressure and other factors, including emotional and psychological ones. That’s the first thing that happens. Then, while under the influence of a low parasympathetic tone, you experience some sort of emotional, psychological or physical stress that activates your sympathetic nervous system.
This shifts your cell metabolism from the mitochondria to the cytoplasm, meaning the cells in your heart shift from using fat for fuel, to generating fuel in a glycolytic way through the fermentation of sugar. Once that glycolytic shift occurs, you enter into glycolytic metabolism where you burn sugar for fuel and make lactic acid. As in other muscles, lactic acid in the heart muscle causes the telltale cramps and pain known as angina.
Since your heart cannot stop contracting to allow the blood flow to flush out the lactic acid, the lactic acid builds up, causing localized metabolic acidosis that necroses or destroys the cardiac tissue. Also, when the tissue becomes acidic, calcium cannot enter the tissue. As a result, the heart muscle cannot contract properly.
Next, pressure in the arteries embedded in the non-moving area of your heart builds, which then breaks off little pieces. These are the “clots” conventional cardiology believes are the cause of the heart attack.
But the clots are not due to plaque, they’re the result of pressure in the non-moving area of your heart, which is the result of not getting calcium into the cells, which is the result of lactic acid forming from the altered metabolism in the heart. This chain of events, Cowan believes, is the real cause of most heart attacks.
2. Collateral circulation failure. Diabetes, smoking and high-stress all affect collateral circulation, not major blood vessels, and all of these are known to raise your risk of a heart attack.
3. Particularly badly placed plaque formation. This is not the norm, but could occur.
Indeed, one of the problems with using carbohydrates as a primary fuel — which a majority of people in the West are doing — is that it generates more reactive oxygen species (ROS) and secondary free radicals. Chronically, this will cause mitochondrial damage. I like to simplify it by saying that carbs are dirty fuels — dirty in the sense that they generate excessive amounts of free radicals that poison the mitochondria.
It’s this dirty fuel — the net carbs — that creates fermentation metabolism and subsequent lactic acid production. The answer is not to take more antioxidants. The answer is to reduce the production of free radicals by reducing net carbs and increasing the amount of healthy dietary fats you eat.
This is a core tenet of a healthy diet, and if you understand Cowan’s explanation above, and how carbs act as a dirty fuel, you’ll have a good understanding of why a high-sugar diet causes heart disease and heart attacks.
Treatment Alternative for Heart Disease
To address the primary issue of decreased parasympathetic tone followed by sympathetic nervous system activation, an adrenal hormone called ouabain, or strophanthin, could be used. Strophanthus is the name of the plant, the active ingredient of which is called g-strophanthin in Europe, and ouabain in the United States.
G-strophanthin is an endogenous (meaning “made in us”) hormone that goes into your blood, to your heart, where it converts the lactic acid into pyruvate, which is actually the preferred fuel for your heart. In this way, g-strophanthin breaks and eliminates the buildup of lactic acid that is causing all the trouble. Not only that, it converts it to a fully usable fuel, allowing your heart to function properly again.
G-strophanthin also helps create more neurotransmitters of the parasympathetic nervous system. So it performs two central functions: 1) It supports your parasympathetic nervous system, and 2), It flushes out lactic acid. Unfortunately, strophanthus can be hard to find. You cannot simply pick it up at your local health food store.
“Strophanthus was first identified by the famous African explorer, Livingston, who apparently saw the natives dip their arrows in it. They would make a really high dose and it would stun their prey … He dipped his toothbrush in a strophanthus extract and noticed the change in his heart rate. It slowed down. Basically, from there, it became a heart medicine.
It’s in the same family as digitalis, but digitalis doesn’t convert lactic acid into pyruvate. Digitalis does not support the parasympathetic system. It’s really different because digitalis is fat soluble, while ouabain, g-[strophanthin] is water soluble. There are a lot of differences.”
How to Find Strophanthus
For over 20 years, strophanthus was the main treatment for angina and heart attack prevention in Germany. Millions of doses were given and hundreds of studies were done. One 1972 study involved 150 patients with angina. After taking strophanthus for one week, 144 were symptom free. After two weeks, 146 were without symptoms. It clearly has a long history of successful clinical use.
