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heart and artery diseases

To do justice to this topic, I first discussed arteriosclerosis and coronary artery disease, which arises from arteriosclerosis of the coronary arteries. Below are topics related to non-vascular heart disease. When it comes to arteriosclerosis, the pharmaceutical companies' prejudices and marketing strategies need to be scrutinized.  If you describe a therapy that has been introduced worldwide as a lie, you run the risk of being cornered by crackpots and conspiracy theorists becomes. In the meantime, however, it has been proven that a cholesterol lie was dished out as a result of a bribe in favor of the margarine industry, which demonized the consumption of animal fats and praised margarine as the only sensible alternative to butter.

Other non-atherosclerotic heart diseases

Arteriosclerosis (also atherosclerosis)


Atherosclerosis means that deposits appear in the inner layer (intima) of the arteries. As shown in the figure, these can reach a considerable extent. These deposits do not always consist only of cholesterol and other fats. If more calcium flows into the vessel wall, calcifications also occur, which are easily visible in ultrasound or cardio-CT. Bit by bit I would like to present a few facts that will give you a better overview of the real risk factors. But first, back to cholesterol:



The widespread opinion among doctors, even cardiologists, is that cholesterol is harmful and promotes arteriosclerosis. Doctors still differentiate between the so-called HDL and LDL cholesterol, i.e. the apparently good and bad cholesterol. But things are not as simple as they seem. In fact, I've also observed that a low LDL-HDL ratio (preferably below 3.0) seems to be a good protective factor. But a higher ratio is not necessarily associated with a higher risk of atherosclerosis. This is because it has been proven that LDL is not evil per se. Because evolution did not set it up in such a way that LDL cholesterol is produced in the body at great expense in order to store it in the vascular walls, but it has been proven that only the oxidized LDL, i.e. the burned LDL cholesterol, leads to deposits in the arterial walls. The oxidized LDL  is caused by environmental toxins and free radicals. The weakening of the mitochondria also leads to an increase in free radicals. Some people will think that you can easily get a grip on cholesterol-lowering drugs, the so-called statins. However, my own research has found that stopping statins can often reduce harmful oxidized LDL. So stopping the cholesterol-lowering medication improved the situation. The improvement in the LDL-HDL ratio after the administration of statins is therefore very often only a matter of laboratory cosmetics. Pharmaceutical companies repeatedly claim that statins also have an anti-inflammatory effect. This would ensure that the plaques (deposits in the vessel walls) would not be injured and thus the formation of clots, which lead to heart attacks or strokes, would be suppressed. However, the effect is only very slight and can be achieved with other natural remedies without side effects. Studies by pharmaceutical companies are often presented in a very impressive way. The good effect of statins on mortality is also repeatedly praised here. Large studies have shown that in patients who already have coronary artery disease, mortality can be reduced by 0.6% per year. i.e. but also that 1000 patients have to take the preparations with many side effects in order to save in the year six. This can also be easily achieved with other measures. For many, including me, it seemed obvious that statins should be prescribed before coronary artery disease develops, since then one can have an early and long-lasting influence on cholesterol. However, a related study was also disappointing. Mortality in treated and untreated participants was the same. This means that there is no advantage in starting treatment early.

The use of statins is particularly problematic in those over 60 years of age. Because the publication of a study from 2016 showed that the use of cholesterol-lowering drugs in over 60-year-olds had no positive effect. The statins prescribed to about 15 million Americans are completely useless. There was no association between  LDL levels and deaths from heart disease. 92% of the patients with high cholesterol even lived longer than the patients with lowered cholesterol levels. Some scientists concluded that it is not the statins but a healthy lifestyle that is important for keeping the heart healthy. This thesis was also supported by Professor Sherif Sultan, expert in vascular and endovascular surgery at the University of Ireland. When I was a student at a meeting of the cardiologists at the University Hospital in Frankfurt, it was about the newly developed statins that were just coming onto the market. One cardiologist cautioned that lowering cholesterol is not necessarily associated with less atherosclerosis. To which his colleague replied: "You can well imagine, if the daily dose for a newly developed drug is 1.50 DM, that the producing pharmaceutical companies will find a way in view of the large number of patients with elevated cholesterol, the drug_cc781905- 5cde-3194-bb3b-136bad5cf58d_ into the market." At that time I still believed in the only good thing in medicine and that everyone involved in the healthcare system would try to heal. Today I have to say that the cardiological colleague understood the situation correctly assessed with wise foresight.

