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This page is meant to correct errors and explain misrepresentation about information presented to the public.
This page attempts to hold the medical field to a high standard.....the truth!

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Vitamin E does NOT Cause Prostate Cancer

Around Oct. 11th, 2011 there were various news organizations that reported a study that linked vitamin E usage to an INCREASED risk of prostate cancer. There are many news organization that followed suit in reporting this study.

Below is a video explaining why this is a misleading study.

 

 

Additional Information:

D- alpha- Tocopherol = GOOD
DL-alpha-Tocopherol = BAD (also BAD = all rac-alpha-tocopherol acetate, tocopherol acetate)

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D-alpha- Tocopherol = natural

DL-alpha- Tocopherol (or tocopheryl) = synthetic

all-racemic DL- alpha- Tocopheryl (acetate or succinate) = synthetic

D-alpha- Tocopheryl (acetate or succinate) = semi-synthetic

 

α-Tocopherol is an important lipid-soluble antioxidant. It performs its functions as antioxidant in what is known by the glutathione peroxidase pathway and it protects cell membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction. This would remove the free radical intermediates and prevent the oxidation reaction from continuing. The oxidized α-tocopheroxyl radicals produced in this process may be recycled back to the active reduced form through reduction by other antioxidants, such as ascorbate (vitamin C), retinol or ubiquinol.

Other forms of vitamin E have their own unique properties; for example, gamma-tocopherol is a nucleophile that can react with electrophilic mutagens.

Still, there are other functions that have also been recognized to be of importance. α-Tocopherol has a regulatory effect on enzymatic activities. For instance, protein kinase C (PKC), which plays a role in smooth muscle growth, can be inhibited by α-tocopherol. α-Tocopherol has a stimulatory effect on the dephosphorylation enzyme, protein phosphatase 2A, which in turn, cleaves phosphate groups from PKC leading to its deactivation, bringing the smooth muscle growth to a halt.

Vitamin E also has an effect on gene expression. Macrophages rich in cholesterol are found in the atherogenetic tissue. Scavenger receptor CD36 is a class B scavenger receptor found to be up-regulated by oxidized low density lipoprotein (LDL) and binds it. Treatment with alpha tocopherol was found to down regulate the CD36 scavenger receptor gene expression as well as the scavenger receptor class A (SR-A).

In addition to the effect it has been shown to have on SRA and CD36, α-tocopherol also has an effect on expression of the connective tissue growth factor (CTGF). CTGF gene, when expressed, is responsible for the repair of the wounds and regeneration of the extracellular tissue that is lost or damaged during atherosclerosis.

Moreover, vitamin E also plays a role in neurological functions, and inhibition of platelet aggregation and it has even been suggested that the most important function of vitamin E is as a signaling molecule.