The Estrogenic Effects of Trans-Resveratrol

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    The Estrogenic Effects of Trans-Resveratrol


    There's been the random mention in several threads on Resveratrol of estrogenic effects. I've yet to see any of it explained, though many people seem interested or concerned. I thought the topic should have its own thread. So lets have at it.
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    From what I recall one of the earliest studies on resveratrol in rats or mice showed estrogenic effects, but partially due the dosing protocol and how it was administrated it was largely discredited. mind you this is just vague memories talking
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    I'm actually wondering if it started as someone/people misconstruing the talk of resveratrol's binding affinity for estrogen receptors as being a negative. But then Dinoiii seems to have some further info, or at least clues that there's more going on. Hopefully we'll get some folks who have read AND understood the studies.
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    there definitely was one of the earliest studies that showed estrogenic effects. i'm working out of corporate office + meetings all day today, but if theres not more data here tonite i'll try and find it after my flight to seattle
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    This is a PM that Primordial Perf just sent me:

    The estrogenic potency of resveratrol is a very complex topic. I’ve been through hundreds of resveratrol studies yet have not found a simple way to explain its effects which would be relevant to the BB community. It all dependant on the cell type, cell health, other growth factors, transcriptional activity, ligands, res concentration, delivery method, ect. The bottom line is that Resveratrol is not going to cause the same side effects as high E2 no matter how much you take. It has estrogenic effects in some tissues, but the effects are vastly different because of the different co-factor activation and transcriptional activity of resveratrol. It plays very nicely and it does good things for the body.

    But I’ll tell you why you’ve been seeing so many questionable threads …

    One of our competitors just found out that we are advertising on this board, so he came here to start ‘negative’ threads about resveratrol. It seems silly, but this guy will go to any length to stir up trouble for us. I chose not to engage in his resveratrol threads since it always turns into a mudslinging fight that wastes everyone’s time. (that’s his only purpose anyway) If you notice, the ONLY negative study of resveratrol being a “super-estrogen” is from a 1997 study which was severely flawed (by use of ethanol as a drug carrier) and refuted by every subsequent study done since then.

    Hopefully this clears things up. You can post this up if you want.


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    yeah, that was the one I recalled, the ethanol carrier which none of the later studies showed the similar results
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    Easy, were you the one who was taking rediculous amounts of Trans-res for a while, like seven grams a day or some such?
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    4 g of 50% yes
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    Quote Originally Posted by EasyEJL View Post
    4 g of 50% yes
    How was it? Do you have a report of it anywhere? It'd really help me a lot to hear about it's effects outside of PCT.

    I'm thinking that it might be a good idea to run a heavy dose of res for a while by itself, with bloodwork. This way I'll have a better idea of what doses do what, or at least know what the effects of the res are, versus other things. Kind of running a PCT in pieces, so I've got a clearer image of what's going on when it's all together and needs to work.
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    Quote Originally Posted by bound View Post
    There's been the random mention in several threads on Resveratrol of estrogenic effects. I've yet to see any of it explained, though many people seem interested or concerned. I thought the topic should have its own thread. So lets have at it.
    Interesting indeed. Dinoiii made mention of this I think? I see Eric pmed u about it as well.

    I haven't seen any neg studies on it of course they are far and few but I did see one with mice involved. I wish it were a human trial but what can u do? Anyway I would like to hear from others too.

    But let me pose this question, do u take flaxseed oil? Its estrogenic too, but I think much like revs it doesn't impact the E2, is that right, someone can correct that if I am wrong.

    But no all estrogen is bad. Still interested in other posters thoughts.
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    Quote Originally Posted by bound View Post
    How was it? Do you have a report of it anywhere? It'd really help me a lot to hear about it's effects outside of post cycle therapy.

