Atherosclerosis

Atherosclerosis is the process by which the deposition of cholesterol plaques takes place on the wall of blood vessels and makes those vessels narrow, ultimately getting blocked by those fatty deposits. Atherosclerosis finally leads ischemia to the heart muscle and can cause damage to the heart muscle. The complete blockage of the arteries leads to myocardial infarction (MI). According to the World Health Organization, the major cause of death in the world as a whole by the year 2020 will be acute coronary occlusion (Murray and Lopez, 1997).

As mentioned earlier, tocotrienols differ from tocopherols only in three double bonds in the isoprenoid chain which appear to be essential for the inhibition of cholesterogenesis by higher cell penetration and followed by better interaction with the deposited plaques (Qureshi et al., 1986). In some clinical trials with hypercholesterolemics patients, tocotrienols significantly reduced the serum cholesterols (Qureshi et al., 1991b). In another similar kind of clinical trial, tocotrienols lowered both the serum cholesterols, total cholesterol (TC), and more interestingly the LDL (Tan et al., 1991). In the late 1980s, it was found that one of the major cause of lipid oxidation was the oxidation of LDL. Therefore, Tan et al.'s (1991) observation draws many researchers attention toward tocotrienols as a better anti-lipid oxida-tive agent. Later on, a diet rich in tocotrienols, especially dietary tocotrienols from a TRF palm oil, reduced the concentration of plasma cholesterol and apolipoprotein B, platelet factor 4, and thromboxane B2, indicating its ability to protect against platelet aggregation and endothelial dysfunction (Qureshi et al., 1991a,b). In mammalian cells, HMG-CoA reductase enzyme was found to regulate the cholesterol production. Tocotrienols, mainly g-isoform or the tocotrienols mixture, significantly suppress the secretion of HMG-CoA reductase, ultimately lowering the production of cholesterols in the cells (Parker et al., 1993; Pearce et al., 1992, 1994). Another possible mechanism of protection from lipid peroxidation by tocotrienols was found by isoprenoid-mediated suppression of mevalonate synthesis that depletes tumor tissues of two intermediate products, farnesyl pyrophosphate and geranylgeranyl pyrophosphate, which are incorporated posttranslationally into growth control-associated proteins (Elson and Qureshi, 1995). From the above observations, researchers have also started to compare tocotrienols with any statin group of medicine. In one of the study, Qureshi et al. (2001b) showed that when tocotrienols were applied with lovastatin or when lovastatin was compared to tocotrienol action, there was no difference in terms of cholesterol lowering power in chicken. Very interestingly, it was found apart from these two mechanism of tocotrienols; tocotrienols are also protecting from hypercholesterolemic phase by activating the conversion of LDL to high-density lipoprotein (HDL) through the inter phase VLDL-VDL and finally HDL (Qureshi et al, 1995, 2001a). In hypercholesterolemic phase, it was also observed either g-tocotrienol or the tocotrienols mixture increases the number of HDL, which then interact with LDL to reduce the concentration of LDL in the plasma (Qureshi et al., 1995), HDL may also go by phagocytosis to lower the LDL concentration. In another clinical trial, 100 mg/day of TRF derived from rice bran oil effectively lower the serum cholesterol in hypercholesterolemic patients (Qureshi et al., 2002). The same study showed that a-tocopherol induce the HMG-CoA reductase and that is why in higher doses of TRF, the opposite effect is observed to some extent compared to 100 mg/day of TRF (Qureshi et al., 2002). This may be due to the fact that tocotrienols were found to go on conversion into tocopherols in vivo (Qureshi et al., 2001a). This study clearly showed it is only tocotrienols which are responsible for the lowering of serum cholesterol, but not tocopherols. Tocopherols may increase the cholesterol level by inducing HMG-CoA reductase (Qureshi et al., 2002).

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Lower Your Cholesterol In Just 33 Days

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