It's amazing how little cardiologists know about the medications they prescribe. At a lecture by a cardiologist about statins, I pointed out that by reducing the production of cholesterol in the cell, the formation of the coenzyme Q 10, which is important for us, would be reduced at the same time. The cardiologist knew nothing about this. The Canadian and Japanese package inserts for the preparations state that if statins are prescribed, coenzyme Q10 must also be prescribed. Coenzyme Q 10 is one of the most important catalysts in the mitochondria for energy production. Every cell needs it to function properly. Among other things, the deficiency can lead to cardiac insufficiency. This may be one reason why those over 60 lived shorter lives after lowering their cholesterol levels.

A few years ago, another property of LDL cholesterol came into focus. LDL cholesterol is not a single substance, but consists of different LDL subunits. In general, the small, dense LDL subclasses have proven to be dangerous for the arteries. Laboratories can now break down the subclasses and thus make a better statement about the vascular risk. To what extent this risk factor is related to oxidized LDL is not described in the literature. However, it is obvious to me that even the small, dense LDL subtypes only become dangerous through oxidation. Thus, an exclusive determination of the LDL subclasses is not very meaningful for me. In any case, the oxidized LDL should also be determined.

Those who can manage to change their lifestyle have clear advantages:

A 2016 study showed that patients with coronary artery disease also benefit from a better lifestyle. When they quit smoking, changed to a low-meat and low-fat diet, and exercised regularly, the narrowing of the coronary arteries decreased by 4.5% in one year and by as much as 7.9% after five years. In the control group without significant lifestyle changes, the narrowing of the coronary vessels had increased by 27.7% in five years.

During my residency in a cardiology rehabilitation clinic in the 90s, we prescribed a lot of low-cholesterol diets. We checked the laboratory data at approx. 3-week intervals. Total cholesterol dropped almost regularly. The LDL/HDL ratio also deteriorated regularly. I was already questioning the benefits of the diet. The oxidized LDL was not determined at that time. Only a few years ago, the low-cholesterol diet was removed from the guidelines due to its ineffectiveness. For about 50 years, the population worldwide was treated to a senseless low-cholesterol diet because the margarine industry was "smearing"!

In my experience, it is crucial to also consider the other risk factors. Many risk factors are not considered by general practitioners, internists and cardiologists. This may be due to the fact that no expensive patented drugs have been developed to treat these risk factors. That is why the pharmaceutical companies do not sponsor any training courses on these topics. The majority of doctors only attend training courses sponsored by pharmaceutical companies, for which the doctors also receive the necessary training points.


Risk factors that are neglected include:


Inherited, this is a breakdown of the amino acid methionine. This produces homocysteine as a toxic intermediate product that accumulates in higher concentrations if further degradation is disrupted. It is not only considered a risk factor for atherosclerosis, but also for depression, dementia and macular degeneration. The damaging influence on the macula (place of sharpest vision) is controversial. However, positive effects on the macula have already been observed when homocysteine levels are reduced. Homocysteine can be reduced by administering vitamins B6, B12 and folic acid.

Lipoprotein A

Lipoprotein A is a  transport protein that ensures the transport of fats in the blood. Elevated levels, which promote arteriosclerosis, can be genetically determined. From experience I can say that I sometimes only found the increased lipoprotein A as a risk factor in patients suffering from arteriosclerosis. An increase in lipoprotein A is not always genetic, but can also be promoted by kidney disease, diabetes mellitus and hypothyroidism. Various vitamins, including vitamin B3, can lower lipoprotein A levels.

