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Atherosclerosis, the cause of ischemic heart disease , is the condition where the coating of oxidized fats (atheroma) is deposited in the blood vessels. Atherosclerosis is the most common of civilization diseases ( Barac2009mdv ). Oxidation of fat in the blood is proportional to the amount of fatty acids (LDL) in the blood and the amount of free radicals in the blood. The amount of free radicals in turn correlates with the amount of oxygen - therefore, the atheromas are formed only in the arteries. The capture of oxidized fats on the inner surface of the vessels (endothelium) invokes macrophages that try to clear the contaminants by absorbing and degrading oxidized fats. If these oxidized fatty particles are too much, the macrophage will eventually die to death, and the lipids that have been poured will be poured again into the vessel wall. This calls for more macrophages waiting for the same fate. The atheroma - a sort of "macrophagian graveyard" that has certain characteristics of an inflammatory deposit - is gradually emerging on the affected site. Cholesterol, which is resistant to degradation, accumulates there. Simplified lesson is that atherosclerosis is mainly an immune process and this fact is not mutually exclusive to the cholesterol hypothesis of cardiovascular disease ( Ignarro2007npa ). Although atherosclerosis is not a cause of myocardial infarction , it is not one of the direct causes of hypertension ( Shimbo2010edr ).

Factors of atherosclerosis

Atherosclerosis begins in early adulthood and progresses without causing problems during life. Developed atherosclerosis is untreatable for the time being. The only cure is prevention. Thinking doctors, therefore, try to protect the patients they care about before proceeding.

According to current knowledge, atherosclerosis causes two things:

  1. Oxidation of fat in the blood.
  2. Unclear immune pathological process .

Oxidation of fat in the blood again requires two things:

  1. Oxygen
  2. Fat in the blood

So we have three parameters to control the development of atherosclerosis: oxygen, blood fat and immunity.


From the point of view of the amount of oxygen in the blood, I would pragmatically divide the activity of the organism into three modes: (a) sleep, (b) calm, (c) physical exertion. In sleep, the oxygen content in the blood is reduced - the body is saved and repaired at night. At rest, for example, in non-stressful mental work, or in light physical activity (walking), the oxygen content is at a basic level of vigilance. In physical exercise mode (physical work, training) the oxygen content is increased by the intensity of the physical activity.

Fat in the blood

Roughly speaking, there are fatty droplets of two types: LDL ( low density lipoprotein - low density lipoprotein ) and HDL ( high density lipoprotein - high density lipoprotein ). They are honestly called "lipoprotein," but in fact they are just a little fat crust with a bit of protein, which prevents them from merging. It's like fat in milk, we have less in blood. HDL droplets are "good" (do not cause atherosclerosis) because they are small. They have a high density because there is little fat in them (fat is light, protein is heavy). LDLs are bad because they are the real, big (and therefore light) fat flesh. They are mainly released from the small intestine into the bloodstream. Blood in the vein vein is milky, after a fat meal. The vein vein, as we know, leads to the liver, where it once again shoots into the capillaries and where the LDL droplets become a chemical raw material for the hepatic cells, so they should not go too much into the large circulation. This, however, appears to be happening to some extent, and LDL droplets in the large blood circulation contribute to the development of atherosclerosis.

Immune factors of atherosclerosis

Beginning with the development of the atherosclerosis deposit (atheroma) appears to be oxidative stress. But it also causes an inflammatory process that leads to the development of atheroma. It is not entirely clear what is the interaction between oxidation of LDL droplets and the inflammatory process in the vessel wall, but both of these factors are mutually supportive and that both are necessary to develop atherosclerosis ( Hajjar2013bri ). Roughly, LDL droplets are oxidized and trapped on the wall of the arteries (or first trapped and then oxidized). The clutter calls the cleaning macrophages that can not be cleaned, the oxidized fat droplets are desired, and appear to be filled with foam ("foam cells") under the microscope. These macrophages then die and the disordered disorder spills back into the vessel wall. (Oiled fats are what can be found in households on a wall near a frying pan, where they are fried in the pan, and when I clean it, I sometimes think I will die of it.) This happens all the way up to the point where the atherosclerotic bearing Mainly cholesterol, which is the most persistent of all fats.


We must realize that the development of atherosclerosis must be wrong in this process. It is normal that the vessel wall becomes dirty occasionally and that the macrophages will come clean. There must be some other factor that will cause routine cleaning to fail and create an atheroma. We do not know exactly what this factor is, but it seems that adaptogens that affect the overall "inflammation" (the susceptibility of the body to inflammation) and those with a cytoprotective effect can act positively against the onset and progression of atherosclerosis.

So how do you protect yourself from atherosclerosis?

