Vitamin E (2008) Neuroprotection by Vitamin E in Glaucoma


See other glaucoma vitamins & supplements.

Learn more information about glaucoma treatment and information.

Vitamin E is known as a major fat-soluble antioxidant. It intercepts free radicals preventing chain reactions of lipid destruction. However the discovery of complex molecules that control vitamin E metabolism fostered the idea that the vitamin E may be more than an antioxidant.

Vitamin E is now known to affect the expression and activity of immune and inflammatory cells, and to enhance dilation of blood vessels. It is also known to inhibit the activity of protein kinase C (PKC), a family of enzyme-like proteins enzyme that control other proteins and which plays a role in development of glaucoma. PKC inhibitors have been shown to relax the trabecular meshwork and to affect matrix metalloproteinase and PGF2 alpha, both of which can degrade cell structure).

Vitamin E and PKC could also have a vaso-regulatory effect in the retina. In different experimental models, retinal vascular dysfunction due to hyperglycemia was reportedly prevented by vitamin E via the diacylglycerol-PKC pathway1,2.

These findings prompted researchers at Istanbul University to evaluate the clinical potential of vitamin E in glaucoma patients. They reported prevention of visual field loss in this preliminary study, and conclude that vitamin E deserves further attention in preventing glaucomatous damage3.

Study Design and Methods
Thirty glaucomatous patients (60 eyes) with controlled IOP, were randomly divided into three groups. Group (A) received no vitamin E, while groups (B) and (C) were given a daily dose of 300 and 600 mg of vitamin E respectively, as d-alpha tocopheryl acetate for 12 months. Blood levels of vitamin E were measured via HPLC.

Disease progression for each subject was monitored via visual field measurements and color Doppler imaging of ophthalmic and posterior ciliary arteries at baseline, and at 6 and 12 months. Retinal blood flow of ophthalmic and posterior ciliary arteries was evaluated, and resistivity and pulsatility indexes were obtained. Mean deviation values for Fastpac visual fields were recorded at all time points, and the difference in mean deviation values calculated. The change in mean deviations of Groups (B) and (C) were compared with Group (A), and the Mann-Whitney U-test was employed for statistical analysis.

There were no significant differences between the groups in mean ages, IOP, best corrected visual acuities of 10/10 ratios and disease etiologies. The average differences between the pulsatility indexes (PI) and resistivity indexes (RI) of both ophthalmic arteries and posterior ciliary arteries of both supplemented groups were significantly lower than those of the non-supplemented groups at 6 months and 1 year. RI decreases observed in posterior ciliary arteries at both time points, and PI decreases observed in ophthalmic arteries at the 6th month were statistically significant.

Compared with those receiving vitamin E, non-treated subjects showed a statistically significant reduction in visual field (change in mean deviation) at 6 and 12 months).

  1. Kunisaki M et al. Vitamin E prevents diabetes-induced abnormal retinal blood flow via the diacylglycerol-protein kinase C pathway. Am J Physiol 269:239-46, 1995.
  2. Lee IK et al. d-alpha tocopherol prevents hyperglycemia induced activation of the diacylglycerol (DAG)-protein kinase C pathway in vascular smooth muscle cells by an increase in DAG kinase activity. Diabetes Res Clin Pract 45:183-90, 1999.
  3. Engin KN et al. Clinical evaluation of the neuroprotective effect of alpha tocopherol in glaucomatous damage. Eur J Ophthalmol 17:528-33, 2007.