haidut
Member
Hi all,
As you know Ray has written extensively on the benefits of Vitamin E though its actions as an estrogen antagonist. I opsted some studies that show that tocopherols act directly like estrogen "receptor" antagonist and this may explain some of their anti-estrogenic properties. However, receptor antagonists (e.g. cyproheptadine) typically do not decrease plasma levels of the hormone/substance they are antagonizing. So, I was wondering how come several studies with mixed tocopherols (escpecially a mix with high gamma contents) reduced plasma levels of estrogen. I just found this study that appears to confirm that in addition to being an estrogen "receptor" antagonist, tocopherols are also aromatase inhibitors - i.e. they also reduce the synthesis of new estrogen "in vivo".
http://www.fasebj.org/content/early/200 ... e.full.pdf
This would make vitamin E even more attractive substance for Peat-minded people since reducing estrogen (AKA the "shock hormone") is one of the main goals of the Peat-style diets and regimens. Interestingly, tocopherols were also found to suppress androgen signaling WITHOUT suppressing androgen metabolism. So, what other substance is known to have this effect - i.e. estrogen receptor antagonist, aromatase inhibitor, and anti androgenic? The answer is - progesterone!
And of course, not surprisingly, Peat and others scientists working with vitamin E have written extensively about its progesterone-like qualities and progesterone-sparing effects. So, in a sense, vitamin E is a surrogate for progesterone.
The study compared vitamin E to lycopene in terms of prostate cancer inhibition and found that lycopene has 5-alpha reductase inhibiting properties, while vitamin E did not. So, lycopene works similarly to the well-known "chemical castration" drugs like Finasteride (i.e. Propecia) while vitamin E does not.
I strongly recommend reading the full study, but for those that do not have the patience here are some notable quotes:
"...In contrast to lycopene supplementation, vitamin E treatment did not influence steroid 5-α-reductase expression in the prostate tumors. Vitamin E, however, significantly reduced aromatase expression, suggesting reduced estrogen synthesis. Also, in contrast to lycopene treatment, neither IGF-I nor the ROS generating iNOS or NADPH oxidase were affected by vitamin E. "
"...In the vitamin E-treated group, the reduced androgen target gene expression is in agreement with studies demonstrating that vitamin E inhibits the androgen receptor (25). In addition, vitamin E affected estrogen metabolism by down-regulating aromatase expression."
"...Vitamin E reduced androgen signaling without affecting androgen metabolism. Lycopene interfered with local testosterone activation by down-regulating 5-α-reductase and consequently reduced steroid target genes expression (cystatin-related protein 1 and 2, prostatic spermine binding protein, prostatic steroid binding protein C1, C2 and C3 chain, probasin)."
The human equivalent dosage for achieving these effects is about 7mg/kg - 9 mg/kg vitamin E. This is close to the human equivalents of 1g - 1.5g daily reported by the studies using the high-gamma mixed tocopherols (γ-TmT) for breast cancer listed below. Also of note, is the fact the vitamin E used was only alpha-tocopherol, not mixed tocopherols. This is in line with the other study I posted showing alpha-tocopherol to be an estrogen receptor antagonist.
Vitamin E is an estrogen receptor antagonist
Furthermore, the above dose of about 1.5g for a person of 100kg weight, matches well with yet another study on using gamma-tocopherol rich mixture to treat prostate cancer.
Dietary tocopherols inhibit PhIP-induced prostate carcinogenesis in CYP1A-humanized mice. - PubMed - NCBI
"...In the present study, we investigated the effects of different preparations of tocopherols on PhIP-induced prostate carcinogenesis. The dosages of γ-TmT (0.3% in diet) or δ-T, γ-T and α-T (0.2% in diet) were selected from the optimal doses observed in previous studies and correspond to the intake of 1.5 g or 1.0 g of tocopherols, respectively, for a person consuming 500 g of diet per day [20–22,27]. These doses, although higher than the nutritional level, have been reported to be nontoxic [28]. Dietary γ-TmT and δ-T were found to inhibit the development of mPIN lesions and related molecular events, while γ-T and α-T were less effective. The results suggest that the inhibitory effect of tocopherols involves the reduction in cellular oxidative and nitrosative stress and inhibition of the PI3K/ AKT signaling pathway."
Btw, the vitamin E used in this study was dl-alpha-tocopheryl acetate (Rovimix E50 brand). Peat wrote that DL-alpha-tocopheryl acetate has only about 50% of the activity of pure alpha-tocopherol. This suggests that if pure alpha-tocopherol is used, a person may be able to achieve the same effects with only half the dose used in the study.
Finally, since lycopene is found primarily in tomatoes and bright-colored vegetables like bell peppers - that may another reason to take it easy on the vegetable intake. Ray talks about tomatoes containing serotonin, and when you add lycopene with its "castration" properties I think this makes the case for avoiding the nightshades plants family even stronger.