“In fact, in the ’50s and ’60s, there was a test called a strophanthin challenge test … All physicians know, sometimes a person comes in with chest pain. We don’t know if it’s because they’re breathing too hard or if it’s muscle pain or something.
You want to figure out whether that’s from their heart. They [would] give them g-strophanthin. If the pain went away, it was considered from their heart. That was the g-strophanthin challenge test, because simply, it flushes the lactic acid. No lactic acid, no pain. But it’s not just for pain relief. It actually breaks the cycle that leads to heart attacks,” Cowan says.
“Now, there are very few places to get it. There’s one compounding pharmacy in Germany, which you can import [from]. There’s a company in Brazil that makes an extract of the strophanthus seeds. That’s what I’ve been using mostly for about 10, 15 years. I’ve had it tested so I know how much ouabain per milliliter is in there.
It’s been one of the best medicines I’ve ever used. People [who] can’t walk to the mailbox, they take it for a couple of weeks, they can walk to the mailbox, go skiing, etc. It relieves their chest pain and it does the exact things that you would hope a medicine would do.”
To make strophanthus more available, Cowan suggests finding a practitioner who is willing to give it to you and supervise your medical condition. Then contact Cowan’s office via HumanHeartCosmicHeart.com. Cowan will talk to the practitioner and explain how strophanthus works and how it should be taken. The practitioner can then obtain it through the website and give it to you.
Enhanced External Counterpulsation — Another Alternative Treatment for Heart Disease
Enhanced External Counterpulsation (EECP) is an alternative for bypass, provided you’re not dealing with a proximal left anterior descending (LAD) obstruction. EECP will increase collateral circulation, which is another common factor responsible for heart attacks.
“EECP.com will tell you if or where there is a site that does this in your area. It’s a Medicare insurance-approved therapy, believe it or not. There are studies that show just EECP alone will relieve about 80 percent of angina. It definitely has some conventional literature behind its effectiveness. It’s very simple and straightforward,” Cowan says.
As explained earlier, the reason you don’t experience a heart attack due to blockage is because you’re protected by collateral circulation. However, if you have diabetes or chronic inflammation, that will eventually deteriorate your small blood vessels (capillaries), reducing this built-in protection.
EECP works by inflating compression cuffs on your thighs and calves that are synchronized with your EKG. When your heart is in diastole (relaxed), the balloons inflate, squeezing the blood. This is a very powerful and safe alternative to coronary bypass surgery for most. Rather than bypassing one or two large arteries you create thousands of new capillary beds that supply even more blood than bypassed vessels.
The sessions are about one hour long, and one requires about 35 sessions to receive benefit. It has insurance approval for angina, and even if you had to pay the $5,000 dollars out of pocket, it is certainly far safer than having your chest cracked open.
It is also very effective for many other conditions like heart failure and diastolic dysfunction (which is an emerging cardiac epidemic). Many professional and elite athletes use it as an aid to maintain cardiac fitness when they are injured and unable to actively exercise.
EECP Triggers Growth of New Blood Vessels
By doing that for an hour, five days a week for seven weeks (a total of 35 treatments), your body will form new blood vessels, thereby improving your collateral circulation. It’s as simple as that. Your body will literally sprout new blood vessels in response to the increased pressure. In addition to eliminating angina, the new flow may also increase your physical endurance and sexual function by 20 and 40 percent. The effects typically last five to eight years.
“Some people call this ‘passive exercise,’ because [that’s] the only other thing I know of that actually really encourages the sprouting of new blood vessels. [H]igh-intensity strength training … encourages new blood vessel formation. If you’re going to make muscle, you have to make more small blood vessels to nourish the flow.
That’s what happens. Anytime you’re doing high-intensity strength training or running up hills or whatever it is you’re doing, that also does it. It makes more collateral circulation,” Cowan explains.
“The problem is a lot of people who come with heart disease, you can’t tell them to do high-intensity training or hardly any exercise. The only thing they can do is just lay on the bed and do this passive exercise. Then they have much more capacity. Then they can get into more of a strength training or some sort of exercise program, and have a much greater capacity.”