    I'm thinking that it might be a good idea to run a heavy dose of res for a while by itself, with bloodwork. This way I'll have a better idea of what doses do what, or at least know what the effects of the res are, versus other things. Kind of running a PCT in pieces, so I've got a clearer image of what's going on when it's all together and needs to work.
    I don't really have a good separate log as i'm an idiot and I put too many supplements together at once. So its buried in other logs. But I can say I noticed the difference SIGNIFICANTLY from when I was at 1g 50%/day to 2g/day to 4g/day. at 4g/day I sexually felt like I was 17 again
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    Understand the differences of ER-alpha and ER-beta.

    ER-alpha: receives proliferation signals from E2

    ER-beta: facilitates the return of ER-alpha to the nucleus and restores responsiveness to E2


    * While trans-resveratrol apparently harbors an inhibitory action on ER-alpha, the same can NOT be said for ER-beta. This is NOT going to contribute to short-term effects.

    This is one of the rationales as to why tamoxifen (though I still believe its negatives outnumber this as a positive) actually downregulates the ER-beta en route to treatment of breast cancer (cellular proliferation) as well as gyno (cell proliferation). This also offers up rationale as to why the so-called "delayed-gyno" scares existed some time back. ER-beta was likely not taken care of. If ER-beta is taken care of as well (almost an indiscriminate antagonism), you will actually prolong the refractory response to E2 in mammary tissue.

    Right now, resveratrol research is in its infancy, BUT we do know it does NOT seem to antagonize the ER-beta (this is a problem).


    If this doesn't make sense, feel free to continue the discussion below.


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    Wow I can usually understand most this stuff but that blew right by me.
    Does this basically mean that if you hit ER-alpha but not ER-beta there could be an E2 "rebound" type of effect when discontinued?
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    +1. Dinoiii, you lost me on that one, too.
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    LOL, I think I understand but not sure. I will re-read it a few times.

    U will break it down for us simpletons right D??
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    It inhibits ER-A- which is good right? It doesn't do that for the ER-B. We want it to inhibit ER-B as well correct?

    D, at some point I want to talk about Trans- Revs outside of PCT.
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    Thumbs up


    Quote Originally Posted by UNCfan1 View Post
    It inhibits ER-A- which is good right? It doesn't do that for the ER-B. We want it to inhibit ER-B as well correct?

    D, at some point I want to talk about Trans- Revs outside of post cycle therapy.
    This thread isn't just PCT oriented. As long as it's about Res, add what you want.
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    Quote Originally Posted by dinoiii View Post
    Understand the differences of ER-alpha and ER-beta.

    ER-alpha: receives proliferation signals from E2

    ER-beta: facilitates the return of ER-alpha to the nucleus and restores responsiveness to E2


    * While trans-resveratrol apparently harbors an inhibitory action on ER-alpha, the same can NOT be said for ER-beta. This is NOT going to contribute to short-term effects.

    This is one of the rationales as to why tamoxifen (though I still believe its negatives outnumber this as a positive) actually downregulates the ER-beta en route to treatment of breast cancer (cellular proliferation) as well as gyno (cell proliferation). This also offers up rationale as to why the so-called "delayed-gyno" scares existed some time back. ER-beta was likely not taken care of. If ER-beta is taken care of as well (almost an indiscriminate antagonism), you will actually prolong the refractory response to E2 in mammary tissue.

    Right now, resveratrol research is in its infancy, BUT we do know it does NOT seem to antagonize the ER-beta (this is a problem).


    If this doesn't make sense, feel free to continue the discussion below.


    D_
    thats what i was trying to say but no body cared to listen.. and before you say that one of the studies is for breast cancer cells and normal cells exhibit different properties, aren't SERMS designed to treat breast cancer.. so if tamoxifen citrate also works in normal tissue the way it does, why wouldn't resveratrol?


    Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Medical School, 303 E. Chicago Avenue, Chicago, IL 60611, USA.