ADMA (Asymmetric dimethylarginine)

ADMA is a derivative of the amino acid L-arginine and also promotes arteriosclerosis. It is often elevated in kidney disease, diabetes mellitus, and elevated cholesterol levels. ADMA interferes with the synthesis of nitric oxide and can thereby produce the nitrosative and oxidative stress that promote arteriosclerosis. The risk factor can be reduced by administering the antagonist L-arginine.

trans fats

Cardiologists also rarely mention trans fats because there are no patented drugs to lower them. Rather, attention must be paid to diet. An important guiding principle for this would be: "If men made it, don't eat it!". This means that, above all, fast food and convenience foods should be avoided. According to WHO estimates, 500,000 deaths per year are attributable to Trans fats promote arteriosclerosis, stroke and heart attack.

In the kitchen, we can very easily create the dangerous trans fats ourselves through ignorance. If we overheat the healthy unsaturated fats when frying, trans fats are created by changing the double bonds in the unsaturated oils. Therefore, the right oil for heating should be selected. Pumpkin seed oil, linseed oil and walnut oil should never be heated. Virgin olive oil and butter tolerate temperature increases up to a maximum of 180°. Clarified butter, ghee, coconut oil, rapeseed oil, palm kernel oil and the new high-oleic oils tolerate temperatures of up to 230°. As already described, margarine should be avoided, since the processing of vegetable oils produces trans fats and therefore margarine is usually much more harmful to health than butter. The only exceptions are a few margarine brands that are available in health food stores. Otherwise, high trans fat concentrations are mainly found in baked goods such as croissants, biscuits and donuts, in chips, flips, popcorn, fast food, French fries and pizza.

Why are trans fats so problematic?

Our cell walls are largely made up of phospholipids. The phospholipids consist partly of long-chain fats. If trans fats are used to produce these fats, the phospholipids and thus the entire cell wall do not have the quality that is necessary. A “rotten” cell wall then occurs. This means that substances that should remain outside can also pass through the cell wall. It is assumed that, among other things, there is an increased influx of calcium into the cell.

This also applies to the vascular cells. Therefore, calcifications are often found here.

lack of vital substances

The lack of certain vital substances as a risk factor for arteriosclerosis is well known. The vitamins vitamin D3, K2, C, E, B12, B6, B1 and the amino acid L arginine are important. In general, however, one should not only think about the administration of vitamin supplements, but also a balanced organic diet with a high proportion of vegetables for detoxification and to reduce hyperacidity.

heavy metal pollution

This risk factor becomes extensive on the subjectchelation therapy described.

Meatbolic Syndrome

The metabolic syndrome describes the interaction of four risk factors: high blood pressure, diabetes mellitus, obesity (overweight) and elevated blood lipid levels (triglycerides or oxidized LDL cholesterol). In general, only the unfavorable LDL-HDL ratio is spoken of in relation to cholesterol. However, I explained that the main risk is oxidized LDL cholesterol (see above). The metabolic syndrome can be improved by regular exercise and a change in diet, the aim of which is, among other things, to lose weight.

testosterone deficiency

Testosterone deficiency in men as a risk factor for arteriosclerosis is rarely considered. The risk factor is practically unknown among cardiologists. An eleven-year study with 702 participants found that testosterone levels in the lower quarter of the normal range already entailed a 2.3-fold increased risk of diabetes mellitus or metabolic syndrome. Any average doctor who hasn't dealt with hormone therapy will tell a patient with testosterone levels that high that everything is fine because testosterone is in the normal range. However, as the study showed, that is not the case. Standard values in medicine are often defined too low, since they are based on the gender and age-specific average of the population group. In this population group, however, there are already pathological deviations that are wrongly used to calculate the average. A therapy withnature-identical hormonesso it can be quite helpful.

The widely known individual risk factors

Sugar and thus also diabetes mellitus, smoking, high blood pressure, lack of exercise, stress, sleep apnea syndrome, triglycerides (neutral fats). Here, too, there are corresponding therapies for every point.