Hopefully this interview has intrigued, encouraged and inspired you to pursue and investigate this topic in more detail, because the potential to transform your life and the lives of those you love is certainly available. Cardiovascular disease, heart attacks and strokes are enormously common, and they simply do not need to be.
To learn more, I highly recommend picking up a copy of Cowan’s book, “Human Heart, Cosmic Heart: A Doctor’s Quest to Understand, Treat, and Prevent Cardiovascular Disease.” You can also find more information on HumanHeartCosmicHeart.com. I also published an article written by Cowan in 2014, in which he provides his perspective on the real cause of heart attacks, which you can read through.
“Hopefully, we’ll have some sort of newsletter and be able to really develop a community of people who are interested in looking at a whole different way of understanding and approaching heart disease,” Cowan says.
What You Really Need to Know About Heart Disease and Its Treatment
December 24, 2017
- Recent research shows stents do not improve angina, thereby negating the sole remaining medical indication for angioplasty or the placement of a stent to unblock a blocked artery
- Earlier research showed angioplasty does not reduce mortality, nonfatal myocardial infarction or hospitalization rates for acute coronary syndrome
- Coronary artery disease is not a disease per se. It’s a symptom of “a diffuse systemic disease,” caused primarily by poor diet, inactivity, insulin resistance and stress
- The largest study done on heart attack incidence revealed only 41 percent of people who have a heart attack actually have a blocked artery. Of those, 50 percent of the blockages occurred after the heart attack. This means at least 80 percent of heart attacks are not associated with blocked arteries at all
- Three primary causes of heart attacks are decreased parasympathetic tone followed by sympathetic nervous system activation, lack of microcirculation and lactic acid buildup in the heart muscle
By Dr. Mercola
Heart disease is one of the most common chronic health problems in the United States, and we’re wasting tens of billions of dollars on ineffective treatments and surgical procedures. In this interview, Dr. Thomas Cowan, a practicing physician and founding board member of the Weston A. Price Foundation, shares recently published data1,2 showing the ineffectiveness of stents — a commonly performed surgical procedure used to remediate damage from coronary artery disease.
Stents Were Never Indicated for Anything but Angina Relief
There are a number of parameters that are crucial for evaluating the efficacy of a treatment for heart disease. For instance, will the patient actually live longer as a result of that intervention? Mortality is one parameter of assessment. Another parameter is the risk of heart attack as a result of the intervention. Alleviation of angina (chest pain) is a third. “There’s probably more, but those are the three big ones,” Cowan says.
Earlier research had already dismissed the use of percutaneous interventions (PCI) for most of these parameters, showing the use of stents had no impact on long-term rates of death, nonfatal myocardial infarctions (MI) or hospitalization rates for acute coronary syndrome. The sole indication for the use of stents was angina, as some of the findings showed it helped reduce prevalence of chest pain.
“What [that] means is the state of the literature, before this current Lancet study, was that doing stents or other interventions … has never been shown to help people live longer or to prevent further heart attacks. They have been shown to be of aid in people who are having an acute MI, but in anything but that indication, the state of the science was that they don’t help people live longer, and they don’t prevent further heart attacks.
As this study says, the indication was for relieving angina … It was actually not appropriate, and possibly even not allowed, to tell somebody we were doing a bypass or stent so that you would live longer or not have a heart attack. You could tell them that you could do it because you’re having chest pain, and this will relieve your chest pain,” Cowan notes.
Do Stents Actually Relieve Angina?
Interestingly, there had never been a double-blind study assessing whether, in fact, stent placement relieves angina. The reason for this lack of data was because doing such a study was considered unethical. In a nutshell, it was assumed that stents were beneficial, and therefore denying patients of this benefit would place them at risk.
Eventually, though, a group of interventional cardiologists in England got approval from the review board to perform a comparative study in which half the patients with stable angina received a stent, while the other half received sham surgery. The sham surgery consisted of inserting and removing a catheter in the artery without actually placing a stent. The level of chest pain and exercise tolerance was then assessed and compared between the two groups.