    The phytochemical resveratrol, which is found in grapes and wine, has been reported to have a variety of anti-inflammatory, anti-platelet, and anti-carcinogenic effects. Based on its structural similarity to diethylstilbestrol, a synthetic estrogen, we examined whether resveratrol might be a phytoestrogen. At concentrations (approximately 3-10 microM) comparable to those required for its other biological effects, resveratrol inhibited the binding of labeled estradiol to the estrogen receptor and it activated transcription of estrogen-responsive reporter genes transfected into human breast cancer cells. This transcriptional activation was estrogen receptor-dependent, required an estrogen response element in the reporter gene, and was inhibited by specific estrogen antagonists. In some cell types (e.g., MCF-7 cells), resveratrol functioned as a superagonist (i.e., produced a greater maximal transcriptional response than estradiol) whereas in others it produced activation equal to or less than that of estradiol. Resveratrol also increased the expression of native estrogen-regulated genes, and it stimulated the proliferation of estrogen-dependent T47D breast cancer cells. We conclude that resveratrol is a phytoestrogen and that it exhibits variable degrees of estrogen receptor agonism in different test systems. The estrogenic actions of resveratrol broaden the spectrum of its biological actions and may be relevant to the reported cardiovascular benefits of drinking wine.
    PMID: 9391166 [PubMed - indexed for MEDLINE]
    Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Kentucky 40292, USA.

    Epidemiological evidence indicates that phytoestrogens inhibit cancer formation and growth, reduce cholesterol levels, and show benefits in treating osteoporosis. At least some of these activities are mediated through the interaction of phytoestrogens with estrogen receptors alpha and beta (ERalpha and ERbeta). Resveratrol, trans-3,5,4'-trihydroxystilbene, is a phytoestrogen in grapes that is present in red wine. Resveratrol was shown to bind ER in cytosolic extracts from MCF-7 and rat uteri. However, the contribution of ERalpha vs. ERbeta in this binding is unknown. Here we report that resveratrol binds ERbeta and ERalpha with comparable affinity, but with 7,000-fold lower affinity than estradiol (E2). Thus, resveratrol differs from other phytoestrogens that bind ERbeta with higher affinity than ERalpha. Resveratrol acts as an estrogen agonist and stimulates ERE-driven reporter gene activity in CHO-K1 cells expressing either ERalpha or ERbeta. The estrogen agonist activity of resveratrol depends on the ERE sequence and the type of ER. Resveratrol-liganded ERbeta has higher transcriptional activity than E2-liganded ERbeta at a single palindromic ERE. This indicates that those tissues that uniquely express ERbeta or that express higher levels of ERbeta than ERalpha may be more sensitive to resveratrol's estrogen agonist activity. For the natural, imperfect EREs from the human c-fos, pS2, and progesterone receptor (PR) genes, resveratrol shows activity comparable to that induced by E2. We report that resveratrol exhibits E2 antagonist activity for ERalpha with select EREs. In contrast, resveratrol shows no E2 antagonist activity with ERbeta. These data indicate that resveratrol differentially affects the transcriptional activity of ERalpha and ERbeta in an ERE sequence-dependent manner.
    PMID: 11014220 [PubMed - indexed for MEDLINE]
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    Quote Originally Posted by jasonschaffin View Post
    Wow I can usually understand most this stuff but that blew right by me.
    Does this basically mean that if you hit ER-alpha but not ER-beta there could be an E2 "rebound" type of effect when discontinued?
    More or less. And here I thought I watched my lingo in this one too.

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    Quote Originally Posted by UNCfan1 View Post
    It inhibits ER-A- which is good right? It doesn't do that for the ER-B. We want it to inhibit ER-B as well correct?

    D, at some point I want to talk about Trans- Revs outside of post cycle therapy.
    Blocking ER-B would yield a longer refractory response to E2, potentially lasting the length of a post-cycle therapeutic stance, so effectively YES.

    In the same breath...outside of the post-cycle timeframe, I am uncertain it matters, but then it may merely act as an expense outside of the life extension camps and sirt genes.



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    Quote Originally Posted by drksun View Post
    thats what i was trying to say but no body cared to listen..

