What foods cause oxidized cholesterol
How harmful is oxidized LDL?
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Hans-Helmut Martin / Jacqueline Hoffmann
Low density lipoproteins (LDL) are necessary to transport fat and cholesterol in the blood to the cells. In oxidized form, however, they damage the vessel walls.
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Cardiovascular diseases are one of the most common causes of death in western industrialized countries. They are characterized by atherosclerosis, a pathological change in the arterial walls. The focus of this consideration is on lipoproteins, which act as a transport medium for fats and cholesterol in the blood. The lipoproteins are differentiated according to their density. LDL stands for Low Density Lipoprotein and is a low density lipoprotein and particularly high in cholesterol. This is because LDL is the main transport medium for cholesterol in plasma and transports it from the liver to the peripheral tissue. There it is absorbed into the cells via LDL receptors. Cholesterol is an important component of the cell membrane, the starting material for hormones, bile acids and vitamin D.
LDL is therefore a very desirable component of the blood, even if it is considered problematic in larger quantities. The high LDL level is not the only critical factor. A particular danger is that the LDL particles can oxidize. Oxidized LDL has changed on the outer shell of the lipoprotein in such a way that it no longer reaches the cell via the LDL receptors and remains in the blood. Among other things, free radicals are responsible for the oxidation of LDL. Possible triggers for the formation of free radicals are cigarette smoke and exhaust gases, metabolic products, stress and inflammatory processes in the body. Malnutrition is also an important factor. Free radicals are also created during cell respiration and energy generation. At the same time, the oxidized LDL becomes a reactive radical and can damage the vessel wall.Defense cells such as monocytes and macrophages are used to remove oxidized LDL and repair damage to the vessel wall. These phagocytes preferentially absorb oxidized LDL and, through the accumulation of these fat fractions, become so-called foam cells, which are supposed to seal the vessel wall again. The downside: foam cells form the basis of atherosclerotic plaques. An unfavorable cycle begins: LDL that has penetrated through the damaged vessel wall can in turn be oxidized and absorbed by other immune cells. From this self-reinforcing process, atherosclerosis develops. It has been known for many years that atherosclerosis also involves oxidative and inflammatory processes (see also p. 198). Antibodies against oxidized LDL are therefore also discussed as a diagnostic marker for atherosclerosis.
So preventing atherosclerosis is not just about lowering LDL levels. Quitting smoking, reducing stress and eating a predominantly plant-based diet with antioxidant vitamins (C and E), phytochemicals and fiber are just as important.
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Biesalski HK (2015). Pocket atlas of nutrition. Thieme, 6th revised edition, Stuttgart
Kobbe A (2011). Antibodies against oxidized LDL as a risk marker for atherosclerosis. Dissertation, University Medical Center Hamburg-Eppendorf
Mügge A (1998). The role of reactive oxygen species in atherosclerosis. Z Kardiol 87, 851-861
Ng CH et al (2008). Oxidized cholesterol is more hypercholesterolaemic and atherogenic than non-oxidized cholesterol in hamsters. British Journal of Nutrition, 99, 749-755, doi: 10.1017 / S0007114507842784
Schmiedel V (2006). Cholesterol - finally plain language. Trias, 2nd completely revised edition, Stuttgart
Source: UGBforum 4/18, p. 200
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