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Redefining Heart Disease

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Redefining Heart Disease

Posted by RG [5135.3312] on March 05, 2007 at 17:17:30:

would venture that there are not five western trained physicians on the planet who are not completely convinced that the cause of heart attacks are the blockages in the coronary arteries. In fact, a common synonym for a heart attack is to say the patient has had a coronary, meaning he has an illness of his coronary arteries. The whole edifice of cardiology, whether conventional or alternative, is based on strategies for detecting, stopping, clearing, or bypassing blockages in the coronary arteries. Some say the blockages are from cholesterol, others say it is homocsyteine, still others say it is inflammation that causes the blockages, even perhaps in the form of an undetected infection. When therapeutic strategies based on these fail, the next step is to bypass the blockages with an operation called a coronary artery bypass graft (or CABG for those into sauerkraut), or roto-rooter them out with the whole array of modern devices available to the modern cardiologists. The presumption of all this is the “fact” that it is the coronary arteries that are the root of the trouble. I, and others, beg to differ.

In a 1998 editorial in The American Journal of Cardiology (1998 Oct 1; 82(7): 896-897), Dr. W.W. O’Neill commented about a paradox in recent findings. In a number of trials of myocardial infarctions (hereafter referred to as MIs, more commonly known as heart attacks), many of the patients who suffered recent MIs were not found to have blockages in the arteries that led to the area of the heart that had suffered the infarction. This should have been big news, for what this cardiologist was saying was that when we look carefully at the angiograms (the test where we squirt dye into the arteries in the heart to see if they are blocked) of people who are having or who have recently had an MI, in some we find the artery is blocked and in others we don’t. This is actually a shocking statement, but to realize how shocking and controversial it really is we need to look at some history here.

Back in the late 1930s and early 1940s, heart attacks were first becoming prominent in American society, due largely to the rapid change in the American diet. Doctors wondered what was causing this relatively new phenomenon. Many theories were proposed, but the one that stuck was called the Thrombogenic Theory of Myocardial Infarction. Essentially this theory postulated that heart tissue, like any other tissue in the body, has a blood supply. When this blood supply is compromised by, say, plaque buildup in that blood vessel, then the cells “downriver” from the blockage will have their blood supply choked off, and under certain situations those cells will be deprived of their necessary food and oxygen and eventually will die. When they are dying because of inadequate flow, there is a painful feeling around the heart which we call Angina. When the cells actually die, we can that an Infarction. This is often a catastrophic event and many patients die as a result of the dysfunction of the heart itself as a consequence of their MI, or heart attack.

Many cardiologists and other doctors disagreed early on with this theory. They asked why it is only the heart that infarcts in this way. After all, this plaque development is in no way specific to the coronary (heart) arteries. Why do we not hear of liver attacks, foot attacks, and so on? Another criticism of the theory revolved around the well known phenomenon of collateral circulation: In many parts of the body, when an artery is blocked, the body “bypasses” the blocked vessel and makes a secondary (so-called collateral) circulation. Why not in the heart as well? These were the two main reasons many physicians didn’t buy the blocked coronary artery theory.

Since the thrombogenic theory was accepted in the early 40s as bottom line fact-of-the-matter, there have been a number of studies that have attempted to document that all people having MIs have blocked arteries to that area of the heart. But these studies have all failed miserably to show this connection. In a paper by Murakami in 1998 (Am J Cardiology, 1998;82 :839-44), the author found that, of those with an acute MI, 49% have a recent thrombus (blockage), 30% have no thrombus, 14% had moderate plaque (not considered enough to cause an MI), and 7% had “another condition”. Roberts, in an earlier paper (Circulation, 1972; 49:1), showed that in cases of acute MI with sudden death, 50-60% had evidence of sufficient thrombus to account for the MI. Spain and Bradess’s 25-year autopsy study of patients who died of heart attacks found 25% had sufficient thrombus to account for their MI and 75% had atherosclerosis (arterial blockages of some degree) (Am J Med Sci, 1960; 240:701). And finally and perhaps most importantly, these same authors in another paper (Circulation 1960, 22: 816) found that the longer the time elapsed between the MI and the autopsy, the more likely they were to find blockages. After one hour only 16% had sufficient blockage to account for the MI, whereas after 24 hours the total increased to 53%. The authors concluded that the arterial blockage is the CONSEQUENCE, not the cause, of the heart attack. This is why in every study I have seen, the longer the time interval between the MI and either the angiogram or autopsy, the more likely you are to see the blockage. How can we account for the results of these studies? Even if the number is 75%, the highest in the literature, what happened to the other 25%? Why did they also have an MI if their arteries weren’t blocked?

