QUABAIN

The Real Story of Ouabain

by Thomas Cowan | 

Sadly, the story of ouabain, the active ingredient in the plant strophanthus, is largely and somewhat mysteriously unknown. Few family doctors, internists and even cardiologists know of its effectiveness in treating and preventing heart disease and heart attacks, and it therefore remains unavailable to most heart patients.

 
A book written by German Naturopath Rolf-Jurgen Petry called “Ouabain: The Possible Victory Over Myocardial Infarction,” is a solution to this vacuum of information. However, it’s available only in its original German.  We’ve recently posted an  article on our website titled “The Story of Ouabain,” which outlines the book’s main points. Dr. Petry became interested in the story of strophanthus/ouabain decades ago, and after his medical training spent many years reading all the original research done on ouabain.   This article is a must-read for anyone interested in heart disease or the etiology, prevention and treatment of myocardial infarction (MI, commonly called “heart attacks”).
 
Dr. Petry not only lays out the history of the benefit of strophanthus/ouabain in the prevention and treatment of MI, but he also addresses directly the many common misconceptions medical doctors and researchers continue to have about its use.  The first of these misconceptions is that since ouabain is in the family of cardiac glycosides, like the more commonly used heart drug digitalis/digoxin, it must affect the body in the same way.   In reality, the research conclusively demonstrates that at the doses used in practice, as in the strophanthus extract we are using, ouabain not only doesn’t inhibit the sodium/potassium pump, as does digitalis, it actually stimulates the action of this pump.
 
Therefore, while digitalis is relatively contraindicated for people with angina or MI, ouabain clearly helps these patients.  One well-documented way in which ouabain helps people with heart disease has to do with red blood cells and platelets. In one type of cardiac dysfunction that leads to an MI, the red blood cells and  platelets become swollen and, as a result, are unable to move easily through the narrow capillaries.   This process creates further congestion and clotting in the small vessels, which creates decreased blood flow and further dysfunction in the heart cells. Giving aspirin to heart patients is meant to increase the blood flow through the capillary network.   Ouabain, by stimulating the sodium/potassium pump in the platelets and RBCs, has a similar effect.  Stimulation of the pump makes the RBCs and platelets less swollen (by increasing the sodium excretion out of the cell) and therefore more able to glide through the narrow passages of the capillaries.  This increases blood flow and prevents clots with NONE of the negative consequences of aspirin or other blood thinners. 
 
 Another misconception Dr. Petry clears up is connected to animal studies that show that some animals with hypertension have elevated endogenous (self-produced) ouabain in their blood.   This finding has led to the common belief that the elevated ouabain causes their elevated blood pressure.  This theory is clearly in opposition to the actual studies on people treated with oral ouabain. In my own experience, people with elevated blood pressure experience a lowering of their blood pressure with oaubain, and people with normal BP show no effects. In reality, the conclusion that the elevated ouabain levels in animals cause hypertension is backward.  The elevated endogenously produced ouabain is the animals’ attempt to self-treat their elevated pressure levels, not the cause.  The proof of this conclusion is that in all such studies, the elevated ouabain levels were found to be “cardioprotective.”    That is, the animals with high BP who raised their own ouabain levels (as a protection) clearly showed less heart damage than those animals with lower ouabain levels.  This result mimics what happens when we give patients with high BP a small dose of oral ouabain. It not only lowers the BP, but it also protects their cardiovascular system.  In essence, ouabain acts as both blood thinner (like aspirin or Plavix) and as a first-line hypertensive drug (beta blockers or diuretics), again, with none of the unwanted side effects. 
 
Furthermore, Dr. Petry also demonstrates with multiple studies that unlike digitalis, oral ouabain lowers the oxygen needs of the myocardial cells.  Lowered oxygen requirements mean more efficient respiration, which translates into less susceptibility to injury.  Interestingly, this is the exact rationale for giving beta blockers or calcium channel blockers to heart patients.  Again, while beta blockers cause people to feel fatigued, make them impotent and depressed, worsen lipid profiles and exacerbate diabetes, oral ouabain makes people feel better, more energetic and is being investigated for its beneficial effects on such diverse conditions as breast cancer, Parkinson’s disease and asthma.
 
At the end of reading this article and thoroughly investigating the decades of clinical use and research on the use of strophanthus/ouabain, I hope everyone asks themselves the question: which would I rather use or prescribe, the toxic medicines of conventional therapeutics or nature’s gift to the heart, strophanthus?
 
On a final note, we want to emphasize that if you are a patient who is interested in using strophanthus/ouabain for your own health, please find a health-care practitioner who is willing to work with you on this medicine.  Have them call our office at  (415) 334-1010, and we can sign them up to participate in a short phone conference in which I address how to use this valuable medicine.  At that point, they will have access to the medicine and my full support in learning how to incorporate strophanthus/ouabain in their practice. 
 
Finally, just this week, we introduced a new  beet-root juice powder,which is another valuable medicine in the prevention and treatment of cardiovascular disease.  This is a U.S. organically grown, freeze-dried powder that easily dissolves in water and is an easy way to incorporate the benefits of beet juice in your diet.  It’s rich in nitrates, which are the precursors of nitrous oxide, which relaxes blood vessels, similar to the drug nitroglycerine.

 

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WHAT'S THE REAL CAUSE OF HEART ATTACKS?

Thomas S. Cowan, MD

http://www.fourwinds10.net/siterun_data/health/intentional_death/news.php?q=1418833899

 

 

 

Dec. 17, 2014

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 (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 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 studies 5 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, 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.

http://articles.mercola.com/sites/articles/archive/2014/12/17/real-cause-heart-attacks.aspx

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PERSPECTIVE CUNICAL PRACTICE

