Proteins are attached to fats to facilitate their transport though the bloodstream. One example is a waxy fat, cholesterol, which is transported in the blood attached to proteins in the form of lipoproteins. Low density lipoproteins (LDL) transport cholesterol away from the liver, while the high density lipoproteins (HDL) transport cholesterol back to the liver for storage or for elimination in the bile. There is a close association between elevated levels of LDL cholesterol and coronary heart disease, which is a leading cause of death all over the world.
Low density lipoproteins are assembled in the liver. They are not known to contribute to heart disease unless they are oxidized by free radicals. The creation of atherosclerotic plaque and its progression to heart disease is only partially understood. When LDL levels in the blood are elevated, the oxidation of LDL may lead to the accumulation of fatty slabs on the inside of the arterial walls. This is the leading theory of the development of atherosclerotic plaque. The elevated levels of oxidized LDL stimulate macrophages to attack the LDL using free radicals. This causes more oxidized LDL. The macrophages become bloated foam cells and these foam cells attach to the inside of the artery. This can lead to blockage of the coronary arteries and a heart attack.
Vitamin E is built into LDL for protection from oxidation that can lead to clogged arteries.
Four published, large-scale, randomized, double-blind clinical intervention studies tested the effectiveness of supplemental vitamin E to reduce heart attacks. Three of these studies used 50 mg of vitamin E in the synthetic form and found little correlation with heart attacks. However, the study using 268 mg to 567 mg of vitamin E in the natural alpha-tocopherol form found a strong correlation with reduced heart attacks. Vitamin E protects LDL from oxidation. In the liver, a protein called alphatocopherol transfer protein incorporates alpha-tocopherol into LDL during the assembly of LDL. The alpha-tocopherol is there to protect the LDL from free radicals. Although alpha-tocopherol is preferentially loaded into LDL, some of the other tocopherols can also be incorporated into LDL. Half of the synthetic forms of vitamin E cannot be loaded into LDL
Low density lipoproteins are assembled in the liver. They are not known to contribute to heart disease unless they are oxidized by free radicals. The creation of atherosclerotic plaque and its progression to heart disease is only partially understood. When LDL levels in the blood are elevated, the oxidation of LDL may lead to the accumulation of fatty slabs on the inside of the arterial walls. This is the leading theory of the development of atherosclerotic plaque. The elevated levels of oxidized LDL stimulate macrophages to attack the LDL using free radicals. This causes more oxidized LDL. The macrophages become bloated foam cells and these foam cells attach to the inside of the artery. This can lead to blockage of the coronary arteries and a heart attack.
Vitamin E is built into LDL for protection from oxidation that can lead to clogged arteries.
Four published, large-scale, randomized, double-blind clinical intervention studies tested the effectiveness of supplemental vitamin E to reduce heart attacks. Three of these studies used 50 mg of vitamin E in the synthetic form and found little correlation with heart attacks. However, the study using 268 mg to 567 mg of vitamin E in the natural alpha-tocopherol form found a strong correlation with reduced heart attacks. Vitamin E protects LDL from oxidation. In the liver, a protein called alphatocopherol transfer protein incorporates alpha-tocopherol into LDL during the assembly of LDL. The alpha-tocopherol is there to protect the LDL from free radicals. Although alpha-tocopherol is preferentially loaded into LDL, some of the other tocopherols can also be incorporated into LDL. Half of the synthetic forms of vitamin E cannot be loaded into LDL
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