Because of my interest in the heart, I have been studying this seeming paradox for a long time. The usual explanations for this inconsistency between the theory and the facts is that some people have a spasm of their coronary arteries which, in the absence of the plaque, is enough to kill them in some cases. The trouble with this theory is that as far as I know no one has ever seen this occur, and it seems a bit implausible that a completely healthy artery somehow goes into a spasm, and next thing you know, the person dies. The more I thought about it, I felt something was wrong with this whole story.

Very recently, through a serendipitous internet encounter, I ran across a different theory which may explain the whole series of facts surrounding the cause and thus the treatment of MI/angina. The myogenic theory proposed by the Brazilian cardiologist Dr. Mesquita states that, rather than coronary artery disease causing MIs, the blockages are actually the consequence of the MI. According to Mesquita’s theory, the heart, because it is such an active organ and has such a high oxygen demand (like the brain, the other site of “infarctions” which we call strokes), is always a bit tenuous in its ability to extract enough oxygen from the blood. Exercise or other physical or mental activity increases the need for the heart cells to extract even more oxygen. As a result of stress, particularly chronic stress, the small blood vessels in the heart become constricted, which then compromises what we call the micro-circulation in and around the heart cells. This leads to decreased oxygen supply, especially with physical exertion, then anaerobic metabolism (meaning without air), then acidosis as the lactic acid builds up through this metabolism with an oxygen deficit and eventual death of the cells. After the cells die, an inflammatory reaction occurs which eventually compromises the artery leading to that artery, filling it with inflammatory debris that we see on autopsy and angiograms.

Let me try to explain this in another way. Under stress, especially chronic stress, the body over-excretes adrenaline and other stress hormones. These hormones cause the small blood vessels all over the body to constrict, which is why doctors and dentists, when they don’t want a tissue to bleed while they are suturing, inject Adrenaline in the area. Constricted blood vessels – and these are the small vessels, capillaries, not the coronary arteries – choke off the blood flow and hinder the removal of the wastes, predominantly acidic waste products. If this continues for many years and is exacerbated by increased demand like exercise, then the heart cells can die or become infarcted. It has nothing to do with plaque or blockages in the bigger arteries as these the body can easily bypass as they build up very slowly through the years. This explanation fits all of the known facts about the timing and development as well as the epidemiology of MIs, particularly in relationship to the crucial role that chronic stress plays on the development of MIs. I would also add that it is perfectly compatible with my claim that the heart is not the “pump” of the body.

This decades-long study by Dr. Mesquita is a truly remarkable contribution to our understanding of cardiology and the etiology of heart disease. Because of this, I have included in this issue a report by Carlos Monteiro on Dr. Mesquita’s studies (see below).

If this Myogenic theory is correct, then the billions of dollars spent on clearing out arterial blockages is essentially an exercise in futility, which is pretty much what the studies on longevity have shown. I am not saying that after an acute MI it is not important to “flush out” the artery. After the event, this flushing can be helpful, although probably not needed. What I am saying is that this clearing of arterial blockages does nothing to address the true cause of this illness.

The next step is to ask the question: Is there any way to affect the heart cells so that they are able to extract oxygen more efficiently and therefore be less susceptible to the acidosis that is the underlying basis of the MI? One thing, of course, is to avoid stress, but there is another perhaps more straightforward possibility. It has been known for centuries that there are a few plant medicines that clearly increase the efficiency of the heart cells. The medicines in these plants are called cardiac inotropes because they increase the ability of the heart to “pump” blood by increasing the efficiency of the cells and improving the overall contractibility and elasticity of the heart. The two main plants that do this are Strophanthus, an African vine, and Digitalis, common foxglove. I discuss these two in the next piece in this edition.