Lo and behold, there was no difference in chest pain (angina) between the treatment group and the sham group. This means that the one and only indication for doing a stent, which is to relieve angina, is also invalid. “It’s hard to come up with what the indication is at this point, except in the rare instance of an acute MI,” Cowan says.
Blocked Arteries Are but One Symptom of a Diffuse Systemic Disease
The ultimate tragedy here, aside from the exorbitant cost, is that patients continue receiving this useless intervention even though there are several simple strategies that are known to be effective, are far less expensive and pose no risk to the patient.
“The Atlantic … [had] one of the most … provocative, quotes I’ve ever heard from a standard cardiologist,” Cowan says. “This was from Dr. Mandrola … [H]er quote … summarizes exactly what we’re talking about … [Q]uote: ‘This study will begin to change the mindset of cardiologists and patients that focal blockages need to be fixed.’
Focal blockages are these blocked arteries that they put the stents in. Quote: ‘Instead, these findings help doctors and patients understand that coronary artery disease is a diffuse systemic disease. A focal blockage is just one manifestation of a larger disease’ …
Now, the thing that was so shocking to me about that is… this is literally the first time I’ve ever heard a cardiologist admit that there is a diffuse focal disease here, of which blocked arteries is only one of the manifestations. That is such a heretical position. I’ve never heard a cardiologist say that. They say, ‘You have blocked arteries. That’s your problem. We’re going to unblock your arteries.’
To suggest that what they have is a systemic disease changes everything. I can’t emphasize that enough. This is not a blocked artery disease. A blocked artery may or may not be significant symptom in this disease. The question that I would ask every listener [to pose to their cardiologist is] … ‘I wonder what diffuse systemic disease this [blocked artery] is a manifestation of?’
I mean, that’s the question. ‘I’ve heard there’s a cardiologist who’s saying that this blocked artery is only one manifestation,’ which then, of course, is a perfect explanation for why stents don’t work. [Blocked arteries are] not the disease. They’re just one of the symptoms of the disease. ‘If that’s the case, then what’s my disease?’ I would be very interested to hear the answer.”
High Cholesterol Does Not Cause Heart Attacks
As noted by Cowan, many cardiologists would probably answer that question saying the underlying problem is high cholesterol. Alas, the evidence does not support this position either. “I actually looked up four papers, [one] in JAMA, three in The Lancet, showing that life expectancy tends to increase as cholesterol goes up, and that there is no relationship between high cholesterol and death,” Cowan says.
Many other studies have also come to this conclusion. In short, the “diffuse systemic disease” behind blocked arteries is NOT high cholesterol. So, what is? The answer to this question is detailed in Cowan’s book, “Human Heart, Cosmic Heart,” which we reviewed in an earlier interview. The book explores and tries to answer the question of why people have heart attacks if it’s not blocked arteries.
In his 2004 book, “The Etiopathogenesis of Coronary Heart Disease,”3 the late Dr. Giorgio Baroldi wrote that the largest study done on heart attack incidence revealed only 41 percent of people who have a heart attack actually have a blocked artery, and of those, 50 percent of the blockages occur after the heart attack, not prior to it. This means at least 80 percent of heart attacks are not associated with blocked arteries at all. So, what’s really the cause of a heart attack? Cowan explains:
“It’s obviously complex, and there’s a number of manifestations, but the three most important things that I point out in my book is, No. 1 … at least 90 percent of people who have a heart attack have an autonomic nervous system imbalance. Specifically, they have a suppressed parasympathetic nervous system tone, which is caused by a number of things, including chronic stress, poor sleep, high blood pressure, diabetes, i.e. a high-sugar, low-fat type of diet [and] smoking …
Conventional cardiologists are certainly aware of the role of the autonomic nervous system, which is why standard cardiology care includes beta blockers, which block the sympathetic nervous system, but again, the actual research on this does not show chronic high sympathetic activity. It shows chronic low parasympathetic activity. I would admit they’re similar, but they’re not the same.