Ouabain - the insulin of the heart 


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
(13). There are marked differences between the effects of digoxin and ouabain. Only ouabain in small doses stimulates the sodium pump (14,15); digoxin does not show this effect (16). Moreover, digoxin was shown to induce changes in intracellular membrane traffic in neuronal 
tion. Despite these therapeutic advances, heart failure is still associated with an annual morta]jty rate of 10% (1). The 
cells, whereas ouabain does not possess this ability and even antagonised digoxin effect ( 17). A recent study confumed the long-known clinical 
search for better treatments and optimisation of existing ones remain major challenges in cardiology. 
Modulation of myocardial metabolism has become an accepted new approach to improve the performance of the dysfunctional myocardium (2). Alternatively, proven agents such as digitalis glycosides continue to be of interest. Digoxin is still used extensively worldwide, and it remains one of the most commonly prescribed drugs. The Digitalis Investigation Group trial has indicated that digoxin is quite effective in reducing cardiovascular hospitalisations (3). A proposal for a !arge digoxin study is being considered for funding in Europe (4). However, arrhythmia and a narrow tberapeutic index Iimit its therapeutic application (5,6). Although often used as research tool, the cardiac glycoside ouabain (referred to as g-Strophanthin in German) has become a niche product in treatment of heart diseases. Decades of practical use indicate benefits in prevention and treatment of acute heart attacks. Prophylactic and therapeutic use of ouabain is recommended in insufficiencies of the left ventricle. Several clinical sturlies with orally administered ouabain report exceptionally positive results for the treatment of cardiovascular diseases (7-9). This clinical experience disappeared in time, yet there is mounting evidence that supports a re-evaluation of ouabain in the treatment of heart disease. In 1991, ouabain was identified as an endogenous hormone. This discovery has Iead to an intense re-examination of the drug, its pbysiological functions and its mode of action (10--12). Based on its chemical structure, ouabain is considered as a typical digitalis derivative. All digitalis derivatives bind to and inhibit the ubiquitous transmembrane protein Na+, K+-ATPase and increase the force of contraction of heart muscle. However, there are diverse biological responses to different derivatives both at the cellular and at the molecular Ievel 
experience that ouabain has an inhibitory effect on cardiotoxicity induced by digitalis glycosides. Ouabain at a low dosage delayed the statt of arrythmia induced by digoxin on guinea pig papillary muscle. In addition, ouabain at a low dosage but not at a high dosage delayed the development of digoxin-induced arrhythmia in anaesthetised guinea pigs (18). Thus, the long-known characteristic dose dependency of ouabain effects (19) has been confumed. 
Clinical experience with ouabain 
According to canonical explanations, ouabain and other digitalis derivatives should have similar therapeutic effects. However, clinical experience clearly indicates that ouabain is different from other digitalis derivatives. A most pronounced difference is the fast onset of action by ouabain. This effect was the basis for the chance discovery of ouabain in 1859 by tbe English botanist Kirk. He bad discovered the fast onset of action of ouabain on the heart by using a toothbrusb contaminated witb Strophanthus seeds. The rapid onset of effect of oral ouabain was used in medical practice for a 'Strophanthin-quick-test': patients with suspected heart disease were given two tablets of 3 mg that they had to chew and distribute in the mouth. In the case of heart disease, a relief of complaints was observed within 5-10 min. Tbis test was used routinely in German physicians' offices weil into the 1970s. Based on decades of extensive clinical experience with ouabain, the tberapeutic profile of tbe drug and the disease profiles for which the use of ouabain is appropriate have been summarised in monograpbs and reviews (19-21). The main benefit is in prevention and treatment of acute heart attacks. Prophylactic and therapeutic use of ouabain is recommended in: 
© 2010 Blackwell Publishing ltd lnt J Clin Pract, November 2010, 64, 12, 1591-1594 doi: 10.1111/j.1742-1241.2010.02395.x 
Ouabain is different from digitaUs glycosides 
1591 
1592 Perspective 
congestive heart insufficiency without pronounced hypertrophy, coronary sclerosis, cardiogenic hypertension, asthrna cardiale, exercise-induced cardiac insufficiency, angina pectoris and arrhythrnias, including those that occur on treatrnent with digitalis. lt is stated that ouabain 'has proven to be the rnost acceptable, rnost effective antidote for digitalis intoxication.' Edens described 'the intravenous Strophanthin treatrnent as the safest tteatrnent of organic-induced angina pectoris, including heart attack.' Digitalis causes a worsening of syrnptorns and is therefore contta-indicated. While under digitalis ECG abnorrnalities and arrhythrnias can occur, these syrnptorns are either alleviated or cornpletely abolished by ouabain (22,23). In addition, there are nurnerous clinical reports that ouabain lowers blood pressure in patients with heart diseases (24,25). In the 1950s, a fierce scientific dispute erupted over the bioavailability of orally adrninistered ouabain. In the 1970s, optirnised enteric-coated forrnulations were introduced that have enteral absorption rates of up to 80% in cats (26). A drug based on such a forrnulation today is registered for insufficiency of the left ventticle in Gerrnany, sold as prescription drug under the brand narne Strodival®rnr by Medapharrna (Meda Pharrna GmbH & Co. KG, Bad Hornburg v.d.H., Gerrnany). An investigation published in 2001 reports systernic bioavailability of 43-50% after oral adrninisttation in guinea pigs (27). 
Ouabain modulates cardiac metabolism 
Based on extensive clinical observations, it had been postulated that ouabain stirnulates rnyocardial rnetabolisrn (19-21). Mechanistic sturlies have revealed that ouabain, in conttast to digitalis derivatives, indeed has pronounced effects on the cardiac rnetabolisrn. In dogs, ouabain increases lactic acid utilisation by the rnyocardiurn. Yet, digitoxin inhibits lactic acid utilisation by the rnyocardiurn (28). Ouabain as well as k-strophanthin reduce lactic acid concentration in the blood of patients with heart diseases (29,30). The rnetabolic effect of ouabain is not lirnited to stirnulation of lactic acid utilisation. Upon oral adrninisttation to male rats, ouabain increases the acetyl-coenzyme A/coenzyme A ratio in the rnyocardiurn (31). Conttary to digitoxin, ouabain stirnulates fatty acid utilisation in the rnyocardiurn (32,33). Ouabain arnplifies rnetabolic stirnulation induced by acetylcholine and inhibits increased oxygen consurnption induced by adrenaline (34). In the failing human rnyocardiurn, the positive haernodynarnic effects of ouabain are not associated with additional 
energy consurnption (35). In conttast, in healthy male subjects, digoxin reduces resring rnetabolic rate, respiratory quotient and fat oxidation (36). In an infarct rnodel with the guinea pig heart, digoxin has no stimulating effects on cardiac metabolism (37). The digitalis derivative Lanatoside-C has no effect on substrate utilisation of the rnyocardiurn (38). In addition to the effects on fatty acid rnetabolisrn, ouabain stirnulates rnyocardial protein syntheses (39). Digitoxin inhibits rnyocardial protein synthesis (31). von Ardenne dernonstrated that in rnyocardial infarction induced by ligature in rat and rabbit hearts, the pH in rnyocardial tissue drops rnarkedly. This acidification ttiggers a chain reaction that Ieads to cell death (40). Administration of ouabain in a myocardial infarct model in rats raises the pH of acidic cardiac tissue within a few rninutes by up to 0.5 units. Digitoxin does not alter the pH. In addition, ouabain increases the rheological properties of blood by enhancing the plasticity of erythrocytes (41). Digitoxin does not influence the flexibility of erythrocytes. The pH sensitivity of the rnyocardium is well documented. A drop in pH below 6.2 Ieads to irreversible darnage. Therefore, in cardiac surgery, strict pH conttol is imperative (42). In the 'Strophanthin era', German surgeons routinely applied 0.3 mg ouabain pre-operatively and thereby observed significantly fewer complications (43). The metabolic effects of ouabain are supported by in vivo studies. Ouabain significantly increases the endurance perforrnance of rats. Hyperttophy of the heart is reduced by adrninisttation of ouabain (44). Orally adrninistered ouabain improves physical endurance in guinea pigs ( 45) as well as in healthy volunteers (41). Digoxin, however, does not irnprove the perforrnance of patients with coronary arterial disease. In a double-blind crossover study with k-sttophanthidin and digoxin, only k-sttophanthidin irnproved the perforrnance of coronary patients (46). Additional evidence confirms the rnechanistic differences between ouabain and digitalis glycosides. Ouabain and digitalis derivatives develop their effects in different cellular spaces. Digitalis derivatives rnust penettate into the cell interior to exert their effects, whereas ouabain develops its effect in the extracellular space (47). The pharrnacokinetic behaviour of i.v.-administered ouabain and digitalis derivatives likewise suggests that their therapeutic effects are based on different receptors. The effect of i.v.-adrninistered ouabain starts irnrnediately after injection, reaches a maximum after 5 min, last 5-7 h and then rapidly declines (22). With i.v. -administered digoxin, effects slowly start 5-30 min 
