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s8nlilhlpr
Banned
Anthony Roberts said:
You realize almost all vitamins are water soluble correct? A, D, E, K are the fat soluble ones that can build up to toxicity levels. Anything else just gets pissed out.....I'm curious why you don't know this?
R
Ross
Guest
tru dat
A
Anthony Roberts
Guest
s8nlilhlpr said:
I do know that. I never even mentioned toxicity...you (wrongly) assumed I was talking about that. However, the same mechanism which allows B6 to lower progesterone also makes it lower androgen transcription. Fairly common knowledge I thought.
Why would you want to lower androgen gene transcription?
During PCT that is the worst idea - ever. It's a terrible recommendation to include any b6 in your PCT over the RDA. Just like I said earlier. Sorry I didn't clarify why it's such a shockingly bad idea...I thought everyone was aware of that fact on B6, since I posted it on steroid.com several months ago.
Triple J
New member
the reason for using b6 to combat prolactin is that it is a direct precursor involved in dopamine formation, (increasing dopamine lowers prolactin) there are legit studies demonstrating its effectiveness for this. it is generally a good idea to support healthy dopamine levels during PCT as dopamine levels tend to fall with declining androgens.
i am doubtful of, and not aware of any studies in humans showing b6 lowers androgen gene transcription but willing to learn more on this topic, it certainly is not common knowledge to me
i am doubtful of, and not aware of any studies in humans showing b6 lowers androgen gene transcription but willing to learn more on this topic, it certainly is not common knowledge to me
A
Anthony Roberts
Guest
Triple J said:
J Biol Chem. 1992 Feb 25;267(6):3819-24.
Vitamin B6 modulates transcriptional activation by multiple members of the steroid hormone receptor superfamily.
Allgood VE,
Cidlowski JA.
Department of Physiology, University of North Carolina, Chapel Hill 27599-7545.
Recent studies have shown that vitamin B6 modulates transcriptional activation by the human glucocorticoid receptor in HeLa S3 cells. We have now examined the possibility that vitamin B6 might similarly influence transcriptional activation by the glucocorticoid receptor in other cell types, as well as gene expression mediated by other members of the steroid hormone receptor superfamily. We show that elevated vitamin B6 concentrations suppress by 40-65% the level of transcription mediated through the endogenous murine L cell glucocorticoid receptor, as well as the human receptor transfected into E8.2 and T47D cells. In contrast, glucocorticoid receptor-mediated transcription was enhanced 60-110% in mild vitamin deficiency. The level of hormone-independent constitutive gene expression was not affected by these same alterations in vitamin B6 concentration. These studies indicated that the transcriptional modulatory effects of the vitamin were neither restricted to specific cell types nor limited to the human form of the glucocorticoid receptor. We next determined if hormone-induced transcription by several other steroid receptors (androgen, progesterone, and estrogen receptors) was analogously affected by alterations in vitamin B6 concentration. Analysis of gene expression mediated through the mouse mammary tumor virus promoter revealed that transcriptional activation of both the androgen and progesterone receptors was reduced by 35-40% under conditions of elevated vitamin B6 and enhanced by 60-90% in deficiency, again under conditions where constitutive expression was unaffected. Using a different promoter, the estrogen-regulated vitellogenin promoter, we found that transcriptional activation of the estrogen receptor was similarly affected. Estrogen-induced gene expression was reduced by 30% under conditions of elevated intracellular vitamin B6 and enhanced by 85% in vitamin deficiency. Thus, vitamin B6 modulates transcriptional activation by multiple classes of steroid hormone receptors. The similarities in vitamin B6 effects on transcription mediated through different promoters, the mouse mammary tumor virus and vitellogenin promoters, suggest that this vitamin may modulate the expression of a diverse array of hormonally responsive genes. These observations together support the hypothesis that vitamin B6 represents a physiological modulator of steroid hormone action.
Triple J
New member
well thx for sharing that. its not enough information for me personally to jump to any conclusions though. it seems to also suggest a deficiency state would enhance transcription by 60-90%. so would you advise creating such a deficiency? obviously there are many factors that come into play so this is not a cut and dried issue.
A
Anthony Roberts
Guest
Triple J said:
Much more information is available.
I only looked this up originally because B6 had been recommended for so long that I thought it may operate on the entire superfamily of receptors, based on what I know of it. I found more than just this study, but I posted the one that I think proves my point the best.
So the short answer is that there is much more information available on this topic, in medical journals, and I think you'll agree with me that it's not a great thing to put additional amounts of in PCT.
If you take a look at what I said, I simply say that going over the RDA isn't a great idea, I don't say anything about creating a deficiency.
The degree to which it will help control progesterone is the degree to which it will hurt androgen transcription. So I think it's Cut and Dried as to whether you should use more than the RDA (you shouldn't).
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