    Hmmmm...perhaps you weren't talking loud enough??? Dunno...




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    Quote Originally Posted by dinoiii View Post
    Blocking ER-B would yield a longer refractory response to E2, potentially lasting the length of a post-cycle therapeutic stance, so effectively YES.

    In the same breath...outside of the post-cycle timeframe, I am uncertain it matters, but then it may merely act as an expense outside of the life extension camps and sirt genes.



    D_
    So if Resveratrol acts as a ER-b agonist, this will up regulate ER-a? But isn't ER-a being antagonized by the Resveratrol? What about trans- to cis- conversion in the liver? Isn't the cis- isomer more estrogenic? I know UV light will also cause the conversion.
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    Quote Originally Posted by jasonschaffin View Post
    Wow I can usually understand most this stuff but that blew right by me.
    Does this basically mean that if you hit ER-alpha but not ER-beta there could be an E2 "rebound" type of effect when discontinued?
    Quote Originally Posted by dinoiii View Post
    More or less. And here I thought I watched my lingo in this one too.

    D_
    So is there something else that can be used to complement the trans-res (something to work synergistically with it)?
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    Quote Originally Posted by stxnas View Post
    So is there something else that can be used to complement the trans-res (something to work synergistically with it)?

    I believe(but don't quote me) that piperin and iicarin both help extend the half-life or increase bioavailability of the res. I think one of the tough things about res is that it gets broken down rather quickly. One or two of the ingredients in AI's PCS complement the res, or you can go transdermal which helps, too, like Dermacrine Sustain. Both have very good reviews, and seem to have been used in conjunction pretty often in post cycle therapies.

    This is all stuff that I remember from reading, but do some searching to double check me. Also, try PM'ing CROWLER or PRIMORDIAL PERF, I'm sure that either of them would be happy to help you out with info, they're the reps for the two companies that I mentioned above.
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    I meant in reference to the apparent conundrum that is mentioned above...I appreciate the reply though...
    RcB Since 09-06-2011 20:55 EST, Post 49
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    OOOOooh. I get it. Took the question the other way, obviously.

    You mean something like I3C? (indol-3-carbinol)
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    Quote Originally Posted by drksun View Post
    So if Resveratrol acts as a ER-b agonist, this will up regulate ER-a? But isn't ER-a being antagonized by the Resveratrol? What about trans- to cis- conversion in the liver? Isn't the cis- isomer more estrogenic? I know UV light will also cause the conversion.
    Remember that there are different Estrogen Receptors corresponding to different types of Estrogens (E1, E2, E3). The predominant consideration here is that there is the same binding affinity with ER-alpha and ER-beta with resveratrol (which translates differently when considering E2-liganded alpha and beta), so the difference does NOT happen at the level of binding - BUT the transcriptional level (post-binding). So, effectively the answer is NO, ER-alpha is NOT being antagonized by resveratrol due to transcriptional differences.

    I am unsure whether an "up-regulation" in the truest sense (and often times this is the case, its not an upregulation of steroidal receptors but secondary to saturation of said receptors) occurs with ER-alpha in response to this process, but the discrpency still exists as I have illustrated in prior posts.


    As for quick answers to your latter questions:

    Yes, there is higher estrogenic action of the cis isomer, but guarantee of shunting to trans form via stability factors lies with the two mechanisms that mediate entrance into hepatic metabolism. Only one is a passive entrance into the hepatic cells and then a carrier-mediated one would account for the predominance. Thanks to this last process, resveratrol, while tightly bound to blood proteins (which is the transport medium apparent in many in-vivo models), could be largely delivered to body tissues, which is problematic still.

    cis conversion does NOT solely occur in the liver though as you already pointed out one of the major stability factors. In another thread on this board, Dr.D and myself have described some other fundamental issues here.



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    Quote Originally Posted by stxnas View Post
    So is there something else that can be used to complement the trans-res (something to work synergistically with it)?
    As far as OTC?