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Digitalis and Strophanthus

Digitalis is probably the oldest heart medicine, in fact one of the oldest medicines of any type, still in common use. Commonly known as the beautiful plant Foxglove, one still finds digitalis growing in most herbal and flower gardens in the western hemisphere. It is a striking plant, growing very tall and straight with amazing speckled bells coming off a central stalk. The mythos surrounding digitalis is that it makes the heart glad and is an especially good friend of the old man. Traditionally, it has been used for the condition known as dropsy in which, appropriately enough, the circulation slows down and can’t go uphill through the veins anymore. Eventually gravity takes over and the blood and fluid fall to the feet and into the lungs. The feet become swollen and lifeless, and the choking fluid builds up in the lungs. In modern times, we call this condition congestive heart failure.

Digitalis is a positive inotropic agent, which means it makes the heart “pumping” action more effective. In terms of how I see the heart, rather than increasing the pumping action of the heart, I would say it increases the flow of the circulation and improves the elasticity of the cardiac chambers. When the heart chambers are more elastic, they can hold back the blood more efficiently. Therefore when the gates open the forward flow is more effective. Almost miraculously, when patients with dropsy are given digitalis, within days they can breathe again, the fluid circulates, the swelling goes out of the feet and in many cases even erections, so dependent as they are on blood flow, will return. Truly the friend of the old man.

On a cellular level, science has shown that digitalis works its magic on the cell membrane, increasing the activity of the sodium/potassium pump, thereby keeping the electrical charge on the cells intact. This is important from the myogenic theory point of view, as it is the activity of the sodium/potassium pump that prevents acidosis from occuring. Acidosis is the central pathological mechanism behind myocardial infarction. Even better, digitalis has this effect not only for the heart cells but for every cell of the body. Many famous alternative oncologists, such as Max Gerson, MD, view this sodium/potassium imbalance and subsequent acidosis as the central mechanism in the development of cancer. (For more information on digitalis use in the treatment of cancer, visit the Digitalis page on our website.)

In a number of studies over the years, a surprising finding keeps showing up which has only recently become explainable. In autopsies and other studies of patients who died of or had an MI, trace amounts of digitalis compounds (digoxin and digitoxin) have been found in the blood, even in patients who had never taken the drug. As with opium and endorphins, the two main ingredients in digitalis are mimics of the endogenous (meaning normally within the body) hormones that regulate the contractions and rhythms of the heart. In other words, digitalis in some ways is an externalized replica of the way the heart communicates with itself. It is the plant form of the communication of the heart.

It should be no surprise then that studies of the use of digitalis for angina and myocardial infarction show digitalis’s remarkable ability to prevent or reverse the symptoms of myocardial disease, even in acute situations.

I first encountered Strophanthus about 25 years ago from my primary teacher in medicine, a German physician by the name of Otto Wolff, MD. He was passionate about Strophanthus, even having gone so far as to make a few treks into the African jungles to observe the habits of this tremendous creeping vine firsthand. He observed the indigenous native tribesmen who dipped their arrows into a slurry made of an extract of the seeds of Strophanthus, which they used to temporarily paralyze their prey. The Strophanthus seeds were found to contain an oily substance with a chemical called oubain, which was found to be a potent cardiac inotrope, even stronger that digitalis.

Initial enthusiasm for strophanthus as a medicine was tempered when it was claimed that the oubain could not be absorbed into the body through the oral route. As time went on, much to Dr. Wolff’s disappointment, it was nearly abandoned as a medicine. Then a few studies were done in association with the one remaining manufacturer of oubain, the medicine now being called Strodival. One study of patients with angina showed 81% of patients had complete remission of their anginal (chest pain) symptoms, as compared to 72% of the control group who did not take Strodival and whose angina worsened (World Research Foundation report). A second study showed that after MI, the use of Strodival decreased the evidence of progression of the MI – often within minutes – in 85% of the subjects, a remarkable result. It was found that, as with digitalis, the heart uses oubain in its endogenous communication system. It is as if digitalis and strophanthus contain exact copies of the hormones that the heart uses to regulate its own beat and elasticity.