Thoughts?
As you know Ray has written extensively on the benefits of Vitamin E though its actions as an estrogen antagonist. I opsted some studies that show that tocopherols act directly like estrogen "receptor" antagonist and this may explain some of their anti-estrogenic properties. However, receptor antagonists (e.g. cyproheptadine) typically do not decrease plasma levels of the hormone/substance they are antagonizing. So, I was wondering how come several studies with mixed tocopherols (escpecially a mix with high gamma contents) reduced plasma levels of estrogen. I just found this study that appears to confirm that in addition to being an estrogen "receptor" antagonist, tocopherols are also aromatase inhibitors - i.e. they also reduce the synthesis of new estrogen "in vivo".
http://www.fasebj.org/content/early/200 ... e.full.pdf
This would make vitamin E even more attractive substance for Peat-minded people since reducing estrogen (AKA the "shock hormone") is one of the main goals of the Peat-style diets and regimens. Interestingly, tocopherols were also found to suppress androgen signaling WITHOUT suppressing androgen metabolism. So, what other substance is known to have this effect - i.e. estrogen receptor antagonist, aromatase inhibitor, and anti androgenic? The answer is - progesterone!
And of course, not surprisingly, Peat and others scientists working with vitamin E have written extensively about its progesterone-like qualities and progesterone-sparing effects. So, in a sense, vitamin E is a surrogate for progesterone.
The study compared vitamin E to lycopene in terms of prostate cancer inhibition and found that lycopene has 5-alpha reductase inhibiting properties, while vitamin E did not. So, lycopene works similarly to the well-known "chemical castration" drugs like Finasteride (i.e. Propecia) while vitamin E does not.
I strongly recommend reading the full study, but for those that do not have the patience here are some notable quotes:
"...In contrast to lycopene supplementation, vitamin E treatment did not influence steroid 5-α-reductase expression in the prostate tumors. Vitamin E, however, significantly reduced aromatase expression, suggesting reduced estrogen synthesis. Also, in contrast to lycopene treatment, neither IGF-I nor the ROS generating iNOS or NADPH oxidase were affected by vitamin E. "
"...In the vitamin E-treated group, the reduced androgen target gene expression is in agreement with studies demonstrating that vitamin E inhibits the androgen receptor (25). In addition, vitamin E affected estrogen metabolism by down-regulating aromatase expression."
"...Vitamin E reduced androgen signaling without affecting androgen metabolism. Lycopene interfered with local testosterone activation by down-regulating 5-α-reductase and consequently reduced steroid target genes expression (cystatin-related protein 1 and 2, prostatic spermine binding protein, prostatic steroid binding protein C1, C2 and C3 chain, probasin)."
The human equivalent dosage for achieving these effects is about 7mg/kg - 9 mg/kg vitamin E. This is close to the human equivalents of 1g - 1.5g daily reported by the studies using the high-gamma mixed tocopherols (γ-TmT) for breast cancer listed below. Also of note, is the fact the vitamin E used was only alpha-tocopherol, not mixed tocopherols. This is in line with the other study I posted showing alpha-tocopherol to be an estrogen receptor antagonist.
Vitamin E is an estrogen receptor antagonist
Furthermore, the above dose of about 1.5g for a person of 100kg weight, matches well with yet another study on using gamma-tocopherol rich mixture to treat prostate cancer.
Dietary tocopherols inhibit PhIP-induced prostate carcinogenesis in CYP1A-humanized mice. - PubMed - NCBI
"...In the present study, we investigated the effects of different preparations of tocopherols on PhIP-induced prostate carcinogenesis. The dosages of γ-TmT (0.3% in diet) or δ-T, γ-T and α-T (0.2% in diet) were selected from the optimal doses observed in previous studies and correspond to the intake of 1.5 g or 1.0 g of tocopherols, respectively, for a person consuming 500 g of diet per day [20–22,27]. These doses, although higher than the nutritional level, have been reported to be nontoxic [28]. Dietary γ-TmT and δ-T were found to inhibit the development of mPIN lesions and related molecular events, while γ-T and α-T were less effective. The results suggest that the inhibitory effect of tocopherols involves the reduction in cellular oxidative and nitrosative stress and inhibition of the PI3K/ AKT signaling pathway."
Btw, the vitamin E used in this study was dl-alpha-tocopheryl acetate (Rovimix E50 brand). Peat wrote that DL-alpha-tocopheryl acetate has only about 50% of the activity of pure alpha-tocopherol. This suggests that if pure alpha-tocopherol is used, a person may be able to achieve the same effects with only half the dose used in the study.
Finally, since lycopene is found primarily in tomatoes and bright-colored vegetables like bell peppers - that may another reason to take it easy on the vegetable intake. Ray talks about tomatoes containing serotonin, and when you add lycopene with its "castration" properties I think this makes the case for avoiding the nightshades plants family even stronger.
Thoughts?
Last edited:
