Detrimental changes to platelet aggregation can be caused by an imbalance in dietary intake of the essential fatty acids. This is because both α-linolenic acid (ALA, C18:3 (n-3)) and linoleic acid (LA, C18:2 (n-6)) are converted to other fatty acids that have an influence on the production of compounds required for platelet aggregation. In particular, LA can be converted to arachidonic acid (AA, C20:4 (n-6)), which can increase platelet aggregation, whereas ALA is converted to eicosapentanoic acid (EPA, C20:5 (n-3)) which can decrease platelet aggregation. Conversion of AA through the cyclooxygenase enzyme to series 2 thromboxanes increases platelet aggregation, and this is an oxidative process. Therefore, antioxidants may inhibit platelet aggregation because they modulate the oxidative environment within cells and this might influence thromboxane levels. Because the conversion of AA to series 2 thromboxanes occurs in the cell membranes, lipid soluble antioxidants such as vitamin E may be important modulators.
Researchers1 have investigated the effects of vitamin E on platelet aggregation in subjects with type I diabetes. Using a randomised placebo controlled double-blind study design, researchers fed diabetic subjects either 1 gram of vitamin E per day or a placebo. After stimulation of platelet aggregation through use of ADP, and generation of oxidative products such as thromboxane through addition of AA, the platelet function was estimated. The vitamin E treatment resulted in a significant decrease in platelet aggregation when compared to the placebo. This was accompanied by a reduction in malonaldehyde from the platelets indicating that lipid peroxidation was reduced with vitamin E treatment. High doses of vitamin E therefore appear beneficial at preventing platelet aggregation in type I diabetics. However, whether this would translate into a cardioprotective effect in healthy individuals at dietary levels of vitamin E is controversial.
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