My short answer to this question is: I do not know. Popular statins and cholesterol lowering seem to go away and cause more or less a side effect than the very cause of atherosclerosis. Popular antioxidants are very important , but our body already knows about them, so if we eat healthy, we do not need to think too much about them. The popular exercise is also not what it used to be. Aerobic overloading, as it turns out, leads to oxidative overload and damage to the body ( Tsai2001odd ), and some "antioxidants" under these conditions turn into pro-oxidants ( Tomasello2012dar ). It gets right the farmer's insight that whosoever has gone down, he will be struck. On the other hand, the zero practice is also bad, because most people today (from the point of view of the pramovkaeka) do not practice at all. It is not clear what to advise, in addition to the general recommendation of a return to nature and nature.

Atherosclerosis and cholesterol

Because cholesterol is the most quantitative in atherosms, it has long been suspected of causing atherosclerosis. However, it turns out that atherosclerosis has (as I wrote above) oxidative and immune connections. It is perhaps a hypothesis that cholesterol accumulates in atheromas simply because it is most resistant to degradation. Cholesterol malignancy and statin efficacy demonstrated in herbivorous rabbits ( Shen2013eae and many other similar studies) are not automatically related to humans. It seems that cholesterol in our diet is far from worrying, so butter and eggs are once again healthy foods ( Fernandez2012rdc , Trapani2012rdc ). Statins are important only for some risk groups ( Koh2009ctp ).

Atherosclerosis, stress and smoking

Even though I think that smoking is now overtaking smoking, it is necessary to say that smoking is demonstrably associated with cardiovascular damage and the smoking ban is 100% indicated in all cardiac events. All forms of smoking, including pipes, cigars and marijuana damage the vessels ( Katsiki2013svr ). The damaging effect on the blood vessels has both smoke (tar, carbon monoxide) and nicotine ( Leone2013vpf ). However, I have prepared the floor to say that epidemiological studies on the relationship between smoking and illness do not have the same statistical weight as it seems. I will not quote anything, just say what I mean: I would start by knowing that patients with schizophrenia are smoking. And I think they smoke because it helps them, and I call on the experimenters to explore this hypothesis. I suppose this hypothesis is valid. I also know that people who are prone to stress are also smoking. This could also explain why smokers and lower category workers smoke a lot. It is logical that stress on human psyche is rather negative, so what helps mentally ill can also help mental well-being in stress. We also know that people with poor living conditions suffer more from stress. And - now I come to the conclusion - I think that part of the cardiovascular damage seen in smokers may be stressful due to the poor conditions in which the smokers were found and in whom smoking was accustomed. If stress was caused by a poor life situation, part of the vascular damage can be due to cheap food and poor diet. Therefore, I urge researchers to take into account smoking smoke studies that sometimes smoking is only correlated with a poor life situation that is the cause of health damage. This is a problem that will not solve nicotine bans.

Atherosclerosis, eating and exercise

Atherosclerosis, therefore, begins with dirty blood vessels oxidized by fatty LDL droplets, which mainly come from food. Empirically, it is known that the greatest formation of atheromas is in places where the maximum oxygen content is present, whereas in the veins where oxygen is already consumed, the atheromas do not form at all. Another factor is speed and turbulence of the blood stream. Vessels with the highest oxygen content and high flow rates, such as coronary heart arteries, are the first to suffer from atheroma formation.

So I should advise that we do not run a marathon with a thin intestine full of fat mutton? Especially when I sometimes run and swim with my stomach? Probably yes. So do not run with a full stomach. But I must admit that I personally have the impression that my small intestine does not need this advice. I have the impression that my stomach filled with jogging precisely regulates what and how quickly it goes to the small intestine that regulates what and how quickly it drives into the gate vein. Or is it advisable to advise on overall saving, less physical activity at all, as some physicians call it today? Or eat less, how has it been recommended for many years to prolong life?

Atherosclerosis can be prevented and treated with adaptogens

About adaptogenes with preventive and curative effects against atherosclerosis write in detail on a more general page on heart disease . A completely exceptional position in the prevention and treatment of cardiovascular problems is ginseng.

Protective effect of ginseng against atherosclerosis

From the point of view of scientific medicine, ginseng's systemic anti-inflammatory effect and protective effect on blood vessels (mainly via NO signal cascade ) has been known for a relatively long time. Direct effects on atherosclerosis have been experimentally demonstrated relatively recently in ginsenoside Rb 1 ( He2007peg , Xu2011egr ) and ginsenoside Rd ( Li2011gpc ). Strong indications of a possible effect on atherosclerosis exist with ginsenoside Rg2 ( Cho2013gri ) and compound K ( Lee2011gmc , Park2013cai ). The effect directly on atherosclerosis of coronary arteries was experimentally detected in ginsenoside Rb 1 ( Zhou2005grb ).

Other adaptogens with the effect of atherosclerosis

I will not continue to enumerate because atherosclerosis is a lifestyle disease, and practically any type of vegetable or healthy food somehow reduces the risk of civilization diseases.

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