What’s dangerous to people’s health is chronic stress, chronic sleep deprivation, high carbohydrate diet, low mitochondrial function. All the things that you talk about in your book [‘Fat for Fuel‘] that leads to low sympathetic tone. Then, in the face of a sympathetic stressor, you have a heart attack. It’s not the same to say it’s a sympathetic overactivity, which is why I think we could do a lot better than blocking the sympathetic nervous system.”
The Riddle’s Solution
The second reason for heart attacks, Cowan explains, is lack of microcirculation to the heart. To understand how the blood flows to and through your heart, check out the Riddle’s Solution section on heartattacknew.com’s FAQ page.4 There, you’ll find detailed images of what the actual blood flow looks like. Contrary to popular belief, blood flow is not restricted to just two, three or four coronary arteries (opinions differ on the actual number).
Rather, you have a multitude of smaller blood vessels, capillaries, feeding blood into your heart, and if one or more of your main arteries get blocked, your body will automatically sprout new blood vessels to make up for the reduced flow. In other words, your body performs its own bypass. According to Cowan, your body is “perfectly capable of bringing the blood to whatever area of the heart it needs, and as long as your capillary network is intact, you will be protected from having a heart attack.”
Naturally, this raises the question of what might cause an individual to not have a robust network of capillaries. Not surprisingly, the same factors that cause low sympathetic tone also lead to loss of microcirculation. For example, smoking has a corrosive effect on microcirculation, not just in your extremities but also your heart. A high-sugar, low-fat diet, prediabetes and diabetes, and chronic inflammation also reduce microcirculation.
“We know that overt diabetes actually corrodes and destroys your microcirculation, your capillary network,” Cowan says. “That’s a predominant reason. We have millions of people living on high-carbohydrate diets, low-fat diets, which has an inflammatory effect on their microcirculation. There are other reasons, too, but those are probably the big ones.”
Naturally, one of the most effective ways to encourage and improve microcirculation is physical movement, so chronic inactivity will also deteriorate your body’s ability to maintain healthy microcirculation. “Again, conventional cardiology is aware of this issue. That’s why they use Plavix and aspirin, to keep the microcirculation intact,” Cowan notes.
The Role of Mitochondria in Heart Attacks
Another area of concern is your mitochondria. Unfortunately, this is an area that conventional cardiology is still largely unfamiliar with. In essence, angina is a symptom of poor mitochondrial function, causing a buildup of lactic acid that triggers cramps and pain. When this pain and cramping occurs in your heart, it’s called angina. The lactic acid buildup also restricts blood flow and makes the tissue more toxic.
When a cramp occurs in your leg, you stop moving it, which allows some of the lactic acid to drain off. But your heart cannot stop, so the glycolytic fermentation continues, and the lactic acid continues to build up, eventually interfering with the ability of calcium to get into the muscle. This in turn renders the muscle — in this case your heart — unable to contract, which is exactly what you see on a stress echo or a nuclear thallium scan.
“You see a dyskinetic or an akinetic muscle, which means it doesn’t move, because the calcium can’t get into the cells because the tissue has become too acidic,” Cowan explains. “Eventually, the acidosis continues, and that becomes the cause of necrosis of the tissue, which is what we call a heart attack …
By the way … [the] dyskinetic area … the part of the heart that’s not moving, creates pressure … in the artery embedded in that part of the heart, which causes clots to break off. That explains why you get clots forming after the heart attack, not before. This lactic acidosis buildup is one of the key events, without which you won’t have angina, and you won’t have the progression to necrosis.
Those are the three [primary causes of heart attacks]: The autonomic nervous system, the microcirculation and lactic acid buildup. Luckily, there are safe, nontoxic, effective ways to address each of those, either individually or together.”
Enhanced External Counterpulsation — A Noninvasive Treatment Alternative
One highly effective and noninvasive treatment option that will help improve microcirculation to your heart — which, again, is a common factor responsible for heart attacks — is enhanced external counterpulsation (EECP). It’s a Medicare insurance-approved therapy, and studies show EECP alone can relieve about 80 percent of angina.
