By Uffe Ravnskov MD
Why is atherosclerosis seen only in arteries, you may ask. Veins are also supplied by the vasa vasorum. Why don't the LDL-complexes obstruct the vasa vasorum of the veins? Good question, but there is a good answer also.
The pressure in veins is very low, lower than in their vasa vasorum. Venous blood flows slowly and steadily and therefore, the LDL clumps have no problem passing by.
In the arteries the pressure is high, much higher than in their vasa vasorum. Each stroke of the heart stops the blood flow completely in the vasa vasorum; the blood is only able to pass by during the short time when the heart is relaxed.
By the same reasoning, atherosclerotic plaques are localized to areas of the intimal surface where the hydrodynamic forces, turbulence of blood flow, and tissue pressure are especially high, namely at the branching points of the arteries and within tortuous arteries. The fact that atherosclerosis is seen only in arteries also contradicts the idea that microbes attack the endothelium directly. If this were true, atherosclerosis would be just as, or more common, in veins.
Two other good questions are: Why is LDL oxidized in the arterial wall and how do you explain the presence of oxidized LDL? There is a logical answer to this. LDL is not oxidized in the arterial wall, of course. Why should our own cells attack a normal and perfect molecule with many important functions? No, LDL is oxidized after having been phagocytosed together with its toxic passengers as part of a normal physiological process.
When white blood cells take up foreign, dangerous material they neutralize it by oxidation and at the same time LDL is oxidized as well. Probably HDL reconstructs LDL, because laboratory experiments have shown that HDL is able to convert oxidized LDL back to normal.(28)
What about the foam cell? Is it really true that the droplets are identical with microorganisms or their toxic products captured by LDL? Have you any evidence? Certainly! In laboratory experiments researchers have added various types of bacteria to solutions containing macrophages and human LDL. When they looked at the mixture with a microscope they saw that the previously normal macrophages had been converted to foam cells.(29) The same was observed in an experiment, where LDL was mixed with homocysteine instead of bacteria.(30)
A contradiction to our hypothesis is that prevention of cardiovascular disease by antibiotics has been largely unsuccessful. However, in these experiments patients have received a single antibiotic, chosen because it was effective against a bacterium called Chlamydia pneumoniae, and the treatment was given for short periods.
It is highly unlikely that such treatment would have had an effect in more than a few patients because as previously mentioned, fifty different bacteria have been localized in atherosclerotic tissue, and it is not possible to combat a virus with an antibiotic. Prevention with antibiotics may even have the opposite effect because it may lead to the development of resistant microorganisms.
It is probably a much better idea to look after bacteria in the blood in patients after an acute heart attack, and if present treat the patient with an appropriate antibiotic.
Another good idea is to eliminate chronic infections. Dental researchers from Italy, for instance, treated 35 otherwise healthy individuals with evidence of periodontal infections. After the treatment, examination of the carotid arterial wall showed that its thickness had diminished significantly and much more than seen in any cholesterol-lowering trial.(31)
Atherosclerosis is a spotty disease
According to the current ideas about atherosclerosis it should be a generalized disease. If LDL-cholesterol enters just because there is too much of it, all of our arteries should be atherosclerotic. To explain its spotty appearance it is said that atherosclerosis only occurs where the dynamic forces are especially strong, but everyone who has looked at the inside of dead people's arteries knows that this is only partially true.
Atherosclerosis is often located haphazardly, particularly in the aorta. This is also what we should expect if atherosclerosis was due to the effect of microbial attacks repeated again and again throughout our life.
The foam cells once again
We think that the presence of foam cells is a normal phenomenon. Their contents may probably escape when the tissue becomes malnourished or dies but most likely the lipid droplets are taken up by other macrophages, which move back into the circulation.
On their way they may temporarily accumulate beneath the endothelium where they are organized as fatty streaks due to the rapid blood flow on the outside. Foam cells are also present in other arteries, and if there are foam cells, there should be vulnerable plaques as well. They have indeed been found located in the carotids, those that carry blood to the brain.(32)
Foam cells are seen beneath the retina, more and more with advancing age.(33) They are found commonly in the glomeruli,(34) the kidneys' capillary mesh where the blood is filtered to produce urine, in particular in sclerotic glomeruli. That a glomerulus is sclerotic means that it is dead and may be compared with a scar or a fibrotic plaque. The number of sclerotic glomeruli also increases with age.
What about the risk factors?
Now to the icebergs. What do they look like and why do they stave in our ship?
For many years we have been presented with a long list of risk factors for cardiovascular disease. Most of them are, with all certainty, secondary to the real cause but we think that some of them are primary, because they fit so well with our hypothesis. Diabetes and smoking for instance are strong risk factors for all kinds of cardiovascular diseases and both diabetic patients and smokers are also susceptible to infections.
Mental stress, another established risk factor, stimulates production of the hormone cortisol, and an excess of cortisol promotes infections. This can be seen in patients with Cushing's disease of the adrenal glands and when cortisol is used as a treatment.
Too much homocysteine in the blood promotes the tendency for LDL to stick together. When their structure has been changed, they stimulate the immune system to produce anti-LDL antibodies just as was the case with oxidized LDL. Hyperhomocysteinemia is also associated with lack of vitamin B, smoking, high blood pressure, mental stress and kidney failure, and all of these conditions are risk factors for cardiovascular disease.
A final comment
If your cholesterol is high, I am confident that you will not worry about it any longer. You will also be able to enjoy good old-fashioned food with lots of butter, cheese and cream. But how should we avoid a heart attack or a stroke? The best way is probably to avoid what stimulates microbial growth and what is harmful to our immune system. A few suggestions are available.
There is increasing evidence that vitamin D plays an important role in our immune system as a protective factor against microorganisms.(34) In accordance, a low concentration in the blood of that vitamin is also a risk factor for cardiovascular disease. Although no clinical trials have been performed to see if supplementation with vitamin D is able to protect us, it may be a good idea to take at least 1000 IU daily, in particular during wintertime.
Our need for vitamin C is also much greater than we have been told for many years. The reason is that the amount of that vitamin inside the white blood cells is 80 times higher than in the blood.
Furthermore, glucose and vitamin C use the same cell door, meaning that if the glucose concentration is too high in the blood, these two molecules compete for access.(36) This may be the reason why diabetics are more susceptible to infections than other people. It also means that the 50-100 mg we have been recommended as a daily input may be far too little. One gram a day is probably a minimum for optimal health, more if we become infected.
To learn how we can best protect ourselves against microorganisms should be a challenge for curious and open-minded researchers.Dr. Uffe Ravnskov MD
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