Vitamin E - Antioxidant or Other Functions?

The following abstract is published here to show that other functions for vitamins might be more valuable than the obvious one. In this case, vitamin E functions are not always antioxidant driven.

J Cell Mol Med. 2004 Jan-Mar;8(1):59-76.

Anti-atherosclerotic effects of vitamin E--myth or reality?

Munteanu A, Zingg JM, Azzi A.

Source

Institute of Biochemistry and Molecular Biology, University of Bern, Bern, Switzerland.

Abstract

Atherosclerosis and its complications such as coronary heart disease, myocardial infarction and stroke are the leading causes of death in the developed world. High blood pressure, diabetes, smoking and a diet high in cholesterol and lipids clearly increase the likelihood of premature atherosclerosis, albeit other factors, such as the individual genetic makeup, may play an additional role. Several epidemiological studies and intervention trials have been performed with vitamin E, and some of them showed that it prevents atherosclerosis. For a long time, vitamin E was assumed to act by decreasing the oxidation of LDL, a key step in atherosclerosis initiation. However, at the cellular level, vitamin E acts by inhibition of smooth muscle cell proliferation, platelet aggregation, monocyte adhesion, oxLDL uptake and cytokine production, all reactions implied in the progression of atherosclerosis. Recent research revealed that these effects are not the result of the antioxidant activity of vitamin E, but rather of precise molecular actions of this compound. It is assumed that specific interactions of vitamin E with enzymes and proteins are at the basis of its non-antioxidant effects. Vitamin E influences the activity of several enzymes (e.g. PKC, PP2A, COX-2, 5-lipooxygenase, nitric oxide synthase, NADPH-oxidase, superoxide dismutase, phopholipase A2) and modulates the expression of genes that are involved in atherosclerosis (e.g. scavenger receptors, integrins, selectins, cytokines, cyclins). These interactions promise to reveal the biological properties of vitamin E and allow designing better strategies for the protection against atherosclerosis progression.

PMID: 15090261 [PubMed - indexed for MEDLINE]   -END

Analysis: Vitamin E research mainly concentrated on the anti-oxidant theory of disease. There were many positive results, such as the 71% reduction in second heart attacks during the CHAOS study, while some failed to show benefits, especially ones using the synthetic form of E, and a few found adverse effects at higher dosages after the initial study period. The authors of the above work missed the opportunity to mention that some of the other family members of vitamin E exhibit these same non anti-oxidant activities, often at a higher activity level than alpha tocopherol alone. **ref**  article

High dosages of only alpha tocopherol, whether natural or synthetic, can interfere with the absorption of the other vitamin E family members arriving in food. Alpha tocopherol is the only family member of vitamin E that can be called vitamin E. article The other members of the vitamin E family include; beta-, delta-, and gamma tocopherol plus alpha-, beta-, delta, and gamma tocotrienol. A - d' - precedes the natural vitamin E forms while a - dl'- precedes the synthetic vitamin E form, dl'alpha tocopherol. The L refers to the 50% of E molecules that came out forming backwards, mirror images, when synthetic E was formed in the Lab. This 50% reverse form reduce the biological actions of synthetic E.

Update on Wednesday, September 9, 2015 at 2:41PM by Team RightWay

It is of interest to know that while vitamin E family has full nutrition effects, the vitamin E form as succinate, the dry vitamin E form, is under consideration as a chemotherapic influence on many forms of cancer. It appears to be able to kill cancer cells while the nutritional form of vitamin E does not. ref

While this still needs further study, it looks very promising. Here on breast cancer. ref

ON CANCER

Another vital study on the Vitamin E family form with greatest anti-cancer effects. Copied here to prevent loss.

BMC Cancer. 2006 Jan 17;6:13.

Comparative effects of RRR-alpha- and RRR-gamma-tocopherol on proliferation and apoptosis in human colon cancer cell lines.

Campbell SE1, Stone WL, Lee S, Whaley S, Yang H, Qui M, Goforth P, Sherman D, McHaffie D, Krishnan K.

Abstract

BACKGROUND:

Mediterranean societies, with diets rich in vitamin E isoforms, have a lower risk for colon cancer than those of northern Europe and the Americas. Vitamin E rich diets may neutralize free radicals generated by fecal bacteria in the gut and prevent DNA damage, but signal transduction activities can occur independent of the antioxidant function. The term vitamin E represents eight structurally related compounds, each differing in their potency and mechanisms of chemoprevention. The RRR-gamma-tocopherol isoform is found primarily in the US diet, while RRR-alpha-tocopherol is highest in the plasma.

METHODS:

The effectiveness of RRR-alpha- and RRR-gamma-tocopherol at inhibiting cell growth and inducing apoptosis in colon cancer cell lines with varying molecular characteristics (SW480, HCT-15, HCT-116 and HT-29) and primary colon cells (CCD-112CoN, nontransformed normal phenotype) was studied. Colon cells were treated with and without RRR-alpha- or RRR-gamma-tocopherol using varying tocopherol concentrations and time intervals. Cell proliferation and apoptosis were measured using the trypan blue assay, annexin V staining, DNA laddering and caspase activation.

RESULTS:

Treatment with RRR-gamma-tocopherol resulted in significant cell death for all cancer cell lines tested, while RRR-alpha-tocopherol did not. Further, RRR-gamma-tocopherol treatment showed no cytotoxicity to normal colon cells CCD-112CoN at the highest concentration and time point tested. RRR-gamma-tocopherol treatment resulted in cleavage of PARP, caspase 3, 7, and 8, but not caspase 9. Differences in the percentage cell death and apoptosis were observed in different cell lines suggesting that molecular differences in these cell lines may influence the ability of RRR-gamma-tocopherol to induce cell death.

CONCLUSION:

This is the first study to demonstrate that multiple colon cancer cell lines containing varying genetic alterations will under go growth reduction and apoptosis in the presence of RRR-gamma-tocopherol without damage to normal colon cells. The amount growth reduction was dependent upon the molecular signatures of the cell lines. Since RRR-gamma-tocopherol is effective at inhibition of cell proliferation at both physiological and pharmacological concentrations dietary RRR-gamma-tocopherol may be chemopreventive, while pharmacological concentrations of RRR-gamma-tocopherol may aid chemotherapy without toxic effects to normal cells demonstrated by most chemotherapeutic agents.                     PMID: 16417629

Really makes one re-think the Government's position that only alpha tocopherol can be called Vitamin E or given vitamin E units. The FDA might have made a HUGE mistake in the 1940's with this decision and as a result, doomed many Americans to a less than healthy life.