Luckily for us, the fears of my dear teacher Otto Wolff may not come to pass. A number of cardiac clinics and hospitals in Europe have rediscovered the cardiac tonic effect of strophanthus as well as its swift onset of action. It is said that a sublingual dose of Strodival will often stop angina within minutes and can also have a positive effect on developing MIs again within a very brief period of time.

I would encourage all my patients with an interest in digitalis and strophanthus in the treatment of angina/MI to read carefully the following article, visit the website, and then get in touch with me to discuss this further.

Re: Redefining Heart Disease Archive in coronary.

Posted by Walt Stoll [93.1889] on March 06, 2007 at 07:23:05:

In Reply to: Redefining Heart Disease posted by RG [5135.3312] on March 05, 2007 at 17:17:30:

Thanks, RG!

It needed to be said.


Re: Redefining Heart Disease

Posted by Steve [3019.3308] on March 06, 2007 at 08:34:30:

In Reply to: Redefining Heart Disease posted by RG [5135.3312] on March 05, 2007 at 17:17:30:


There are a few MD's that are up to speed on what causes Heart Disease and what we can do to prevent it. It is still the number one killer, but doesn't get the press like cancer does. Dr's Sinatra and Sherry Rogers are two that have written extensively about preventing heart disease. Thanks for posting that.

Silver Fox!

Follow Ups:

Re: Redefining Heart Disease Archive in coronary.

Posted by R. [1213.3312] on March 06, 2007 at 21:46:58:

In Reply to: Re: Redefining Heart Disease Archive in coronary. posted by Walt Stoll [93.1889] on March 06, 2007 at 07:23:05:

If you agreed with the article, does this mean you no longer subscribe to the "dietary cholesterol is evil" theory?

Re: Redefining Heart Disease Archive in coronary.

Posted by Walt Stoll [93.1889] on March 07, 2007 at 08:31:11:

In Reply to: Re: Redefining Heart Disease Archive in coronary. posted by R. [1213.3312] on March 06, 2007 at 21:46:58:

Thanks, R.

I never have felt that cholesterol was more than a minor contributor to atherosclerotic vascular disease!

In my opinion it takes high cholesterol associated with a genetic propensity for this anomaly to actually contribute to the problem for it to be significant.

Hope this helps.


Re: Redefining Heart Disease Archive in coronary.

Posted by R. [1213.3312] on March 07, 2007 at 10:21:10:

In Reply to: Re: Redefining Heart Disease Archive in coronary. posted by Walt Stoll [93.1889] on March 07, 2007 at 08:31:11:

The reason I asked is that when I posted, a long time ago, about current dietary recommendations of Ann Louise Gittleman, former Pritikin's dietitian (if I remember correctly), you were quick to state that heart disease rates would increase (or something along these lines) if people followed her advice. (She no longer supports low fat diets, having witnessed harm low fat or no fat diet produced in Pritikin's experements.)

By the way, research of Dr. Ravnskov shows that people with familial hypercholesteremia probably derive benefits from this condition. For example, "As discussed in The Cholesterol Myths (see sidebar), much evidence supports the theory that people born with very high cholesterol, so-called familial hypercholesterolemia, are protected against infection. But if inborn high cholesterol protects against infections, inborn low cholesterol should have the opposite effect. Indeed, this seems to be true.

Children with the Smith-Lemli-Opitz syndrome have very low cholesterol because the enzyme that is necessary for the last step in the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the central nervous system. Those who survive are imbecile, they have extremely low cholesterol and suffer from frequent and severe infections. However, if their diet is supplemented with pure cholesterol or extra eggs, their cholesterol goes up and their bouts of infection become less serious and less frequent." []

And from Familial Hypercholesterolemia -
Not as Risky as You May Think
(bottom part of the page):
" Many doctors believe that most patients with familial hypercholesterolemia (FH) die from CHD at a young age. Obviously, they do not know the surprising finding of the Scientific Steering Committee at the Department of Public Health and Primary Care at Radcliffe Infirmary in Oxford, England. For several years, these researchers followed more than 500 FH patients between the ages of 20 and 74 and compared patient mortality during this period with that of the general population.

