The Estrogen-Blocking Vitamin
Vitamin E is an estrogen antagonist.
It was designated as an antioxidant by Big Pharma to hide the fact that estrogen is carcinogenic.
Most antioxidants are carcinogenic.
Otto Warburg told us cancer cells are oxygen-deficient.
That explains why ozone is used as cancer therapy.
Dr. Warburg didn’t say cancer cells have too much oxygen, requiring an antioxidant.
Estrogen is an antioxidant, and testosterone is an oxidant.
Cancer itself is an antioxidant disease.
(Cancer metastasis is an oxidant condition, but that’s explained in dozens of my other blog entries.)
Ray Peat (“Vitamin E: Estrogen antagonist, energy promoter, and anti-inflammatory,” 2006-2016) wrote …
“Keeping our diet as free as possible of the polyunsaturated fats, to create something like the ‘deficiency’ state that is so protective (against cancer, trauma, poison, shock, inflammation, infection, etc.) in the animal experiments, seems preferable to trying to saturate ourselves with antioxidants, considering the imperfectly defined nature of the vitamin E products, and the known toxicity of many of the other antioxidants on the market.”
Many other studies validate the one below. Google them and see for yourself.
H. Chen, D. Li, T. Saldeen, F. Romeo, & J.L. Mehta (“Mixed tocopherol preparation is superior to alpha-tocopherol alone against hypoxia-reoxygenation injury,” Biochemical and Biophysical Research Communications, Feb. 2002) wrote …
“We compared the effect of a mixed tocopherol preparation with that of alpha-tocopherol alone on superoxide dismutase (SOD) activity and iNOS expression in cultured myocytes exposed to H-R. Myocytes from Sprague-Dawley rat hearts were subjected to hypoxia for 24 h followed by reoxygenation for 3 h H-R. Parallel groups of myocytes were pretreated with alpha-tocopherol alone or a mixed-tocopherol preparation (containing alpha-, gamma-, and delta-tocopherols) (50 microM) for 30 min. H-R resulted in myocyte injury (determined by LDH release), a decrease in SOD activity and an upregulation of iNOS expression/activity. Both tocopherol preparations attenuated cell injury and markedly decreased the effects of H-R on SOD activity and iNOS expression/activity (all P < 0.05 vs H-R group, n = 5). However, mixed-tocopherol preparation was much superior to alpha-tocopherol in terms of myocyte protection from the adverse effect of H-R (P < 0.05). Lack of efficacy of commercial tocopherol preparations in clinical trials may reflect absence of gamma- and delta-tocopherols.”