© 2010 Bladtwell Publishing Ltd lnt J Clin Pract, November 2010, 64, 12, 1591-1594 
after injection, the maximum effect being reached only after 1-4 h (5). 
Conclusion 
Research on ouabain has suffered from the dogma that ouabain is a member of the digitalis glycosides. Recent research illustrates the uniqueness of ouabain and confirms the clinical experiences with ouabain, which have been known for decades. Ouabain modulates the metabolism of the heart; it stimulates substrate utilisation of the myocardium, removes lactate accumulated during heart diseases and reduces the amount of fatty acids in the blood. Ouabain is, as Aschenbrenner has formulated, the insulin of the heart. The uniqueness of ouabain ought to be recognised in future research as well as in clinical practice. Clinical studies with ouabain that correspond to current standards are warranted. 
Disdosure 
No conflict of interest. 
References 
H. Fürstenwerth Unterölbach 3A, Leverkusen, Germany Email: hauke@fuerstenwerth.corn 
Oeland )GF, Daubert j-C, Erdmann E et al. The effect of cardiac re>'}'Ilcbronization on morbidity and mortality in heart fuilure. N Eng/ ] Med 2005; 352: 1539-49. 2 Neubauer S. The fuiling heart - an engine out of fuel. N Eng/ ] Med 2007; 356: 1140-51. 3 Hauptman P), Kelly RA. Digitalis. Circulation 1999; 99: 1265-70. 4 Oeland JGF, Cullington D. Digoxin: Quo Vadis? Circ Heart Fail 2009; 2: 81-5. 5 Eichhorn EJ, Gheorghiade M. Digoxin. Prog Gardiavase Dis 2002; 44: 251-66. 6 Wasserstrom JA, Aistrup GL. Digitalis: new actions for an o1d drug. Am] Physiol Heart Circ Physiol 2005; 289: H1781-93. Dohrmann RE, Dohrmann M. Neuere therapie der instabilen angina pectoris bei koronarer berzkrankbeit. Erfahrungsheilkunde 1984; 33: 183- 90. Dohrmann RE, )anisch HD, Kessel M. Kliniscb-poliklinische Studie über die Wirksamkeit von g-Strophanthin bei Angina pectoris und Myokardinfurkt. Cardiol Bull 1977; 14/ 15: 183-7. 9 Haihuber M, Lantscberat T, Meusburger K. Zur Strophoraltherapie. Med Klin 1954; 36: 1440-3. 10 Bagrov AY, Shapiro )1, Fedorova OV. Endogenous cardiotonic steroids: physiology, pharmacology, and novel therapeutic targets. Pharmacol Rev 2009; 61: 9-38. 11 Schoner W, Scheiner-Bobis G. Endogenous and exogenous cardiac glycosides: tbeir roles in bypertension, salt metabolism, and cell growth. Am] PhysiDI Gell Physiol 2007; 293: C509-36. 12 Nesher M, Sbpolansky U, Rosen H, Liebtstein D. Tbe digitalis-like steroid bormones: new mecbanisms of action and biological significance. Life Sei 2007; 80: 2093-107. 13 Dvela M, Rosen H, Feldmann T et al. Diverse biological responses to different cardiotonic steroids. Pathophysiology 2007; 14: 159-66. 14 Oberfrank F, Vizi ES, Baker PF et al. Comparison of the effects of a bufodienolide and ouabain on neuronal and smooth musde preparations. Neurosei Res 1991; 10: 235-44. 
Perspective 
15 Gao ), Wymore RS, Wang Y et aL lsoform-specilic stimulation of cardiac Na/K pumps by nanomolar concentrations of glycosides. ] Gen Physiol 2002; 119: 297-312. 16 Balzan S, D'Urso G, Gbione S et al. Selective inhibition of human erythrocyte Na+ I K+ ATPase by cardiac glycosides and by a mammalian digitalis like mctor. Life Sei 2000; 67: 1921-8. 17 Feldmann T, Glnkmann V, Medvenev E et al. Role of endusomal Na+-K+-ATPase and cardiac steroids in tbe regulation of endocytosis. Am] Physiol Gell PhysiiJI 2007; 293: C885-96. 18 Nesber M, Sbpolansky U, Viola N et al. Ouabain attenuates otber cardiac steroid-induced cardiotoxicity. Br ] Pharmacol 2010; 160: 346-54. 19 Zimmermann H. Die klinische Strophanthinlehre von Edens im Liebte neuer ForscbungsergebnisseMed Klin 1951; 46: 1049- 52. part 1: 1028-1031, part II. 20 Edens E. Die Digitalisbehandlung. 3. Auflage, Berlin-Müncben: Verlag Urban&Scbwarzenberg, 1948. 21 Kern B. Der Myokardinfarkt. 3. Auflage, Heidelberg: Haug Verlag, 1974. 22 Sarre H. Die Ursache der gegensätzlichen Wirkung von Strophanthin und Digitalis auf die Coronarinsuffizienz. Klin Wochensehr 1943; 22: 135. 23 Kubicek F, Reisner T. Hypoxietoleranz bei koronarer Herzkrankheit unter der Einwirkung von Digoxin, Beta-Metbyl-Digoxin und g-Stropbanthin. Ther Ggw 1973; 112: 747. 24 Rotbmund W. Über die Ent;tebung der essentiellen Hypertonie. Notabene Medici 1977; 7: 22-32. 25 Kracke R. Zur perlingualen Stropbantbintherapie. Dtsch Med Wochensehr 1954; 79: 81-3. 26 United States Patent 4,202,888, filed on )uly 7, 1977 by KaliChemie Pharma GmbH. 27 Leuschner ), Winkler A. Toxicological sturlies witb ouabain. Naunyn Schmiedebergs Arch Pham•acol. 2001, 363 (Suppl. 4): 139, abdr2ct 54-4. 28 von Blumencron W. Über die Wirkung von Strophanthin und Digitoxin auf den Milchsäurestoffwechsel des Herzens. Klin Wochensehr 1941; 20: 737-9. 29 Renk H. Vergleichende Untersuchungen über das Verbalten des Milchsäurespiegels bei der Therapie der Herzinsuffizienz. Med Klin 1959; 54: 13-6. 30 Loll H, Blumenherger K). Änderungen des Serumspiegels von Intermediärprodukten und Enzymen durch k-Strophanthin. Arzt/ Forsch 1960; 14: 181-5. 31 Kaemmerer K, Kietzmann M. Intermediäre Effekte von g-Stropbantbin und Digitoxin im Tierversuch. Cardiologisch-Angiologisches Bul/1987; 24: 66-70. 32 Riehle M, Bereiter-Hahn). Ouabain and digitoxin as modulators of chick ernbryo cardiomyocyte energy metabolism. Arzneimittelfor>chung 1994; 44: 943-7. 33 Gousios AG, Fells )M. Effects of ouabain on force of contraction, oxygen consumption, and metabolism of free futty acids in tbe perfused rabbit beart. Circ Res 1967; 21: 445-8. 34 Gremels H. Über den Einfluß von Digitalisglykosideu auf die energetischen Vorgänge am Säugetierberzen. Naunyn Schmiedebergs Arch Exp Parhol Pharmaka/ 1937; 186: 625. 35 Hasenfuss G, Mulieri LA, Allen PD et al. lnfluence of isoproterenol and ouabain an excitation-contraction coupling, cross-bridge function and energetics in fuiling human myocardium. Circularion 1996; 94: 3155-60. 36 Lyon X, Schutz Y, Budin T et al. Inhibition ofNa(+)-K(+) ATPase by digoxin and its relation with energy expenditure and nutrient oxidation rate. Am] PhysiDI Endocrinol Metab 1995; 268: E1051-{i. 37 Zannad F, Graham CW, Aronson )K. The effects of digoxin and dopamine on tbe oxygen consumption, Iactate production and haemodynamic performance of an isolated, perfused, working guinea-pig beart. Eur] Pharmaco/1982; 81: 263-71. 38 Blain )M, Eddle.man EE, Siegel A, Bing R). Sturlies on myocardial metabolism: V. Effects of lanatoside-C on the metabolism of the human heart.] Clin Invest 1956; 35: 314. 
© 2010 Blackwell Publishing Ltd lnt J Clin Pract, November 2010, 64, 12, 1591- 1594 
1593 
1594 Perspective 
39 Kaemmerer K, Kietzmann M. Verhalten der Eiweißsynthese im Herzmuskelgewebe von Ratten nach oraler Gabe von g-Strophanthin. Berl Munch Tierarzd Wochensehr 1986; 98: 262-7. 40 von Ardenne M. Research on the mechanism of myocardial infarctions and on counteracting measures, a new galenic furm of the fust acting g-strophanthin. Agressologie 1978; 19: B-22. 41 Saradcth T, Ernst E. Hämorheologische Effekte durch g-Strophanthin. Erfahrungsheilkunde 1991; 40: 775-6. 42 Healey CM, Kumbhani Dj, Healey NA et al. Impact of intraoperative myoca.rdial tissue acidosis on postoperative adverse outcomes and cost of care fur patients undergoing prolonged aortic clamping during cardiopulmonary bypass. Am] Surg 2009; 197: 203-10. 43 Kem B. Straphanthin-Report, page 43, edited by W. Mauss, Studienkreis für Infarktprobleme, Stuttgart, 1984. 
44 Kuschinsky G. Die Verhütung von Erschöpfungszuständen des Herzens durch Digitalissubstanzen. Klin Wochensehr 1947; 24: 502- 3. 45 Muskopf E, Dietz H. Experimentelle und klinische Untersuchungen über eine zuverlässige orale Strophanthintherapie. Med Welt 1955; 39: 1375-7. 46 Ago•loni PG, Doria E, Bcrti M et al. Bcttcr cfficacy of Kstrophanthidin versus digoxin in subjects with dilated cardiomyopathy and ehrenie heart insufficiency. Cardiologia 1992; 37: 323-9. 47 Löhr E, Makoski HB, Göbbeler T et al. Beitrag zur Membranpermeabilität von Cardiaca (g-Strophanthin, Digoxin und Oxyfedrin) auf Grund von Mikro-Autotadiographien am Meerschweinchenherzen. Arzneimittelforschung 1971; 21: 566. 