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    Quote Originally Posted by bound View Post
    I believe(but don't quote me) that piperin and iicarin both help extend the half-life or increase bioavailability of the res. I think one of the tough things about res is that it gets broken down rather quickly. One or two of the ingredients in AI's PCS complement the res, or you can go transdermal which helps, too, like Dermacrine Sustain. Both have very good reviews, and seem to have been used in conjunction pretty often in post cycle therapies.

    This is all stuff that I remember from reading, but do some searching to double check me. Also, try PM'ing CROWLER or PRIMORDIAL PERF, I'm sure that either of them would be happy to help you out with info, they're the reps for the two companies that I mentioned above.
    As discussed in the TD Form thread which had a lot of talk about TD Res, there are many fundamental flaws not being considered for whatever reason with this product.

    As for extension of half-life with Icariin and/or piperine, I would love to see that data. Understand that bioperine/piperine actually DECREASES bioavailability of certain substances and I am unsure that the patent-holder here has EVER released data with concurrent resveratrol administration. If so, I would ask to see that data as well.

    Trans-res to me as suggested for reasons in the TD form thread is a premature concept that holds little scientific weight the way that it is being purported and I will challenge anyone suggesting the contrary to show a lick of evidence to what is being suggested here. And, I mean credible 3rd party stuff...not some random in-house suggestion from data we'll likely never see.


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    Quote Originally Posted by bound View Post
    OOOOooh. I get it. Took the question the other way, obviously.

    You mean something like I3C? (indol-3-carbinol)
    I3C may cut off any ER-alpha issues in theory by shunting down various pathways and/or through its modest AI properties, but this is really going to be case-by-case dependent upon what we are talking about (PCT vs. NHA vs. Some other offering).


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    I believe you more or less answered my question with the post above (and yes I meant OTC products, if possible). I wasn't aware that there would be a difference in protocol for useage in pct vs an NHA stack for test boosting.

    Quote Originally Posted by stxnas View Post
    So is there something else that can be used to complement the trans-res (something to work synergistically with it)?
    Quote Originally Posted by dinoiii View Post
    As far as OTC?


    D_
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    Quote Originally Posted by stxnas View Post
    I believe you more or less answered my question with the post above (and yes I meant OTC products, if possible). I wasn't aware that there would be a difference in protocol for useage in post cycle therapy vs an NHA stack for test boosting.
    ALL supplementation schemes are case-dependent as are any/all PCT recommendations. A one-size-fits-all more often than not DOES NOT EXIST!!!

    We could even get into detail about different types of PCT and long-acting ester effects and the like, but for many a grandiose science presentation would likely make their head spin.


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    Hmm, never thought about it like that...I was more along the lines of looking at both instances as just trying to boost natty test production
    RcB Since 09-06-2011 20:55 EST, Post 49
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    Quote Originally Posted by dinoiii View Post
    As discussed in the TD Form thread which had a lot of talk about TD Res, there are many fundamental flaws not being considered for whatever reason with this product.

    As for extension of half-life with Icariin and/or piperine, I would love to see that data. Understand that bioperine/piperine actually DECREASES bioavailability of certain substances and I am unsure that the patent-holder here has EVER released data with concurrent resveratrol administration. If so, I would ask to see that data as well.

    Trans-res to me as suggested for reasons in the TD form thread is a premature concept that holds little scientific weight the way that it is being purported and I will challenge anyone suggesting the contrary to show a lick of evidence to what is being suggested here. And, I mean credible 3rd party stuff...not some random in-house suggestion from data we'll likely never see.