First of all, the anamnesis (medical history) is important. Risk factors such as cardiovascular diseases in relatives, smoking, high blood pressure, diabetes and risk factors from previous laboratory tests can possibly be determined here. Then an ultrasound of the cervical arteries is necessary in any case. These can be displayed very well and deposits can be measured down to a tenth of a millimeter. The flow can also be determined well. A heart ultrasound is also useful, even if the coronary arteries cannot be assessed here. Other problems such as heart pressure syndrome (relaxation disorder), heart muscle thickening, enlarged heart cavities, arteriosclerosis of the aorta or sclerosis of the aortic valve can be measured here in addition to the pump function. Heart valve defects are also noticeable here. As described, the coronary vessels cannot be assessed on ultrasound. However, there is a correlation (ratio) of the change in the cervical arteries to the coronary arteries. The agreement of the vascular changes is described as approx. 90%. An abdominal ultrasound can be interesting to assess the condition of the main artery (aorta). Deposits here usually do not lead to significant narrowing. However, the aorta can expand, the so-called aortic aneurysm.  This expansion is not always caused by arteriosclerosis, but sometimes also by a congenital weakness of the connective tissue, for example in Marfan syndrome. If the aneurysm has reached considerable dimensions, it must be operated on, since there is usually no rescue if the aorta ruptures.

A statement about the coronary vessels can often also be made by the stress ECG. If corresponding changes occur in the ECG that indicate a circulatory bottleneck, further clarification by cardio CT or cardiac catheterization is urgently recommended. However, for example, a severe narrowing of one of the three coronary arteries can appear unremarkable in the stress ECG. Therefore, further clarification may be necessary even if the stress ECG is unremarkable. If high blood pressure and possibly chest pain occur during the stress ECG, the symptoms can also be blood pressure-related without the coronary arteries having to be constricted. A good blood pressure control and a repeat of the stress ECG after a few weeks are recommended here.

If abnormalities are observed during these examinations, the risk factors for arteriosclerosis should also be determined.

If there are decisive indications of coronary heart disease, for example symptoms such as cardiac arrhythmia, shortness of breath or angina pectoris, further clarification by cardio CT or cardiac catheterization is advisable. In my opinion, the allegations against the medical profession by Prof. Karl Lauterbach and some medical journalists that too many heart catheter examinations are being carried out are unjustified. The argument that only one in four patients examined has coronary artery disease requiring treatment and is therefore examined too often is unacceptable to me. If Lauterbach is such a gifted doctor that only those patients who are really ill are "fished out" for the heart catheter based on the preliminary examinations, then we could learn a lot from him. In fact, not even the best cardiologists can do this. If only 25% of the patients receive a therapy that is essential for survival through the heart catheter, I think it is tolerable that in 75% the examination was apparently not necessary. But this group also benefits from the study. Because they had symptoms and were seriously concerned. After the examination, you feel reassured and relieved. According to Lauterbach's argument, if we refer fewer patients for cardiac catheterization, more patients will die of heart disease.

Arteriosclerosis also affects other arteries outside the heart. As a rule, symptoms only appear when the narrowing is 70% or more. There is also no need for hasty interventions, because arteriosclerosis does not worsen overnight. When we diagnose advanced arteriosclerosis in a 70-year-old, it has developed since adolescence.