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What Causes Heart Attacks
In this article, I lay out the case that the spectrum of heart disease that 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 in the coronary arteries (the arteries that supply the heart). As we ali know, the conventional view of the cause of heart disease is that the central events occur in the arteries. In this article, I will go into more detail about why the conventional theory is largely misleading, and then I will describe the precise and welldocumented events that do lead to heart attacks. This new understanding is crucial because, as the past 50 or 50 years have shown, pursuing the coronaryartery theory has cost this nation billions of dollars in surgical costs most of which are unnecessary - and billions in medications that cause as much harm as any benefits, and has led many people to adopt a low-fat diet and which only worsens the problem. In contrast, by understanding the real pathophysiological events behind the evolution of Mls, we will be led to a proper "Nourishing Traditions"style diet, the use of the safe and inexpensive medicine g-strophanthin, and rnost important, we will be forced to look at how heart disease is a true manifestation of the cost of modern life to human health. To overcome the epidemic of heart disease, we need a new medical paradigm, a new economic system, and a new ecological consciousness; in short, a new way of life. The coronary theory misses ali of this, just as it
by Dr. Thomas Cowan
misinterprets the actual pathological events. . In writing this article, I am indebted to the work of Dr. Knut Sroka and his website www.heartattacknew. com. For ali who are interested in this important subject, it is advised to read the entire website and watch the video on the website. For health professionals and researchers, your understanding of this subject is incomplete without reading and studying two items found in the print version of the website: The Etiapathagenesis oi Caronary Heart Oisease: A Heretical Theory 8ased an Marphalagy, by G. Baroldi, and "On the Genesis of Myocardial Ischemia," by Sroka.
Rebuttal of the Conventional Theory Until recently, it was thought that most Mls were caused by progressive blackage created by plaque buildup in the major arteries leading ta the heart (there are four major coronary arteries). The plaque was thought to be cholesterol buildup 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 (blockage) with either an angioplasty or stent, or, if that was not possible, to bypass the area with coronary bypass grafting (CABG). Simple problem, simple solution. However, problems became apparent through a number of avenues. First, a story related by a cardiologist at a Northern California
heart symposium, at which I was a speaker, points to the first problem. He told us that during his residency he was part of a trial conducted in rural Alabama with black men. In this trial, angiograms (injections of dye into the coronary arteries to detect blockages) were done on ali the men presenting with chest pains. For the ones who had a single artery blocked, no treatment was prescribed, and the researchers predicted in their notes which part of the heart would have a subsequent heart attack if one occurred. Of course, they ali predicted that it would be in the part of the heart supplied by the blocked coronary artery. Then they waited. Eventually, many of the men did return and did have Mls, but to the researchers' surprise, less than 10% had a heart attack in the area of the heart supplied by the original blocked artery. Second, a large study conducted in 2003 by the Mayo Clinic on the efficacy of bypasses, stents, and angioplasty concluded that: a. bypass surgery relieves symptoms (chest pain); b. bypass surgery does not prevent further heart attacks; c. only high-risk patients, those whose lives are in acute danger, benefit from bypass surgery with regard to a better chance of survival.
In other words, the gold standard for treating arterial blockages has, at best, only minimal benefits. If you watch the video on the heartattacknew.com website and go to the FAQ called "The Riddle's >
TOWNSEND LETTER - MAY 2014 67
of Mls was done in Heidelberg in the 19705.1 The conclusion was that thrornbosis sufficient to cause the MI was found in only 20% of cases. Saroldi, in the largest such study ever done, found sufficient thrombosis in 41% of cases.' He also found that the larger the area of the MI, the more often a stenosis was present, and the longer the time between MI and death, the higher the percentage of stenosis. These two facts allow some researchers to "cherry-pick" the numbers and make the stenosis rate high, as they choose to study only those with large Mls and who live the longest after the MI event. Later in this article, I will explain how the stenosis comes about as a consequence of the MI. Another observation that casts doubt on the relevance of the coronary artery theory of MI has to do with the proposed mechanism of how thrombosed arteries cause ischemia, which is by cutting off the blood supply and thereby the oxygen to the tissues. The reality isthat when careful measurements are done assessing the p02 (oxygen levei) of the myocardial cells during an MI, to the huge surprise of many, there is no oxygen deficit ever shown in an evolving MI.3 The p02 levels do not change at ali throughout the entire event. I will come back to this 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 p02 in the myocardial cells, and in fact the p02 doesn't change, then exactly what did happen? The conclusion is that thrombosis associated with MI is a real phenomenon, but in no pathological study has it been found in more than 50% of deaths, which raises the question, why did the other 50% even have an MI? Second, it's clear from ali pathology studies that thrombosis of significant degrees evolve after the MI occurs, again leading to the question of what caused the MI in the first place. The fact that thrombosis does occur also
Heart Attacks
> Sol.ution," it becomes clear why this is 50. Large, stable blockages - those over 90% - are in almost 100% of the casescompletely compensated by collateral blood vessels. In fact, the view that the heart gets its blood only from the four major vessels is itself false. Starting soon after birth, the normal heart develops an extensive network of small blood vessels called collateral vessels, which eventually compensate for the interruption of flow in any one (or more) of the major vessels. As Sroka correctly points out in the video, coronary angiogram - by failing to show the collateral circulation, and by creating spasms in the coronary arteries through the injection of heavy dye under high pressure - is notoriously inaccurate at assessingthe 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 done on minimally symptomatic patients who show a greater than 90% blockage in one or more coronary arteries. These arteries are almost always fully collateralized; the surgery does not restore blood flow because the body had aiready done its own bypass. Ask yourself: If it were true that an artery more than 90% blocked had no collateral circulation, how would that person still be alive? And does it really make sense that the eventual MI is caused when the stenosis goes from 93% to 98%? This is an insignificant difference and is completely nonsensical. Yet this is what most of the procedures are meant to accomplish, to unblock the stenosis, which, as the video shows, actually has no blood-flow repercussions. It is no wonder that in study after study these procedures faiI to provide any significant benefit to patients. For these reasons, the stableplaque model is being abandoned by conventional cardiology, in favor of a different model for the etiology of
Mls, which, as it turns out, is almost equally invalid.
í
68 TOWNSEND LETTER - MAY 2014
Meet the Unstable Plaque 50, we ali agree that the entire focus of cardiology - the stable, progressing, calcified plaque, the thing that we bypassed and stented for years, the thing that we do CT scans of your arteries for, the thing that we told Vou is from cholesterol buildup in your arteries, the thing that "alternative cardiology," such as the Ornish program, focused on - actually is not 50 important in the etiology of heart attacks. Don't worry, though. We know that the focus of the problem must be the arteries, or 50 conventional thinking goes.Therefore, enter the unstable, or friable, plaque. This insidious fellow doesn't actually create a large blockage; rather, it's a soft, "foamy" plaque that under certain situations (we don't know which situations) rapidly evolves and abruptly closes off the involved artery, creating a downstream oxygen deficit, followed by angina, then ischemia. These soft plaques are thought to be a combination of inflammatory "buildup" and LDL, the exact two things targeted by statin drugs. Therefore, the thinking goes, because this type of plaque can build up in anyone's arteries, at any time, everyone should be on statin drugs to prevent heart attacks. (Some people even advocate putti ng therapeutic doses of statins in municipal water supplies.) Angiogram studies have been presented to show the evolution of these unstable plaques as proof that they are the true cause of the majority of Mls. As I will show in the next section, acute thrombosis does happen in patients having Mls, but it is a consequence, not the cause, of the MI. But how often does it actually happen? Let's look at pathology studies, which are the only accurate way to determine what actually happened, as opposed to angiograms, which are misleading and create many artifacts. The first major autopsy/ pathology study of people who died
ains why emergency procedures mber, the only patients who -t from bypass and stents are ost critical, acute patients) can elpful immediately post-MI to e flow in those patients who ot have adequate collateral ation to that part of their heart. 50 again, ali the existing theories asto the relevance of the coronary arteries in the evolution of the MI are fraught with inconsistencies. If this is 50, what then does cause Mls?
lhe Etiologyof Myocardial Ischemia Any accurate theory of the cause of myocardial ischemia must account for the risk factors most associated _ with heart disease. These are: being male, having diabetes, smoking cigarettes, and experiencing chronic psychological/emotional stress. 'Interestingly, none of these risk factors directly link to pathology of the coronary arteries. Diabetes and cigarette use cause disease in the capillaries, not the large vessels, and stress has no direct effect on coronary arteries that we know of. In addition, during the past five decades or 50, the four main medicines of modern cardiology B-blockers, nitrates, aspirin, and statin drugs - ali have some benefits for heart patients (albeit ali with serious drawbacks as well), which must be addressed in any comprehensive theory of myocardial ischemia, which I will attempt to do here. The real revolution to come in the prevention and treatment of heart disease has been inaugurated through our understanding of the role of the autonomic nervous system in the genesis of ischemia and its measurement through the tool of heart-rate variability. First, some brief background. We have two distinct nervous systems. The first, the central nervous system, controls conscious functions such as rnuscle and nerve function. The second nervous system is called the autonomic (or unconscious) nervous system (AN5), which controls the function of our internal organs. The autonomic