As explained earlier, the reason you don’t experience a heart attack due to blockage is because you’re protected by collateral circulation. However, if you have diabetes or chronic inflammation, that will eventually deteriorate your capillaries, reducing this built-in protection. EECP works by inflating compression cuffs on your thighs and calves that are synchronized with your EKG.
When your heart is in diastole (relaxed), the balloons inflate, forcing blood toward your heart, thereby forcing the growth of new capillaries. It’s a really powerful and safe alternative to coronary bypass surgery for most people. Rather than bypassing one or two large arteries, you create thousands of new capillary beds that supply even more blood than the bypassed vessels. As noted by Cowan:
“New blood vessels mean more blood flow, and the blockage becomes irrelevant. This has been shown to be curative, meaning it will stop people with angina for at least five to seven years with one course of treatment … sometimes longer. It’s Medicare approved.
It’s paid for by insurance. It’s been studied in the literature. Again, at least 80 percent effective for getting rid of patients’ angina, which, by the way, was the last [indication] for stents, which is now no longer [a valid indication].”
The sessions are about one hour long, and most patients will need about 35 sessions to receive benefit. Aside from angina, it’s also effective for heart failure and diastolic dysfunction. Many elite athletes also use it as an aid to maintain cardiac fitness when they are injured and unable to actively exercise, as EECP basically works as a passive form of exercise. To find a provider, visit EECP.com.5
Interestingly, EECP also appears to have hormonal benefits. There are studies showing it results in decreased insulin resistance. Many patients also tend to lose weight, and experience improved blood sugar control. There’s cause to believe these beneficial side effects are related to the fact that it mimics exercise.
I was so intrigued with EECP’s benefits that I actually purchased one. They aren’t cheap; the traditional ones are close to $50,000, but I found a bright young entrepreneur, Louis Manera, who was well connected in the EECP community and is actually in the process of providing great new units at a significant discount. If you are a clinician, or even a patient with heart disease, this is something you might want to consider.
Other Commonsense Prevention Strategies
As noted by Cowan: Heart disease is “a diffuse systemic disease, and every person who goes to a cardiologist, I think, has the … right to know what this diffuse systemic disease is that’s being treated … I have my three-step opinion about what’s going on … The problem is I’ve never heard any cogent explanation in standard cardiology of what diffuse systemic disease they think they’re treating, besides high cholesterol, which turns out to be a red herring … People with higher cholesterol live longer, so that’s not the problem.” To summarize, three of the core, underlying issues at play that cause heart attacks are:
- Decreased parasympathetic tone followed by sympathetic nervous system activation
- Collateral circulation failure (lack of microcirculation to the heart)
- Lactic acid buildup in the heart muscle due to impaired mitochondrial function
So, what can you do to prevent and treat these heart attack triggers? Here’s a quick summary of some of Cowan’s suggestions:
|Eat a whole food-based diet low in net carbs and high in healthy fats, and add in beet juice (or fermented beet powder) to help normalize your blood pressure. Fresh arugula or fermented arugula powder is another option|
|Get plenty of non-exercise movement each day; walk more and incorporate higher intensity exercise as your health allows|
|Intermittently fast. Once you’ve progressed to the point of fasting for 20 hours each day for a month, consider doing a four- or five-day water fast several times a year|
|If you have heart disease, look into EECP, and consider taking g-strophanthin, an adrenal hormone that helps create more parasympathetic nervous system neurotransmitters, thereby supporting your parasympathetic nervous system. It also helps flush out lactic acid. Strophanthus is the name of the plant, the active ingredient of which is called g-strophanthin in Europe, and ouabain in the United States|
|Ground to the earth by walking barefoot on the ground|
|Get sensible sun exposure to optimize your vitamin D status and/or take an oral vitamin D3 supplement with vitamin K2|
|Implement heart-based wellness practices such as connecting with loved ones and practicing gratitude|
For more detailed recommendations, pick up a copy of Cowan’s book, “Human Heart, Cosmic Heart.” You can also find more details on Cowan’s website, FourfoldHealing.com. His book also covers how your heart actually functions, revealing why the idea that your heart acts as a pump is all wrong. It actually operates as a vortex creating machine.6 We also discussed this in a previous interview.
