| |
| Home |
| Scientific Area |
| Olive Oil and Health |
| Medical Guide |
| Quality Area |
| Oil Sector & Spinneret |
| Promotion |
| Normative Area |
| Olive Oil Classification |
| Informative Area |
| Olive Oil in the Kitchen |
| Recipes |
| "Glocal" |
| Press Area |
| Meeting |
| Registration |
OLIVE OIL MONOUNSATURATED, FATTY ACIDS AND LDL OXIDATION
AUTHORS: Prof. Gerd Assman and Prof. Vrsel Wahrburg 1. IntroductionA high LDL cholesterol concentration in the plasma is one of the main risk factors for the development of atherosclerosis .However the principal reasons why the LDL provoke atherosclerosis are not known; that is to say the exact action between LDL infiltration into the artery wall and the consequent atherosclerotic lesion. There is more and more evidence that the LDL have some transformations before they become pathogenic. The data provided by bio-chemical and animal studies hard confirm the hypothesis that the LDL modifications in the oxidation process play a key-role in the atherogenesis. The LDL sensibility to oxidation is determined by several endogenous and exogenous factors, among these the nourishing factors have an extraordinary importance, in particular the types of fatty acids and the anti-oxidant vitamins present in the diet. This document explains the oxidative hypothesis of atherosclerosis and the role of the quality of food fats in this process. 2. The role of the LDL oxidation in the atherogenesisAccording to the so-called “oxidation hypothesis”, one of the starting phases of the atherogenesis is the LDL oxidative modification, and the captation of the lipoproteic particles modified by the macrophages, which on their turn, carry the lipids and form the so-called foamy cells (1), rich in cholesterol. The deposit of foamy cells on the artery wall is the first sign of atherosclerosis and is called adipose stream (2). Although the importance of the oxidative hypothesis has not been stated yet, in the last ten years a lot of data have been collected; these support this thesis. The LDL were shown to oxidise in vivo (3); some antibodies against LDL oxidise ( 4) were discovered in the man¸ the LDL extracted by human atherosclerotic lesions show a lot of physical, chemical and biological properties of the LDL( oxidised in vitro). Moreover the LDL sensibility level to oxidation can be provoked in vitro indicating isolated LDL particles with cells( macrophages, linfocytes, smooth muscle cells), metal ions( copper or iron), enzymes, oxygen radicals or (7-9) ultraviolet light but the mechanism regulating LDL oxidation in-vivo are not known. The LDL were shown to be protected from oxidation in the plasma by anti-oxidative substance as the ascorbic acid, the urea acid or the bilirubin. The most LDL oxidative modifications are likely to happen on the artery wall, where the LDL seem widely isolated by the plasmatic antioxidants. Recent data suggest the metal ions( copper or iron) and the myelo peroxidasis and lipoxygenasis enzymes to play key- roles in the LDL modifications. 10- The LDL exposed to pro-oxidative conditions, lose their anti-oxidants. PUFA ( polyunsaturated fatty acids) oxidation of the LDL into lipidic idro peroxides start when the most antioxidant defences are already lost. The PUFA decomposition drives to several other modifications of the LDL particle, as for example the cholesterol oxidation or the Apo-B (7) modifications; (11)- determining two important effects, at first high biological molecules are generated involving chemiotactic substances for monocytes and linfocytes, citotoxic or able to alter directly the cells of the artery walls( table 1). Then the Apo-B modifications drive to changes in the specificity of the LDL receptor and improve their affinity for the so-called sweeper receptors. The unaltered LDL directly bind to the LDL receptor. As the presence of the receptors for the LDL on the cells is regulated by the intra-cellular content of free cholesterol, the cells can pick up only limited LDL quantities by these receptor. On the other hand, the weeping receptors on the surface of monocytes and macrophages, a family of heterogenic proteins from a structural viewpoint , are not regulated by the intracellular content of cholesterol through feedback. By means of these receptors the cells can pickup the LDL in a deregulated way and depot huge quantities of cholesterol. As these characteristics of the modified LDL are a cause of atherosclerosis, this trend to check LDL sensibility to oxidation should be constant. 3. The olive oil and the oxidative process.Nutrition has undoubtedly a key-role in the process of LDL oxidation. In particular the quality of fats and the content in oxidative elements in the diet contribute to LDL and cells sensibility, and to their consequent damages. There are several possible ways through which the food fatty acids can influence the LDL towards atherogenesis. First, the quantity and the composition of food fats have an influence on the quantities of LDL particles present in the artery wall. The substitution of saturated fatty acids present in the MUFA or PUFA diet lowers down the total cholesterol and the LDL cholesterol levels( for details see: fact sheet: “ Olive oil cardiovascular and coronary risk factors”). The food fatty acids can directly affect the LDL oxidation sensibility, modifying the fatty acid composition present in the artery wall, altering in this way their pro-oxidant activity and their response to the oxidative stresses (11,9). Thanks to its high MUFA content the olive oil seems to have a protective action versus the LDL oxidation. Furthermore the olive oil can provide a supplementary protection giving the LDL strong antioxidants, such as vitamin E and poliphenols. These protective effects of the antioxidants will be explained in detail in a following document, entitled “ Anti- oxidative constituents of the olive oil and the LDL oxidation”. 