nervous system is divided into two branches, which in health are always in a balanced but ready state. The sympathetic, or fight-or-flight, system is centered in our adrenal medulla and uses the chemical adrenaline to tell our bodies that danger is afoot, it's time to run. It does so by activating a series of biochemical responses, the center of which are the glycolytic pathways that accelerate the breakdown of glucose to be used as quick energy 50 that we can make our escape. In contrast, the parasympathetic branch, centered in the adrenal cortex, 15 the rest-and-digest arm of the autonomic nervous system. The particular nerve of the parasympathetic chain that innervates the heart is called the vagus nerve. It slows and relaxes the heart whereas the sympathetic branch accelerates and constricts the heart. It is the imbalance of these two branches that is responsible for the vast majority of heart disease. Using heart-rate variability monitoring, which gives a realtime, accurate depiction of the status of these two branches of the AN5, it has been shown in four studies that patients with ischemic heart disease have, on average, a reduction of parasympathetic activity of more than a third. Typically, the worse the ischemia, the lower the parasympathetic activity (5/134). Furthermore, about 80% of ischemic events have been shown to be preceded by significant, often drastic, reductions in parasympathetic activity related to physical activity, emotional upset, or other causes." This finding contrasts with others that show that people who have normal parasympathetic activity, then have an abrupt increase in sympathetic activity (physical activity, or often 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.7 Presumably, we are meant to have times of excess sympathetic activity: that is normal
Heart Attacks
life. What's dangerous to our health is the ongoing, persistent decrease in our parasympathetic, or liferestoring, activity. This decrease in parasympathetic activity is mediated by the three chemical transmitters of the parasympathetic nervous system: acetylcholine, NO, and cGMP. This is where it becomes fascinating, for it has been shown that women have stronger vagaI activity than men, probably accounting for the sex difference in the incidence of MI.8 Hypertension causes a decrease in vagal activity, smoking causes a decrease in vagal activity, diabetes causes a decrease in vagaI activity, and physical and emotional stressalso causes a decrease in parasympathetic activitv.":" 50 ali the significant risk factors have been shown to downregulate the activity of the regenerative nervous system in the heart. On the other hand, the main drugs used in cardiology - nitrates stimulate NO (nitrous oxide) production, which upregulates the parasympathetic nervous system. Aspirin and statin drugs also stimulate the production of ACH and O, two of the principal mediators of the parasympathetic nervous system (until they cause a rebound decrease in these substances, which then makes the parasympathetic activity even worse). Finally, B blockers are called B-blockers because they block the activity of the sympathetic nervous system. To summarize, the risk factors and interventions that have actually been borne out through time ali help balance the AN5. Whatever their effect on plaque and stenosis development is of minor relevance. 50, what is the sequence of events that leads to an MI? First, and in the vast majority of cases the pathology wi II not proceed unless this condition is met, there is a decreased tonic activity of the parasympathetic nervous system. Then comes an increase in the sympathetic >
TOWNSEND LETTER - MAY 2014 69
Heart Attacks
> nervous system actrvity, usually a physical or emotional stressor, which raises adrenaline production, which directs the myocardial cells to break down glucose using aerobic glycolysis (remember, no change in blood flow as measured by the p02 in the cells has occurred). This development redirects the metabolism of the .heart away from its preferred and most efficient fuel source, which is ketones and fatty acids. This explains why heart patients often feel tired before their events. This also explains why a high-fat, low-glucose diet 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 100% of Mls, with no coronary artery mechanism required.P-" As a result of the increase in lactic acid in the myocardial cells, a localized acidosis occurs. This acidosis causes the calcium to be unable to enter the cells, making the cells less able to contract." This inability to contract causes localized edema, dysfunction of the walls of the heart (called hypokinesis, the hallmark of ischemic disease as seen on stressechoes and nuclear thallium stress tests), and eventually necrosis of the tissue, which we call an MI. The localized tissue edema also alters
the hemodynamics of the arteries embedded in that section of the heart, causing the sheer pressure that ruptures the unstable plaques, which further blocks the artery and worsens the hemodynamics in that area of the heart. Only this explanation tells us why plaques rupture, whattheir role in the MI process is, and when and how they should be addressed; that is, only in the most critical, acute situations. Only this explanation accounts for ali the observable phenomena associated with heart disease. The true origin of heart disease could not be more clear. The final question is, why is this understanding of heart disease relevant, besides being of academic interest? The first and obvious answer isthat if you don't know the cause, you can't find the solution. The solution is to protect our parasympathetic activity, use medicines that support it, and nourish the heart with what it needs. Nourishing our parasympathetic nervous system is basically the same as dismantling a way of life for which humans are ill suited. This way of life, in my view, is otherwise known as industrial civilization. The known things that nourish the parasympathetic nervous system are contact with nature, loving relations, trust, economic security (a hallmark of indigenous peoples the world over), and sex - in a sense, a whole new world. The medicine aspects of the that supports ali parasympathetic
Dr. Tom Cowan discovered lhe work of lhe two men who would have lhe rnost influence on his career while leaching gardening as a Peace Corps volunleer in Swaziland, South Africa. He read Nulrition and Physical Degeneration, by Weslon Price, and a fellow volunteer explained lhe arcane principies 01 Rudolf Steiner's biodynamic agriculture, These events inspired him 10 pursue a medical degree. Tom graduated from Michigan State University College of Human Medicine in 1984. After his residency in family practice at Johnson City Hospital in Johnson City, New York, he seI up an anthroposophical medical practice in Pelerborough, New Hampshire. Dr. . Cowan relocated 10 San Francisco in 2003.
Dr. Cowan has served as vice presidenl of lhe Physicians Associalion for Anthroposophical Medicine and is a lounding board member of lhe Weslon A. Price Foundation. During his career he has studied and written about many subjects in medicine. These include nutrition, horneopathv, anthroposophical medicine, and herbal medicine. He is lhe principal author of lhe book The Fourfold Palh 10 Hea/ing, which was published in 2004 by New Trends . .. Publishing, and is lhe coauthor of The Nourishing Traditions Book of Baby and Cbttd Care, publtshed m 2013. He writes lhe' Ask lhe Doctor" column in Wise Traditions in Food Farming and the Hea/ing Arts, lhe foundation's quarterly magazine, and has lectured throughout lhe US and Carrada. He has three grown children and currently practices medicine in San Francisco, where he resides with his wife, Lynda Smith Cowan. Dr. Cowan sees patients aI his office in San Francisco, does long-distance consults by telephone, and IS acceptmg new patrents, He also gives lectures and presentations,
nervous system is a medicine from the strophanthus plant called ouabain, or g-strophanthin. G-strophanthin is an endogenous hormone made in the adrenal cortex from cholesterol, whose production is inhibited by statin drugs, that does two things that are crucial for heart health and are done by no other medicine. First, it stimulates the production and liberation of ACH, the main neurotransmitter of the parasympathetic nervous system. Second, and crucially, it converts lactic acid - the main metabolic poison in this process - into pyruvate, one of the main and preferred fuels of the myocardial cells. In other words, it converts a "poison" into a nutrient. Perhaps this "magic" is why Chinese medicine practitioners say that the kidneys (i.e., adrenals, where ouabain is made) nourish the heart. In my years of using ouabain in my practice, I have not had a single patient who had an MI while taking it. It is truly the gift to the heart. Finally, this understanding of heart disease leads us to the correct diet, one that is loaded with healthful fats and fat-soluble nutrients, and is low in the processed carbohydrates and sugars that are the hallmark of industrial, civi Iized Iife.
Notes 1. Doerr W et al, Berlin-Heidelberg- ew York: Springer; 1974 2. Baroldi G, Silver M. The Etiopathogenesis of Coronary Hesn. Disease: A Heretica/ Theory Based on Morph%gy. Eurekah.com; 2004. 3. Helfant, RH, Forre51er JS, Hampton JR, Haft JI, Kemp HG, Gorlin R. Coronary heart disease. Differential hemodynamic, metabolic and electrocardiographic effects in subjects with and without angina during atrial pacing. Circu/ation. 1970;42:601-610. 4. Sroka K. On the genesis of myocardial ischemia. Z Csrdiol. 2004;93:768-783. doi:10.1oo7/soo392-0040137-6. S. Takase 8 et al. Heart rate variability in patients with diabetes mellitus, ischemic heart disease and congestive heart fallure J E/ectrocardio/. 1992;25:79-88. 6. Sroka. Op cit. 7. Sroka K et a!. Heart rate variability in myocardial ischemia during daily life. J Electrocardio/. 1997;30:45-56 8. Sroka. Op cit. 9. Sroka. lbid. 10. Sroka. lbid. 1L Sroka. lbid. 12. Sroka. lbid. 13. Sroka. lbid. 14. Scheuer J et aI. Coronary insufficiency: relations between hemodynamic, electrical, and biochemlcal parameters. Circu/ation Res. 1965;17:178-189. 15. Schmidt PG et al, Regional choline acetyltransferase activity in the guinea pig heart. Circuieuon Res. 1978;42:657-660. 16. Katz AM. Effects of ischemia on the cardiac contractile proteins. Cerdiolog». 1972;56:276-283. •

