If you were to lay out all the blood vessels of the human body end to end, you would reach a length of 100,000 kilometers. This would allow you to wrap around the earth about two and a half times! Through these blood vessels, the heart transports oxygen and nutrients to all cells of the body. A well-functioning vessel system consisting of veins, arteries and capillaries is therefore vital.
Arteries transport blood away from the heart. These branch out like a tree into arterioles and into hair-fine capillary vessels. Here the vessel pressure is reduced enough that oxygen, fluid and nutrients can be transported between gaps in the vessel wall cells into the surrounding connective tissue (Pischinger space) and specialized organ cells. Via veins and the lymphatic system, the metabolic processes of the latter cells flow back to the heart.
If the arteries no longer fulfill their function, certain body regions and cells can no longer be adequately supplied with vital oxygen and nutrients, or in the worst case, not at all. Undersupplied cells lose their function and in the worst case can die within a short time (stroke, heart attack). But how does it happen that arteries can no longer fulfill their function?
Definition
In atherosclerosis, so-called plaques accumulate in the arteries, deposits consisting of fat (cholesterol) and calcium salts, which is why it is colloquially said that the arteries "calcify".
These deposits have consequences on the one hand on the vessel wall of the arteries, which becomes stiffer and thicker. On the other hand, deposits reduce the inner opening of the arteries, so that less blood "passes through". The consequences: circulatory disorders up to complete blockage (e.g. heart attack, stroke) or weakening and bulging of the vessel wall (aneurysm).
Risk Factors
The American Heart Association, together with the company Google, announced a 75-million-dollar prize for determining the causes of atherosclerosis. Even today, the exact causes of atherosclerosis are still unknown, but risk factors have emerged from practice over time:
- Smoking
- Overweight
- unhealthy diet
- diabetes
- high cholesterol levels
- high blood pressure
- stress
- harmful environmental factors such as environmental toxins, fine dust, etc.
These factors promote the development of arteriosclerosis, but what really lies behind the dangerous deposits in the blood vessels?
Causes
Several studies now prove that inflammation plays a key role in the development of arteriosclerosis. In January 2017, Professor Axel Haverich from Hannover even declared inflammation to be the main cause of arteriosclerosis.
1. Inflammation is a defense reaction of the body to a danger or a problem. During inflammation, the body releases substances that change the function of certain cells with the aim of quickly identifying and neutralizing the source of danger. For example, the permeability of certain blood vessels is increased. This allows the body's own defense substances to reach their point of action faster, but all other substances also have, so to speak, „free passage“ in the body. The first body's own defense substances can be imagined like a broad-spectrum antibiotic. Since the body has not yet identified the „intruder“, it cannot recognize pathogenic pathogens and diseased cells and therefore destroys all cells in this area, altered/diseased and healthy alike.
Additionally, studies suggest a connection between inflammation and arteriosclerosis. For example, a study from England shows that the risk of a heart attack during a flu illness is six times higher than normal. Prolonged fine dust exposure, which also triggers an inflammatory response in the body, also increases the risk of infarction according to current studies. Other causes of inflammation can be, for example, bacteria, viruses, fungi, injuries, but also oxidative stress.
2. Oxidative stress is caused by so-called free radicals. Free radicals are byproducts of normal metabolism. They are molecules that lack an electron. They therefore try to snatch an electron from other molecules. If they succeed, they in turn leave behind a molecule with a missing electron: a new free radical. This leads to a chain reaction of oxidation.
Fortunately, the human body has so-called antioxidants, molecules with an extra electron, which can neutralize free radicals by releasing their extra electron. However, if the number of free radicals in the body increases, for example through greatly accelerated metabolism (sport) or unhealthy external influences (nicotine, alcohol, UV rays, environmental toxins), the body's own antioxidants are no longer sufficient to neutralize them. The result: oxidative stress. The declining number of the body's own antioxidants with advancing age can also lead to oxidative stress.
Oxidative stress leads to cell damage and as a result, the cells can no longer perform their functions properly or not at all. This causes the body to recognize a problem and start its defense mechanisms, that is, react with inflammation.
Oxidative stress promotes arteriosclerosis therefore indirectly by triggering inflammatory processes in the body, but also directly by free radicals damaging the protein HDL, which normally has the task of transporting cholesterol out of the bloodstream, so that no deposits and thus arteriosclerosis can form.
3. Besides, nitrosative stress, i.e. the formation of "NO" molecules during circulatory disorders, can also be involved. Here in particular, the formation of peroxynitrite must be prevented.
4. Also, vital nutrient deficiencies lead, according to our observation, to substitute incorporation of cholesterol into the vessel walls in order to stabilize them, when adequate proteins, trace elements and vitamins are lacking.
Prevention
It is proven that inflammation and oxidative stress are significant factors in the development of arteriosclerosis. To prevent arteriosclerosis, therefore, inflammation and oxidative stress must be avoided. While injuries and infections as triggers for inflammation cannot be completely prevented, oxidative stress can certainly be combated.
The best remedy against oxidative stress is antioxidants. By donating their additional electron without becoming a free radical themselves, antioxidants interrupt the health-damaging chain reaction of oxidation in the body. However, antioxidants also have the ability to regenerate other antioxidants, i.e. molecules that have already donated their additional electron to neutralize a free radical, by providing them again with an additional electron, so that the molecules can act antioxidatively again and resume free radical scavenging.
Various studies prove the positive influence of antioxidants on the cardiovascular system and vessels. The following vitamins and nutrients are particularly strong antioxidants:
- Vitamin C
- Vitamin E (especially gamma-tocotrienol)
- Vitamin A
- OPC (which, however, is greatly overestimated in relation to R-alpha-lipoic acid)
- Vitamin B12
- Folic acid. -minimal
- Glutathione
- Cysteine
- SOD
- R-Alpha-Lipoic Acid
- Omega-3 Fatty Acids
Many of these valuable nutrients also work anti-inflammatory and protect not only against oxidative stress, but also help to reduce inflammatory processes in the body. This way they support a healthy vascular system and help prevent atherosclerosis and its dangerous consequences.
Various Priosa products from Sanopoly contain these powerful antioxidants in their purest form and highest quality.
Especially the combination of Priosa® immun and Priosa® defense retard Pro (please consult your doctor or naturopath regarding this) has led to many reports of even a reduction in vascular diseases. A study on this has already been initiated. Feasibility is being examined.
1) Axel Haverich, Hans H. Kreipe (2016): Etiology Research Atherosclerosis, Deutsches Ärzteblatt 2016, https://www.aerzteblatt.de/archiv/175264/Ursachenforschung-Arteriosklerose-Warum-wir-die-KHK-nicht-verstehen
2) Inflammation and Atherosclerosis. By Peter Libby, Paul M. Ridker and Attilio Maseri in: Circulation, Vol. 105, No. 9, pp. 1135; March 5, 2002.
The Canakinumab Anti-Inflammatory Thrombosis Outcomes Study, presented by P. Ridker as part of the hotline session of ESC 2017, Abstract 115.
3) https://www.ahajournals.org/doi/abs/10.1161/circulationaha.116.025407
4) Jeffrey C. Kwong et al. (2018): Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection, New England Journal of Medicine 2018; 378:345-353, https://www.nejm.org/doi/full/10.1056/NEJMoa1702090
5) Long term exposure to ambient air pollution and incidence of acute coronary events: prospective cohort study and meta-analysis in 11 European cohorts from the ESCAPE Project, British Medical Journal, 2014 https://www.bmj.com/content/348/bmj.f7412
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