Long-Term Use of High Doses of Vitamin E are Needed to Reduce Oxidative Stress

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Abstracted by Susan Sweeny Johnson, PhD., Biochem, from “The relationship between dose of vitamin E and suppression of oxidative stress in humans., Free Radic. Biol. Med.  November 15, 2007.

Conflicting reports on the efficacy of Vitamin E in preventing stroke or cardiovascular events (1) have been puzzling, since vitamin E is potentially a powerful antioxidant that appears to inhibit lipid oxidation and slow plaque formation in arteries (2).

To evaluate the cause of these conflicting studies, these researchers looked at how long a patient has to take vitamin E supplements to see changes in blood oxidation levels and what doses are necessary to achieve this result.

In the first time course study, 8 patients with blood cholesterol higher than 200 mg/dl and elevated levels oxidative stress were given 3200 IU per day of vitamin E (RRR-d-α-tocopherol acetate) for 20 weeks. Oxidative stress status was monitored over the course of the study by measurements of blood concentrations of F2-isoprostanes. F2-isoprostanes are prostaglandin-like compounds that are formed by free radical-mediated oxidation of arachidonic acid (3). A significant reduction from mean blood levels of F2-isoprostanes at week 0 (61.7±6.5 picograms/ml) did not occur until after 16 weeks of vitamin E supplementation (36.3±2.6 pg/ml) (p<0.005) and levels remained suppressed through weeks 18 and 20 (p<0.005). These results indicate that to see a reduction in oxidative stress, a patient must use vitamin E supplements for at least 16 weeks.

In the second dose study, 35 patients were given a placebo or 100, 200, 400, 800, 1600, or 3200 IU of vitamin E daily for 16 weeks. Their blood levels of F2-isoprostanes were measured at 0 and 16 weeks to determine what level of supplementation was necessary to achieve significant reduction in oxidative stress. There was a significant linear trend between dosage of vitamin E and percentage change in blood concentrations of F2-isoprostanes (p<001). When supplementation reached 800 IU per day, obvious suppression of F2-isoprostanes was observed (30±8%; p<0.094). Significant reduction in F2-isoprostanes was achieved at 1600 IU (35±2%; p<0.03) and 3200 IU (49±10%; p<0.005).

Therefore, in order to see any changes vitamin E supplementation might have on oxidative stress in a patient, they should be taking at least 800 IU per day and preferably 1600 IU per day for at least 16 weeks.

The authors of this paper reviewed numerous studies and found that many of them did not use enough vitamin E over a long enough period of time to see any significant results.

It should be noted that conflicting reports about the safety of taking more than 400 IU per day over extended periods of time (4,5) and the limited reduction in oxidative stress seen with 3200 IU per day supplementation (only 49%) suggest caution on the part of individuals seeking to support cardiovascular health.

Heart disease, stroke and other cardiovascular diseases remain the No. 1 killer of Americans and they are a major cause of permanent disability. More than 70 million Americans of all ages suffer from cardiovascular diseases. These diseases are major causes of permanent disability. Heart disease is the leading cause of premature, permanent disability among American workers. Cardiovascular diseases cost Americans more than any other disease, an estimated $394 billion for medical costs and lost productivity in 2005. Stroke will cost $57 billion. (6)

References:

  1. Vivekananthan, D. P.; Penn, M. S.; Sapp, S. K.; Hsu, A.; Topol, E. J. Use of antioxidant vitamins for the prevention of cardiovascular disease: metaanalysis of randomised trials. Lancet 361:2017–2023; 2003.
  2. Steinberg, D.; Parthasarathy, S.; Carew, T. E.; Khoo, J. C.; Witztum, J. L. Beyond cholesterol: modifications of low-density lipoprotein that increase its atherogenicity. N. Engl. J. Med. 320:915–924; 1989.
  3. Morrow, J. D.; Hill, K. E.; Burk, R. F.; Nammour, T. M.; Badr, K. F.; Roberts, L. J., II. A series of prostaglandin F2-like compounds are produced in vivo in humans by a non-cyclooxygenase, free radicalcatalyzed mechanism. Proc. Natl. Acad. Sci. USA 87:9383–9387; 1990.
  4. Bjelakovic, G.; Nikolova, D.; Gluud, L. L.; Simonetti, R. G.; Gluud, C.Mortality in randomized trials of antioxidant supplements for primary and secondary prevention. JAMA 297:842–857; 2007.
  5. Miller, E. R., III; Pastor-Barriuso, R.; Dalal, D.; Riemersma, R. A.; Appel, L. J.; Guallar, E. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann. Intern. Med. 142:37–46; 2005.
  6. NIH Heart Disease and Stroke Research: Fact Sheet

Cardiovascular Health-General & Misc., Vitamin E