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Qual é mesmo a causa do ataque cardíaco? 
 
por Tom Cowan, médico 
 Tradução: Odi Melo, www.melnex.net 
 
 
Os rins nutrem o coração. 
 (Medicina Tradicional Chinesa) 
 
 
A história sobre como cheguei a entender a causa e, portanto, o tratamento adequado da Síndrome Coronária Aguda (SCA), envolve fascinantes elementos de surpresa e de sorte. A SCA descreve uma constelação de doenças que inclui angina (dor no peito), angina instável (basicamente forte dor no peito) e infarto do miocárdio (IM). Essas 3 doenças formam um conjunto contínuo, sendo a angina o sintoma mais suave e o ataque cardíaco (quando chega a ocorrer morte de células cardíacas) o mais grave. A história do pensamento sobre esse grupo de doenças é fascinante e controvertida. 
 
Parece que os ataques cardíacos eram raros até a década de 1930. A incidência de IMs fatais cresceu rapidamente, de aproximadamente 3.000 por ano naquela década para quase meio milhão na década de 1950. Na verdade, na metade do século essa doença antes rara havia se tornado a principal causa de morte nos EUA. 
 
 
Uma Teoria Controvertida 
 
Como se pode imaginar, quando se tornou claro que estávamos diante de uma epidemia dessa doença, os médicos desenvolveram um grande interesse na sua causa e possível tratamento. Por volta do final da década de 1940, a classe médica propôs uma explicação simples e plausível para o IM, e essa explicação logo tornou-se universalmente aceita. 
 
O atual pensamento sobre ataques cardíacos está centrado no suprimento de sangue às células do miocárdio (coração) através da rede de artérias coronárias, ou seja, das artérias que suprem o próprio coração com sangue. Existem 4 artérias principais, cada uma suprindo sangue a uma região diferente do coração. Os especialistas médicos acreditam que quando uma ou mais dessas artérias fica obstruída por placas (uma doença chamada aterosclerose), o interior da artéria se estreita, o fluxo de sangue fica comprometido e, em situações de stress do miocárdio (como exercícios físicos ou traumas emocionais) esse fluxo insuficiente de sangue causa danos àquela região do coração alimentada pela artéria obstruída. Esse fluxo diminuído de sangue primeiro causa dor (angina), e depois, se for mais grave, causa a morte do tecido cardíaco. 
 
Aqui estava uma teoria elegante e palusível. Voilá! Caso encerrado. A única que ficou faltando descobrir era o que estava causando a obstrução arterial. Essa resposta, que ficou famosa, foi dada pelo Dr. Ancel Keys, na década de 1950. O Dr. Keys apontou o colesterol como culpado, alegando que um excesso de colesterol no sangue forma placas nas artérias. Por mais de 50 anos essa teoria tem sobrevivido sem qualquer alteração significativa. Na verdade, quando alguém tem um ataque cardíaco hoje em dia, geralmente chamamos isso como "coronário", uma referência à suposta fonte do problema – as artéria coronárias. 
 
Essa teoria sobre a causa dos ataques cardíacos está tão arraigada na nossa cultura que, até recentemente, até um médico cético como eu nunca a tinha questionado seriamente. Minha única dúvida quanto à teoria estava relacionada ao material das placas, que mais tarde as pesquisas revelaram ser constituído na maior parte de fragmentos inflamatórios, e não colesterol. Mas eu nunca realmente pensei muito sobre a premissa básica, ou seja, que artérias obstruídas causam ataques cardíacos. 
 
 
 
 
 2
 
Deve ser mencionado que essa teoria sobre a causa dos ataques cardíacos deu origem a uma colossal indústria dedicada ao seu diagnóstico e tratamento. Angiografias, pontes de safena, angioplastias, stents, medicamentos para baixar o colesterol, dietas alimentares de baixo colesterol – tudo isso está 100% baseado na aceitação de artérias obstruídas como sendo "A Causa" das síndromes coronárias agudas. Todo o debate na cardiologia moderna, tanto alternativa como convencional, é sobre como estancar o acúmulo de placas, ou (mais recentemente) como evitar que as placas das artérias se soltem e formem um coágulo, dessa forma obstruindo totalmente alguma artéria já estreitada pelo acúmulo de material. 
 
 
A Conexão Digitalis 
 
Há cerca de uns 2 anos, recebi um e-mail do genro de um cardiologista brasileiro, recentemente falecido e aparentemente renomado, o Dr. Quintiliano H. de Mesquita. Antes de morrer, o Dr. Mesquita tinha publicado um resumo sobre 29 anos de pesquisas realizadas no seu hospital de cardiologia, com dados sobre o que ele chamou de "verdadeira causa e tratamento eficaz de infartos do miocárdio". Seu genro e pesquisador, Carlos Monteiro, me passou por e-mail uma pergunta simples, que era: "Quando o senhor medica seus pacientes de câncer com baixas doses de extrato integral da planta digitalis, isso reduz a incidência de infartos neles?" 
 
Sua pergunta na verdade tinha sido motivada por uma série de artigos sobre a eficácia de baixas doses do extrato integral das folhas de digitalis no tratamento de vários tipos de câncer, que eu havia recentemente publicado no meu site www.fourfoldhealing.com na internet. Respondi sua mensagem perguntando por que ele queria saber isso. Ele então disse que no estudo pioneiro do Dr. Mesquita sobre o que ele chamou de teoria miogênica (ou seja, oriunda do músculo) da doença cardíaca, ele havia casualmente encontrado um resultado inesperado: o digitalis que eles estavam usando para tratar infartos tinha também reduzido radicalmente a incidência de câncer em seus pacientes cardíacos, e o meu site foi o único que eles encontraram que mencionava essa associação. 
 
Como eu nunca tinha ouvido falar da teoria miogênica nem do uso de digitalis para ataques cardíacos, perguntei-lhe o que significava tudo aquilo. Sua resposta foi uma caixa com artigos e livros, todos publicados nos últimos 50 anos e que pareciam refutar a teoria da obstrução coronária nos infartos e respaldar o que ele chamava de a teoria miogênica. Passei os dois meses seguintes debruçado sobre esses estudos até me tornar convencido de que isso talvez fosse a maior novidade médica da década, ou talvez até do século. 
 