    D_
    This is one of the things that I'm still waiting for, too. I've read a few logs by folks whose PCT was based solely on RES products, but as usual with logs, no bloodwork. The first thing that I'm going to do with my new health insurance is get some bloodwork then use res for a while, and see what the numbers say.
    There does seem to be an awful lot of hope for it, but like you said, there just aren't any numbers.
    Thanks for the replies, Dinoiii, hadn't seen you around much.
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    Quote Originally Posted by bound View Post
    This is one of the things that I'm still waiting for, too. I've read a few logs by folks whose post cycle therapy was based solely on RES products, but as usual with logs, no bloodwork. The first thing that I'm going to do with my new health insurance is get some bloodwork then use res for a while, and see what the numbers say.
    There does seem to be an awful lot of hope for it, but like you said, there just aren't any numbers.
    Thanks for the replies, Dinoiii, hadn't seen you around much.
    My PCT for the 1-t cycle i'm on right now will be just the Dermacrine Sustain. It does have chrysin in it as well as a couple other ingredients I can't recall. I do have test, estradiol, fsh, and lh blood levels before cycle, and will take again after PCT
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    Quote Originally Posted by EasyEJL View Post
    My post cycle therapy for the 1-t cycle i'm on right now will be just the Dermacrine Sustain. It does have chrysin in it as well as a couple other ingredients I can't recall. I do have test, estradiol, fsh, and lh blood levels before cycle, and will take again after post cycle therapy
    You got a log going, or will you just post the results?

    edit: Nevermind, turns out there was a nice handy link in your sig that oddly enough, took me right to the log in question....
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    Quote Originally Posted by bound View Post
    You got a log going, or will you just post the results?

    edit: Nevermind, turns out there was a nice handy link in your sig that oddly enough, took me right to the log in question....


    the blood test results are sort of in the middle of the log, but the sample was taken before the start. I was clean of anything testosterone affecting for 2 weeks prior. I knew my test was that low, didn't realize estrogen was so high :P
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    Sorry to chime in out of nowhere, but I thought this might be as good a place as any. I've been lurking here and sifting through threads for a while, since I have been suffering from symptoms of hypogonadism for months and am currently using Dermacrine Sustain to help get my T levels back into a comfort zone, with some mild, inconsistent improvements. It turns out, though, that my Estradiol (E2) is way high as well (as is DHT), so I am looking into AI possibilities to drive down its levels.

    I understand that Estradiol is metabolized by the liver, and that cessation of E2 production does not mean immediate effects, since there remains E2 in the bloodstream. But the answer I can't seem to find anywhere is how long it takes for the liver to process or 'turn over' existing E2 in the system...? Does anybody have any clue about whether we're talkig days or weeks or months? I just really want to be able to evaluate by what point a treatment should be working or not.

    Any info appreciated!
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    Quote Originally Posted by bound View Post
    Easy, were you the one who was taking rediculous amounts of Trans-res for a while, like seven grams a day or some such?
    Im taking around 7 grams of 50% trans-resveratrol now, have been for a while. Im triple dosing AIs PCS as an everyday regime, not for post cycle therapy, as well as doing about 140mg ed of transdermal formestane. My test is naturally on the lower end though, Ill probably be throwing more into the mix (like dermacrine..which is transdermal pregnenalone and dhea) till I see my endo soon. So far so good at seven grams though. I found a good supplier for bulk 50% or 99% trans-resveratrol as well.
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    Quote Originally Posted by EasyEJL View Post
    My post cycle therapy for the 1-t cycle i'm on right now will be just the Dermacrine Sustain. It does have chrysin in it as well as a couple other ingredients I can't recall. I do have test, estradiol, fsh, and lh blood levels before cycle, and will take again after PCT
    The reasons I don't necessarily care for chrysin are:

    [1] Its usual comparative analysis is with aminoglutethimide (CYTADREN) a 1st gen, Type 2 compound. There are MUCH better AIs today.

    [2] The competitive inhibition of steroidal cytochorme systems makes for interesting steroidal metabolism - this can have an effect on long-acting esters as well as any complimentary steroidal post-cycle product.


    Being wary of these considerations is likely a more prudent approach because if it were up to me, there is no way I'd employ chrysin as monotherapy and call it a day.


    D_
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