The general theory about the origin of heart attacks is at least dubious. It is believed that small intimal injuries in the area of the plaques (deposits) lead to clot formation on the built-up surface. This clot would then break loose and block the vessel behind the bottleneck. I don't think this theory is wrong, but there are indications that other heart attack causes are also possible. A case that shakes the current theory is described in the book "Strophantin" by Rolf Jürgen Petry. Here it was observed during a heart catheter examination that there were ECG changes in the sense of a heart attack. At that time, the coronary arteries were still free. Then the cardiologists observed an occlusion of an artery and injected streptokinase through the catheter into the corresponding vessel to dissolve the clog. It opened briefly, only to close again. Here it is highly probable that the infarction did not begin in the vessel and was certainly not caused by a detached blood clot, but that overload and hyperacidity resulted in a blood flow bottleneck in the smallest arteries of the heart muscle. The overload may cause a small inflammation with microedema in the arterioles, which promote clotting at this point. The blood then backs up into the larger coronary arteries. It therefore makes little sense to only look at the vessels. The composition of the blood is also important with regard to an increased willingness to coagulate. Dark field microscopy is important in this regard, as it can detect signs of acidification and the so-called sludge phenomenon. The sludge phenomenon refers to the chain-like clumping to the so-called "rolls of money". It is easy for everyone to see that these clumped red blood cells have difficulty passing through the small arterioles, which have a smaller diameter than the red blood cells. If there is still an increased willingness to clot, the catastrophe is complete. It is a fairy tale that aspirin and the relatively expensive clopidogrel provide adequate protection against unwanted coagulation for everyone. Recent studies have shown that there is a widespread genetic defect that renders these drugs ineffective. However, the side effects are still there. Unfortunately, this genetic disorder cannot yet be routinely detected in the laboratory. Also in the book "Strophanthin" it was reported that most heart attacks are often observed in the coronary arteries, which are not as narrowed as neighboring arteries. Even the most recent literature states that it is impossible to predict in which coronary artery an infarction would occur in the future. This can certainly speak for the origin of the infarction in the arterioles. It will be difficult to prove this theory because it is extremely rare for a heart attack to occur during a cardiac catheterization. A study in Sweden showed that the heart attack rate increased when more wood was used for firing in the houses. The emission of fine dust seems to be the reason for this. In my opinion, this fine dust going straight into the blood could fuel inflammation in the arterioles. The theory of the cause of infarction in the arterioles could trigger a reaction like many other hypotheses before: first it is ridiculed, then it is fought and finally accepted as a matter of course. Opponents of the theory must be able to explain why the EKG showed signs of infarction even though the coronary arteries were still open.


Of course, the phenomenon of infarction described above does not only apply to the heart. It may also play a role in causing strokes. Many heart attacks are not diagnosed or are diagnosed too late because they affect organs where the symptoms are not so clear. Mesenteric artery infarction, which affects the arteries of the intestine, is difficult to diagnose. It manifests itself primarily in the form of abdominal pain, which then disappears again until the circulatory disorder becomes life-threatening due to the death of a section of the perineum. Abdominal pain can have many causes and only rarely is it caused by a heart attack. It is much easier to diagnose a stroke when the patient can no longer speak or is paralyzed on one side. Then immediate help is needed.


with higher degree narrowing of the arteries, from 80% an operation makes sense. In the case of coronary heart disease, this can also mean stretching the coronary arteries with the help of a balloon catheter. As a rule, a stent (tubular wire mesh) is pushed into the dilated area so that the vessel remains open. Bypass operations are also sometimes necessary. Here, a bottleneck in the coronary artery or leg artery is bridged by a diversion obtained from a vein in the body. An artery that runs under the ribs towards the heart (mammary artery) can also be connected directly to a coronary artery. This offers the advantage that it does not develop arteriosclerosis. Arterial sections can also be bridged with Dacron prostheses (artificial arteries). This is often used to bridge constricted leg arteries. Patchplasty in particular is used for the carotid arteries. This involves the surgical expansion of the neck artery, which is then closed with a patch from a vein.

In principle, however, it must always be diagnosed whether narrowing of the arteries is responsible for a supply bottleneck. The smallest arteries (arterioles) can certainly be narrowed, as occurs, for example, in diabetic microangiopathy. Surgery doesn't help, only infusions.The LipoPower Cure PlusInfusion is very helpful for the treatment of arteriosclerotic changes in small and large vessels. Also thechelation therapycounteracts arteriosclerosis. On this subject, a study by C. Hancke Flytie, Denmark 1993 found: in 58 of 65 patients on the waiting list for coronary bypass surgery, the procedure was no longer necessary after chelation therapy. In 24 of 27 patients on the waiting list for an amputation, the procedure was no longer necessary after chelation therapy. A meta-analysis by Terry L. Chappell, MD, and John P. StahlPhD from 19 studies showed:in 22,765 patients there was a positive relationship between improved coronary artery blood flow and EDTA chelation therapy. 87% showed clinical improvement in symptoms by objective testing

It is crucial that the causal risk factors are found and treated. As a result, operations can often be prevented and the small arterioles that cannot be operated on are also treated.

Heart diseases not related to atherosclerosis:

inflammation of the pericardium or muscles

Heart failure (heart failure)

Dilated cardiomyopathy (progressive enlargement and weakness of the heart)

heart valve defect

cardiac arrhythmia and atrial fibrillation

Anker Herzkrankheiten
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