 
A Teoria Miogênica 
 
Resumidamente, a teoria miogênica dos infartos diz que: 
 
1. A teoria da obstrução coronária não explica adequadamente todos os fatos observados em relação aos infartos. 
 2. O principal fator etiológico (causa e efeito) num infarto é um processo químico destrutivo. Especificamente, em situações de stress no miocárdio (músculo do coração), muitas vezes como resultado de doença num pequeno vaso, o tecido do miocárdio recebe oxigênio e nutrientes insuficientes. Isso gera uma acidose lática destrutiva no tecido e que, se não tratada, leva à morte das células do miocárdio. Esse processo, de modo geral, não está relacionado a doenças de artérias coronárias. 
 3. O uso regular de cardiotônicos, principalmente baixas doses do extrato integral de digitalis ou o extrato de outra planta, chamado g-estrofantina, evita essa acidose letal, e assim previne e corrige a real causa dessa síndrome. O resultado é uma substancial redução de morbidade e mortalidade nas doenças cardíacas. 
 
 
 
 3
 
 
Vamos dar uma olhada em alguns dos dados que respaldam essas três conclusões. Primeiro, a teoria da obstrução coronária explica adequadamente os fatos observados? É interessante que nos anos 1940 e 1950, quando a teoria da obstrução coronária foi inicialmente proposta, a maioria dos cardiologistas não a aceitaram. Eles observavam que, embora as artérias coronárias não sejam as únicas a ter placas, o único tecido a sofrer pela diminuição do fluxo de sangue nos ataques cardíacos é o do coração. Em outras palavras, ninguém tem ataque de baço ou de rins, e no entanto as artéria que alimentam esses órgãos também apresentam formação de placas. 
 
Além disso, a literatura revela alguns achados surpreendentes. Num artigo de 1998 por Mirakami,1 o autor constatou que, dentre os que tiveram infartos agudos, 49% tiveram obstrução, 30% não tiveram obstrução coronária, 14% tiveram obstrução insuficiente para prejudicar o fluxo de sangue, e 7% tiveram "outra condição clínica". Num artigo de 1972,2 um pesquisador chamado Roberts demonstrou que, em infartos agudos, apenas 50-60% apresentaram evidência de obstrução suficiente para prejudicar o fluxo sangüíneo. E um estudo de 25 anos de autópsias de pacientes que morreram de infartos agudos, realizado por Spain e Braddess, descobriu que somente 25% tiveram obstrução suficiente para justificar seus infartos, enquanto um total de 75% tiveram apenas uma obstrução de leve a moderada.3 
 
Num segundo artigo,4 esses mesmos autores relataram uma descoberta surpreendente: quando um ataque cardíaco é fatal, quanto maior for o tempo decorrido entre o infarto e a morte (e a subseqüente autópsia), maiores eram as possibilidades de eles encontrarem obstruções significativas. Se o óbito ocorria uma hora após começar o ataque, apenas 16% tinham suficiente obstrução para explicar seus infartos. Se a morte ocorria 24 horas após o começo do ataque, o número com suficiente obstrução para justificar o infarto subia para 53 por cento. Os autores concluíram que as obstruções arteriais são uma conseqüência, e não uma causa dos infartos de miocárdio. 
 
À medida que fui examinando o assunto com mais profundidade, descobri que os mais destacados cardiologistas da nossa história eram céticos a respeito da teoria da artéria coronária nos infartos. Por exemplo, em 1972 o Dr. George E. Burch declarou: "O paciente cardíaco não morre por doença coronária, ele morre por doença do miocárdio".5 Um editorial de 1980 na conceituada publicação médica Circulation afirma: "Esses dados respaldam o conceito de que um trombo coronário oclusivo (ou seja, uma obstrução) não tem um papel fundamental na patogênese do infarto do miocárdio".6  Por último, ainda em 1988 o Dr. Epstein, dos National Institutes of Health, declara: "Descobriram que num estágio avançado de estreitamento das artérias coronárias, o suprimento de sangue aos músculos do coração fica totalmente assegurado via colaterais, que aumentam de tamanho naturalmente em resposta à obstrução".7 Na verdade, os pesquisadores descobriram que quanto mais as coronárias se estreitam, menor é o risco de um infarto do coração. 
 
Esses chocantes estudos são perfeitamente compatíveis com um outro estudo, que abalou o mundo da cardiologia, e publicado em 1988 com o título "Vinte anos de cirurgias de revascularização [pontes de safena]".8  Referindo-se a dois importantes estudos, o Veterans Administration (VA) Study e o NIH Coronary Artery Surgery Study (CASS), os autores fizeram a seguinte declaração: "Nem o estudo VA nem o CASS detectaram diferenças significativas em sobrevivências de longo prazo entre os grupos de tratamento médico e cirúrgico, quando a totalidade dos pacientes foi incluída." Em outras palavras, cirurgias para revascularizar artérias obstruídas [pontes de safena] não melhoraram as chances de sobrevivência dos pacientes – o que não é o resultado que seria de ser esperar se as artérias obstruídas fossem a causa dos ataques cardíacos. Portanto, a evidência para a teoria da artéria coronária no infarto não é convincente. Na verdade, ela é até refutada na literatura relevante. 
 
 
 
 
 
 4 A Teoria Corresponde aos Fatos 
 Mas se os ataques cardíacos não resultam de doenças nas artérias coronárias, então o que causa tantos infartos? A teoria miogênica do Dr. Mesquita, na verdade, é condizente com todas as atuais observações sobre esse problema de saúde. A teoria miogênica postula que, devido a doenças nos pequenos vasos (capilares e arteríolas), resultantes de fatores tais como stress, diabetes, fumo e deficiências nutricionais, as células do coração, que são muito ativas metabolicamente, sofrem de suprimento inadequado de oxigênio e nutrientes. Essa deficiência de oxigênio e nutrientes aumenta nas situações de stress. Quando isso acontece, as células do coração revertem para seu sistema de backup, que é a fermentação anaeróbica para geração de energia – muito similar ao que acontece no músculo da perna quando corremos muito. A fermentação anaeróbica produz ácido lático, que se acumula nos tecidos. Como o coração, ao contrário do músculo da perna, não pode descansar, a acidose avança (se não tratada), causando até mesmo a morte das células do miocárdio. 
 
Como conseqüência desse processo necrótico, fragmentos inflamatórios se acumulam nos tecidos, e são esses fragmentos a verdadeira fonte da obstrução coronária encontrada nas mortes por infarto agudo do miocárdio. Como se poderia prever, quanto maior o intervalo de tempo entre infarto e morte, maiores são as chances de obstrução – exatamente como observado nos estudos.  A única conclusão que se pode tirar disso é que as células do coração morrem primeiro, e só então a artéria se torna obstruída com os fragmentos liberados por ocasião da morte das células no miocárdio, que são exatamente os tipos de fragmentos encontrados nessas artérias obstruídas. 
 
A atual prática de limpeza das obstruções de artérias pode ajudar a remover os fragmentos e restaurar o fluxo de sangue no sistema arterial comprometido, porém isso de forma alguma sugere que as artérias obstruídas representem o evento primário na seqüência que leva ao infarto. De qualquer modo, toda a ênfase dada às obstruções das artérias coronárias é basicamente um beco sem saída e condenado ao fracasso, seja sob o ponto de vista cirúrgico (pontes de safena, stents, etc) ou médico (drogas para baixar colesterol, restrições na dieta alimentar, etc). 
 