3-1 Effects of food fatty acids (derived from oil) on LDL oxidationSeveral researchers compared the influence of MUFA and PUFA diets on LDL oxidation. The oleate- enriched LDL particles have been shown to be particularly resistant to oxidative modifications in the rabbits. One of the first studies analysing this matter in human beings was led by Reaven and his staff (16) who collected some participants fed with very fat liquid diets with 80% MUFA content or 60% PUFA of the total fatty acids. After these MUFA- enriched diets( derived from highly oleic sunflower oil) or PUFA( coming from sunflower oil) the composition of fatty acids present in isolated LDL particles, reflected the composition of the fatty acids in the diet and the distribution of fatty acids was similar in the different lipid traits of the LDL particle. The content of LDL linoleic acid ( C18:2) was strongly linked to the oxidation level. Several other studies were led ( 17-23) with good diets on healthy men hyperlidemic patients (24 -25) and diabetics ( 26) Such studies steadily show how MUFA enriched diets make the LDL more resistant to oxidation, if compared to PUFA diets. For example, Bonanome and his staff (17)compared a rape enriched diet (45% fats, 5% MUFA and 5% PUFA) among 12 healthy men. Even in this case the LDL oxidation level was higher in the PUFA diet than the MUFA diet. Although these results are still a bit ambiguous, some questions are still unsolved. according to the studies led so far. Are the two above mechanisms both involved in the reduced LDL sensibility to oxidation? Can PUFA improve the LDL oxidation or can MUFA reduce it? So far there have been only two existing studies dealing with this aspect: Aviram and Eias ( 27) compared the effects of the olive oil integration (50 grams/die) on the basic diet (30% fats, 50% carbohydrates). After two weeks’ diet rich in olive oil the LDL were discovered as less sensible to oxidation and they presented a lower cellular captation of the macrophages. MUFA integration is likely to cause a LDL sensibility reduction to oxidation. In their study Berry and his staff confirmed such results where they compared a MUFA diet (17% energy, total fats: 33% energy) with a carbohydrates enriched diet (65% energy: MUFA: 7%) leaving PUFA content constant in both the diets. The richest MUFA diet led to a meaningful reduction in LDL oxidation. Such data confirm that the diet rich in oleic acid can reduce LDL oxidation thanks to the MUFA antioxidant properties. 3-2 Food fatty acid effects on the cellular pro-oxidant activity and on their sensibility to the oxidative stress.The food fatty acids can influence also the cellular pro-oxidant activity. Several researches showed how the food integration with different fatty acids can lead to composition changes of the fatty acids present in the cellular membrane of the monocytes and this can influence the production of oxygen radicals in particular the anion in the monocytes and in the macrophages. The production of the anion by these cells undoubtedly contributes to LDL oxidation. Comparing the effects of the food integration with MUFA, the n-3 or n-6 PUFA on the anion generation, a reduction in superoxide production was recorded only after the n-5 fatty acids, while the monocytes coming from MUFA or n-6 PUFA integration did not show any change. The n-3 fatty acid action on oxygen radicals is not known, yet. Further investigations will be needed. 3-3 The role of the olive oil on the atherogenesis of the oxidised LDLAs described above the LDL modified because of oxidation, have atherogenic qualities. Tsimikas and his staff (23) analysed the effects of MUFA and PUFA, present in the diet, on the capacity of the half-oxidise LDL to cause the adhesion and the chemiotaxis of the monocytes. They found out that a higher quantity of oleic acid in the LDL, not only makes LDL particles less ossidable, but it reduces their biologic activity versus atherosclerotic processes. Similar results had already been shown by Mata and his staff (19). 4. Summary and conclusionsThere is more and more evidence on the key-role that LDL modifications can have in the pathogenesis of the atherosclerosis. The LDL oxidation starts with the PUFA peroxidation in the LDL particle. That’s the reason why the composition of LDL fatty acids favours their oxidation process. The composition of LDL fatty acids is influenced by the fatty acids present in the diet and, consequently, the quantity and the quality of the dietary fats influence the LDL oxidation-sensibility. MUFA-enriched diets enforce LDL against the oxidative modifications, if compared to PUFA enriched diets, as the LDL particles add some oleic acid. Furthermore, the composition of fatty acids of the cellular membrane depends on diets: MUFA diets guarantee higher MUFA contents in the cellular membrane and, consequently, the cells become more resistant to the oxidative damages. Finally, a MUFA increase reduces not only the LDL oxidation sensibility, but it lowers also the atherogenic characteristic, when already oxidised. Until many years ago, the attention to the benefits of the Mediterranean diet was focused only on hyperlypidemia and on some cardiovascular diseases. Now it’s clearer that the high assumption of MUFA, typical of the Mediterranean diet, thanks to the use of the olive oil, combines with the advantages of cholesterol reduction and of a lower LDL and cellular sensibility to oxidation, reducing also the atherogenic effects of the LDL. Bibliography
1.Westhuyzen J: The oxidation hypothesis of atherosclerosis: an update. Ann.Clin.Lab.Sci. 1997;27:1-10. |
|
|