“On my Human Heart, Cosmic Heart website, there are articles [explaining why] the heart is not a pump, including an article by Branko Furst, an anesthesiologist in upstate New York. He wrote a book called ‘The Heart and Circulation: An Integrative Model.’
His book was endorsed by the head of cardiac anesthesiology at Harvard Medical School, who said … ‘Furst is right. There’s no way the heart is a pump, and thinking the heart is a pump is the same as believing in Newtonian physics. It’s an outdated concept.'”
Further resources substantiating issues touched on by these articles
WATER IS THE MEANS, MEDIUM AND MESSAGE OF LIFE
Volume 9 (2014), Issue 1MAE-WAN HO
Everyone knows water is essential for life, and generations of scientists have marvelled at the properties of water that make it especially fit for life. Yet this simple, ubiquitous chemical compound has remained completely mysterious until quite recently. New evidence is beginning to unlock the mysteries. Liquid water is quantum coherent even at ordinary temperatures and pressure. It associates with macromolecules and membranes in a liquid crystalline configuration that enables enzymes and nucleic acids to function as quantum molecular machines that transform and transfer energy at close to 100% efficiency. Liquid crystalline water at interfaces also provides the excitation energy that enables it to split into hydrogen and oxygen in photosynthesis, simultaneously generating electricity for intercommunication and for the redox chemistry that ultimately powers the entire biosphere. Water is the means, medium and message of life; ‘the rainbow within that mirrors the one in the sky’.
Illuminating Water and Life
Entropy 2014, 16(9), 4874-4891
This paper reviews the quantum electrodynamics theory of water put forward by Del Giudice and colleagues and how it may provide a useful foundation for a new science of water for life. The interaction of light with liquid water generates quantum coherent domains in which the water molecules oscillate between the ground state and an excited state close to the ionizing potential of water. This produces a plasma of almost free electrons favouring redox reactions, the basis of energy metabolism in living organisms. Coherent domains stabilized by surfaces, such as membranes and macromolecules, provide the excited interfacial water that enables photosynthesis to take place, on which most of life on Earth depends. Excited water is the source of superconducting protons for rapid intercommunication within the body that may be associated with the acupuncture meridians. Coherent domains can also trap electromagnetic frequencies from the environment to orchestrate and activate specific biochemical reactions through resonance, a mechanism for the most precise regulation of gene function.
The Fourth Phase of Water: A role in fascia?
Journal of Bodywork and Movement Therapies
Volume 17 , Issue 4 , 510 – 511, October 2013
How can a Jesus Christ lizard walk on water? Why do pollen grains jitterbug in a puddle? Why do fair weather clouds form such lovely puffy white shapes? And why can you “feel” the movement of fascial water?
“…The stored electrical energy in water can drive various kinds of work, including flow. An example is the axial flow through tubes. We found that immersing tubes made of hydrophilic materials into water produces flow through those tubes, similar to blood flow through blood vessels. The energy derives from the radiant energy absorbed and stored in the water. Nothing more. Flow may persist undiminished for hours, sometimes longer. Additional incident light brings faster flow. This is not a perpetual motion machine: incident radiant energy drives the flow — in much the same way that it drives vascular flow in plants…
…What’s new is the role of radiant energy: powering many of those cellular functions. An example is the blood flowing through your capillaries. That blood suffers high resistance: capillaries are often narrower than the red blood cells that must pass through; those red cells need to scrunch down in order to make their way. Resistance is high. Notwithstanding, the pressure gradient across the capillary bed is negligible. This has seemed paradoxical: without a pressure gradient, what drives the flow through those resistive vessels? If radiant energy helps propel flow through capillaries in the same way that it propels flow through hydrophilic tubes, then the paradox resolves. Radiant energy may constitute an unsuspected source of vascular drive, supplementing cardiac pressure.”
