Surprise! s Hopkins finds that Vitamin E (still) doesn't prevent aging......

[Guest guest]

It's funny you bring up the issue of "dosage", as there is beginning to emerge some data about contrasting effects of "high" and "low" dose. Mechanistic certainty is not a possibility in immediate future, but there are some that are beginning to notice some interesting immunologic "side effects" of vitamin E.

For instance, in this study, they found that low dose vitamin E helped mice suffering from a "runaway" immune system, but that high dose did not help. They also determined that high dose vitamin E inhibits IL-2 secretion, but enhances IL-4 and IL-10 production. These mice have a "lower than normal" amount of IL-2 to begin with, so the authors suggest that IL-2 reduction associated with high dose Vitamin E *promotes* inflammation. Yep, that's right, dose vitamin E right and you can imbalance your cytokines, leading to uncontrolled inflammation.

The authors suggest that high dose vitamin E, according to their data, would be detrimental in conditions featuring unmitigated immunologically-mediated inflammation, such as "lupus" (systemic lupus erythrematosus). However, the low dose of vitamin E, in this context, seemed to help.

All in all, studies such as this suggest that there is a *powerful* "law of dimishing returns" operating with this vitamin that is so frequently thought of as "innocuous".

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http://www.sciencedirect.com/science/journal/08999007

Opposite effects of low and high dose supplementation of vitamin E on survival of MRL/lpr mice

Chia-Chien Hsieh Ph.D. and Bi-Fong Lin Ph.D., Department of Biochemical Science and Technology, Institute of Microbiology and Biochemistry, College of Life Science, National Taiwan University, Taipei, Taiwan, Republic of China Received 13 July

2004; accepted 30 November 2004. Available online 27 July 2005.

Abstract

Objective

The purpose of this study is to investigate the effects of vitamin E supplementation on the autoimmune disease course in MRL/lymphoproliferative mice. Methods

Three-month-old MRL/lymphoproliferative lpr female mice were fed an AIN-76 diet containing 50 mg/kg (control), 250 mg/kg (E5), 375 mg/kg (E7.5), or 500 mg/kg (E10) all-rac--tocopheryl acetate. Eight mice per group were killed for analysis after two months of experimental diets, and the rest of the mice were followed up to observe their proteinuria levels and life span. Results

The data suggest that the life span of the E5 group was longer than the E10 group. Though á-tocopherol content in the plasma, liver, and kidneys increased in the mice fed the diet supplemented with vitamin E, the thiobarbituric acid reactive substance values in the liver and kidneys among these groups were not significantly different. IgM anti-ds-DNA and anticardiolipin antibodies were significantly higher in the E10 group than in those of the other groups. Phytohemagglutinin-stimulated interleukin (IL)-2 secretion was significantly lower, but concanavalinA-stimulated IL-4 and IL-10 production was significantly higher in the E10 group compared with the control group. The in vitro study also showed decreased IL-2 secretion and messenger RNA expression in phytohemagglutinin-stimulated splenocytes cultured in medium supplemented with high doses of vitamin E, but increased IL-2 with low doses of vitamin E. Conclusions

Our data suggest that low and high dose supplementation of vitamin E has the opposite effect on the survival of MRL/lpr mice. The inhibitory effect of Th1 from high vitamin E content may not be beneficial for those suffering from Th2 prone autoimmune diseases, such as systemic lupus erythematosus.

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T. pct35768@...

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