Vitamin E

Vitamin E is another widely researched adjunctive therapy, with various effects throughout the body and on inflammatory diseases. Vitamin E exists as eight different forms including four tocopherols and four tocotrienols. A powerful antioxidant with several antiatherogenic effects, much attention has been focused on vitamin E in the prevention and treatment of cardiovascular disease. Vitamin E exerts beneficial effects on LDL oxidation, pro-inflammatory cytokines, and CRP levels.64 Providing patients with 1,200 international units (IU) per day of alpha-tocopherol significantly lowered interleukin-6 and hsCRP levels in a five-month study.65 Other studies have shown a direct dose-response effect of up to 1,200 IU of vitamin E on anti-inflammatory effects and inhibition of CRP.66 In another study, 1,200 IU of vitamin E reduced elevated CRP levels by 33% in control subjects who were nondiabetic and by 25% in patients with type 2 diabetes after three months of supplementation.45 A similar trial with 800 IU of vitamin E reduced CRP levels by 48% in four weeks.67 Supplementation with alpha-tocopherol is considered to be therapeutically safe, even at 1,200 IU.68 Studies regarding the efficacy of vitamin E supplementation in cardiovascular disease have been conflicting, however. This may be due to the use of alpha-tocopherol exclusively. Studies show that supplementation with alpha-tocopherol depletes levels of serum gamma-tocopherol concentrations by a median change of 58%.69 Some evidence suggests that gamma-tocopherol is more potent than alpha-tocopherol in regard to decreasing platelet aggregation, delaying time to occlusive thrombus, decreasing arterial superoxide anion generation, decreasing lipid peroxidation and LDL oxidation, and increasing endogenous superoxide dismutase (SOD) activity.70 A clinical trial compared a mixed tocopherol preparation rich in gamma-tocopherol for eight weeks with alpha-tocopherol. The results showed that the mixed tocopherols were more potent in preventing platelet aggregation than alpha-tocopherol and modulating increased nitric oxide (NO) release and endothelial constitutive nitric-oxide synthase (ecNOS) activation.71 (Also see the previous section on tocotrienols.)

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