THE HEART IS NOT A PUMP:
Ralph Marinelli 1; Branko Fuerst 2; Hoyte van der Zee 3; Andrew McGinn 4; William Marinelli 5
1. Rudolf Steiner Research Center, Royal Oak, MI
2. Dept. of Anesthesiology, Albany Medical College, Albany, NY
3. Dept. of Anesthesiology and Physiology, Albany Medical College, NY
4. Cardiovascular Consultants Ltd., Minneapolis, MN. Department of Medicine, University of Minnesota, MN
5. Hennipen County Medical Center and Dept. of Medicine, University of Minnesota, MN
In 1932, Bremer of Harvard filmed the blood in the very early embryo circulating in self-propelled mode in spiralling streams before the heart was functioning. Amazingly, he was so impressed with the spiralling nature of the blood flow pattern that he failed to realize that the phenomena before him had demolished the pressure propulsion principle. Earlier in 1920, Steiner, of the Goetheanum in Switzerland had pointed out in lectures to medical doctors that the heart was not a pump forcing inert blood to move with pressure but that the blood was propelled with its own biological momentum, as can be seen in the embryo, and boosts itself with “induced” momenta from the heart. He also stated that the pressure does not cause the blood to circulate but is caused by interrupting the circulation. Experimental corroboration of Steiner’s concepts in the embryo and adult is herein presented.
Branko Furst’s Radical Alternative:
Is the Heart Moved by the Blood, Rather Than Vice Versa?
Pharmacy and Therapeutics. 2017;42(1):33-39.
“Most heart failure trials yield results that are disappointing or difficult to interpret,” Milton Packer, MD, wrote in the April 2016 issue of Circulation: Heart Failure.1 Dr. Packer, Distinguished Scholar in Cardiovascular Science at Baylor University Medical Center in Dallas, has experienced this frustration firsthand as lead investigator of more than 15 large international multicenter heart failure trials. He pointed out that in the late-breaking clinical trials session at the 2015 annual meeting of the American Heart Association, every randomized trial in heart failure “yielded distressing results.” Two medications failed to meet primary end- points (the guanylate cyclase stimulator vericiguat and the beta3adrenergic receptor agonist mirabegron [Myrbetriq, Astellas]); another (oral nitrates) had adverse effects on daily activity; and yet another (the GLP-1 agonist liraglutide) showed no diminution of clinical symptoms but was linked with possible renal-function harm and increased risk of death or heart failure hospitalization.
Such disappointing findings hardly stand alone among research results in heart failure and cardiac support, recent or other- wise. Attempts to replace failing hearts permanently with fully mechanical ones, after years of experimental and clinical trials, have largely been abandoned because of high patient mortality through combinations of thromboembolic, hemorrhagic, and infectious events leading to strokes and multiple organ failure. Despite success at adjusting cardiac outputs, matching hemo- dynamics to organ requirements with mechanical devices has remained elusive.2…”
Ouabain – the insulin of the heart.
Int J Clin Pract. 2010 Nov;64(12):1591-4. doi: 10.1111/j.1742-1241.2010.02395.x.
Today, medical therapies for heart disease are based on a diverse range of drugs. Angiotensin converting enzyme inhlbitors, angiotensin II receptor antagonists, ß-adrenergic receptor antagonists, aldosterone receptor antagonists, as weil as diuretics, and inotropic agents improve clinical symptoms and slow the progression of contractile dysfunc- tion. Despite these therapeutic advances, heart failure is still associated with an annual morta]jty rate of 10% (1). The search for better treatments and optimisation of existing ones remain major challenges in cardiology.
Basic science review: The helix and the heart
The Journal of Thoracic and Cardiovascular Surgery
November 2002, Pages 863-883
Gerald D.Buckberg MD
“It is an enormous privilege and honor to be asked to give the basic science lecture. Please join me on an adventure that I have taken over the past three years. I described this type of voyage to my daughters many years ago as “discovery,” in which you walk down certain common pathways but always see something different on that journey. I will tell you about my concept of how the helix and the heart affect nature, the heart, and the human.
To pursue this new route, I select a comment from my hero, Albert Einstein, who said, “All our science, measured against reality, is primitive and childlike, and yet is the most precious thing we have.” We all have to be students, who are often wrong and always in doubt, while a professor is sometimes wrong and never in doubt. Please join me on my student pathway to see something I discovered recently and will now share with you.”