 
Terapia Miogênica 
 A teoria miogênica nos direciona a um tipo bem diferente de tratamento preventivo das doenças cardíacas, um tipo centrado nas doenças dos pequenos vasos e na prevenção da acidose nos tecidos do coração. A teoria explica também por que o diabetes, o stress e o fumo são fatores de risco tão importantes nos infartos, pois todos esses fatores têm demonstrado afetar principalmente os capilares e os pequenos vasos sangüíneos, e não as grandes artérias coronárias. 
 Mas a história fica ainda mais interessante. Acontece que existem diversos compostos simples, baratos e muito eficazes para prevenção da acidose lática no tecido cardíaco. Esses medicamentos são conhecidos há séculos como cardiotônicos, e vêm sendo utilizados para tratar doenças cardíacas em todos os sistemas médicos tradicionais do mundo. Os dois mais conhecidos são o digitalis (a popular dedaleira) e o estrofanto, uma trepadeira africana. Essas plantas são as fontes dos chamados glucosídeos cardíacos: digoxina e digitoxina, da digitalis, e ouabaína, do estrofanto. 
 A função desses compostos é regular o ritmo e a força da contração cardíaca, e prevenir ou reverter o acúmulo de ácido lático no tecido cardíaco. É por isso que essas plantas têm sido usadas há séculos para tratar insuficiência cardíaca congestiva, distúrbios rítmicos e outros transtornos da função cardíaca. 
 O detalhe interessante é que esses compostos são cópias químicas exatas dos hormônios produzidos pelas glândulas supra-renais. E as supra-renais fabricam esses cardiotônicos a parir do... colesterol! Agora sabemos por que todas essas medidas draconianas na área da dieta alimentar e na área farmacêutica para baixar os níveis de colesterol não têm resultado em decréscimo no índice de infartos, e também por que um grande número de estudos têm demonstrado que, à medida que envelhecemos, aqueles que têm níveis de colesterol mais elevado vivem por mais tempo. Quando baixamos nosso colesterol, estamos sonegando ao nosso organismo justamente a substância que ele precisa para produzir cardiotônicos. 
 
 5
 
A teoria miogênica também explica por que o stress pode causar ataques cardíacos. Em situações de stress, nossas supra-renais precisam trabalhar muito para produzir um grande número de hormônios que regulam o açúcar do sangue e ajudam a reparar o organismo. Se as supra-renais estiverem fracas ou sobrecarregadas, a produção de cardiotônicos é adiada. 
 
Embora existam alguns estudos na literatura convencional que tenham considerado a eficácia da digitalis ou do estrofanto no tratamento do infarto, os resultados clínicos do Dr. Mesquita, ao longo de 29 anos, demonstram uma drástica redução no número de mortes, número de infartos recorrentes, número de anginas e de todos os sintomas no espectro da síndrome coronária aguda, pelo uso oral de glicosídeos da digitalis em baixas dosagens. Esses resultados estão publicados na obra Teoria Miogênica do Enfarte Miocárdico, disponível no site do projeto Infarct Combat, www.infarctcombat.org (e também em sites brasileiros – N. do T.). 
 
Igualmente, o cardiologista alemão Berthold Kern usou a g-estrofantina num estudo para o governo alemão, que demonstrou uma drástica redução de infartos na sua clínica, caindo dos 400 esperados para apenas 20, com o uso desse medicamento.9 Ademais, muitos relatos têm vindo da Alemanha, nos quais os médicos notaram uma redução de até 81 por cento nos ataques de angina, com uso oral de g-estrofantina.10  
 
Na minha clínica, geralmente uso a estrofantina oral, na forma dum preparado chamado Strodival, para todos os meus pacientes de angina e de infartos, e tenho invariavelmente registrado um decréscimo nos episódios de angina, melhora na tolerância a exercícios e, até agora, nenhum infarto. Quando combinada com uma dieta alimentar tradicional nutritiva, óleo de fígado de bacalhau, manteiga clarificada [ghee] rica em vitaminas, CoQ10 (que ajuda a fortalecer o músculo cardíaco) e os nutrientes cardíacos do Regime Padrão (Cardioplus - duas cápsulas 3 vezes ao dia, e Cataplex E2 – dois tabletes 3 vezes ao dia), tenho visto uma enorme melhora na vida dos pacientes portadores dessas terríveis doenças. (Obs.: A folha de digitalis e o Strodival são vendidos apenas sob prescrição médica, e devem ser receitados por médico bem versado no seu uso). 
 
A derradeira ironia é que os médicos tradicionais chineses estavam certos. Os rins (a forma com que eles se referem às glândulas supra-renais) ajudam o organismo a lidar com o stress e a fabricar os hormônios (digoxina e ouabaína) que mantêm saudáveis o nosso maravilhoso coração, forte e pronto para desfrutar toda a plenitude da vida. 
 
 
 
 
 
 
↓ 
 
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Como proteger seus capilares 
 
• Evite um alto índice de açúcar no sangue: O diabetes é um sério fator de risco na deterioração dos capilares. Sua melhor defesa contra o diabetes é uma dieta alimentar rica em gorduras e com poucos carboidratos. Se você tem diabetes, siga o protocolo publicado no site: http://www.westonaprice.org/moderndiseases/diabetes.html  • Não fume! O fumo é um fator de risco na deterioração dos capilares.  • Faça exercícios moderados ao ar livre.  • Evite os óleos vegetais comerciais líquidos, que estão repletos de radicais livres e podem danificar os capilares.  • Siga uma dieta alimentar tradicional e rica em nutrientes. 
 6
 
 
 
 
 
 
 
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↓ 
 
 
 
 
 
 
 
 
 
Por que a placa é um problema 
 
Embora a placa da artéria que leva a uma obstrução possa não ser a principal causa da doença cardíaca, não há dúvida de que o fenônemo da aterosclerose (formação de placas) é realmente um problema para o ser humano, especialmente à medida que envelhecemos. Algumas partes das nossas artérias estão sujeitas a espessamentos e à formação das chamadas estrias gordurosas, por razões ligadas à dinâmica do fluxo, ou seja, a velocidade e turbulência do fluxo de sangue naquela artéria específica. Uma certa quantidade de espessamento, em locais onde o sangue faz muita pressão na artéria, é considerada normal e protetora, e portanto ocorre em todas as pessoas. 
 Mas a formação de placas já é outra situação e pode levar a muitos problemas. Por exemplo, artérias obstruías nas pernas podem causar cãimbras e dor, o que é chamado de claudicação intermitente (dor na perna ao caminhar). No cérebro, a formação de placas leva ao derrame isquêmico (ausência de fluxo sangüíneo). Nos rins, a redução do fluxo de sangue devido à formação de placas é um possível fator contribuinte em alguns casos de hipertensão (pressão alta). Da mesma forma, artérias obstruídas que chegam ao fígado ou ao baço podem resultar na restrição de funções nesses órgãos. 
 As razões da formação dessas placas não são bem claras. Embora os cientistas há tempos culpem os níveis de colesterol no sangue pela formação dessas placas, pesquisadores médicos bem informados atualmente costumam citar a inflamação nos vasos como sendo a causa. Naturalmente, essa inflamação é secundária a outros fatores, como stress, consumo de óleos vegetais processados e deficiências nutricionais (particularmente de vitaminas A e C, e de minerais, como o cobre). 
 Porém a formação de placas não é uma explicação para todo o fenômeno da isquemia do miocárdio. A razão de "ataques" ocorrerem no coração, mas não no baço ou no fígado, é que o uso de energia no coração é muito mais elevado, e também por que o coração nunca pode descansar. Por terem os cientistas descuidado desses fatores, o atual tratamento das doenças cardíacas é muito menos eficaz do que poderia ser. 
 O único outro órgão que se pode dizer que está sujeito a sofrer um "ataque" é o cérebro, quando há um derrame. No entanto, os derrames geralmente acontecem quando um coágulo se forma numa das artérias que aliementam o cérebro.  O processo não é o mesmo do acúmulo de ácido lático no coração. 
 7
 
 
 
 
Referências 
 
1. American Journal of Cardiology; 1998; 82:839-44. 2. Circulation, 1972; 49:1. 3. American Journal of Medical Science, 1960; 240:701. 4. Circulation, 1960, 22:816. 5. American Heart Journal, 1972 Março; 83(3):340-50. 6. Circulation, 1980 Julho; 62(1):17-19. 7. Epstein, SE. American Journal of Cardiology; 1988 Abril 1; 61(10):866-8. 8. Killip, T. New England Journal of Medicine; 1988 Agosto 11; 319(6):366-8. 9. Comunicação não publicada. 10.  Comunicação não publicada. 
 
___________________________________________________________________________________________________________________________________________________________________ 
 
Fonte 
 Wise Traditions The Weston A. Price Foundation, EUA. Volume 8, Número 3 - Fall 2007 Páginas 14 a 19 

 

 

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