During a three- to four-year period, six of 214 FH patients below age 40 died from CHD. This may not seem particularly frightening but as it is rare to die from CHD before the age of 40, the risk for these FH patients was almost 100 times that of the general population.

During a four- to five-year period, eight of 237 FH patients between ages 40 and 59 died, which was five times more than the general population. But during a similar period of time, only one of 75 FH patients between the ages of 60 and 74 died from CHD, when the expected number was two.

If these results are typical for FH, you could say that between ages 20 and 59, about 3 percent of the patients die from CHD, and between ages 60 and 74, less than 2 percent die, in both cases during a period of 3-4 years. The authors stressed that the patients had been referred because of a personal or family history of premature vascular disease and therefore were at a particularly high risk for CHD. Most patients with FH in the general population are unrecognized and untreated. Had the patients studied been representative for all FH patients, their prognosis would probably have been even better.

This view was recently confirmed by Dr. Eric Sijbrands and his coworkers from various medical departments in Amsterdam and Leiden, Netherlands. Out of a large group they found three individuals with very high cholesterol. A genetic analysis confirmed the diagnosis of FH and by tracing their family members backward in time, they came up with a total of 412 individuals. The coronary and total mortality of these members were compared with the mortality of the general Dutch population.

The striking finding was that those who lived during the 19th and early 20th century had normal mortality and lived a normal life span. In fact, those living in the 19th century had a lower mortality than the general population. After 1915 the mortality rose to a maximum between 1935 and 1964, but even at the peak, mortality was less than twice as high as in the general population.

Again, very high cholesterol levels alone do not lead to a heart attack. In fact, high cholesterol may even be protective against other diseases. This was the conclusion of Dr. Sijbrands and his colleagues. As support they cited the fact that genetically modified mice with high cholesterol are protected against severe bacterial infections.

"Doctor, don’t be afraid because of my high cholesterol." These were the words of a 36-year-old lawyer who visited me for the first time for a health examination. And indeed, his cholesterol was high, over 400 mg/dl.

"My father’s cholesterol was even higher," he added. "But he lived happily until he died at age 79 from cancer. And his brother, who also had FH, died at age 83. None of them ever complained of any heart problems." My "patient" is now 53, his brother is 56 and his cousin 61. All of them have extremely high cholesterol values, but none of them has any heart troubles, and none of them has ever taken cholesterol-lowering drugs.

So, if you happen to have FH, don’t be too anxious. Your chances of surviving are pretty good, even surviving to old age.

Scientific Steering Committee on behalf of the Simon Broome Register Group. Risk of fatal coronary heart disease in familial hypercholesterolaemia. British Medical Journal 303, 893-896, 1991; Sijbrands EJG and others. Mortality over two centuries in large pedigree with familial hypercholesterolaemia: family tree mortality study. British Medical Journal 322, 1019-1023, 2001.

From The Cholesterol Myths by Uffe Ravnvskov, MD, PhD, NewTrends Publishing, pp 64-65."

Re: Redefining Heart Disease

Posted by
Brian [5122.1351] on March 07, 2007 at 11:41:13:

In Reply to: Redefining Heart Disease posted by RG [5135.3312] on March 05, 2007 at 17:17:30:


How do we get in touch with you? Feel free to contact me. Thanks.


Follow Ups:

Re: Redefining Heart Disease Archive in coronary.

Posted by Walt Stoll [93.1889] on March 08, 2007 at 07:05:15:

In Reply to: Re: Redefining Heart Disease Archive in coronary. posted by R. [1213.3312] on March 07, 2007 at 10:21:10:

Thanks, R.

Good information about the genetic influence on all of this. We still have a lot to learn from all this.


Follow Ups:

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