i just read that taking trib products will negate the effect of nolva. any input of anything else to be avoided while on nolva would be appreciated. this is a real shocker to me as i regularly use a trib product on pct.
i got this from a post by dinoii. my aunt has cancer and is taking tamox, on the instructions it said notify doctor of any herbal supplements you are taking as they may negate the effects of the tamoxifen, then i read a post by dinoii saying same thing. believe me guys, i am shocked that this is true. i use trib on almost every pct. what i am pissed about is if this is true, why haven't people got the word out to us.Yeah I read youtr post in another thread that said this and I was searching google looking for any evidence on this claim and couldn't find anyone else saying that..
I just started my PCT with nolva and am taking trib.. So I'd like to get to the bottom of this as soon as possible.
i checked with dinoii, he says he can't recall saying trib has that effect, but says that dhea + nolva does= bad. maybe i got it wrong...thanks guys for setting me straight, i also use trib on pct.Well that's pretty standard for any prescription drug ,they want to know what all your taking incase there is any known problem. Just because it says to notify your doc of herbs ur taking doesn't mean any herb is going to negate the effects.. If you search for trib and nolca pct all you find is good reviews.. What did dinoii say? Have a link?
Dhea and nolva bad???? I seriously think you need to question your source.i checked with dinoii, he says he can't recall saying trib has that effect, but says that dhea + nolva does= bad. maybe i got it wrong...thanks guys for setting me straight, i also use trib on pct.
Yes.can i just take nolva by itself?
I recall Dr.D saying around week 3 its ok to start activate, but im not sure how this stands today though.how about Divanol in pct (mass fx, activate etc etc) I heard that taking these in PCT is bad because it actually just increases your free test and not you actual test, and your body reacts by having some shutdown. Has anyone ever heard this before and how much truth to this is there?
Dinoiii is a pretty smart dude. From what I can tell he deals w/all sorts of people coming off different AAS cycles and has lab reports on many different drugs used to bring the HPTA back. I believe that he says that the DHEA has some sort of estrogen activity that could negate/lower the effect of the SERM. I don't know at what dose he says this happens or to exactly what effect. If we can get him over here I'm sure he could explain 1,000,000x better. Or you could ask him in his own subforum, probably the easiest way to a good answer.Dhea and nolva bad???? I seriously think you need to question your source.
DHEA in PCT?
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: Mol Cell Endocrinol. 2003 May 30;203(1-2):13-23. Links
Evidence that dehydroepiandrosterone, DHEA, directly inhibits GnRH gene expression in GT1-7 hypothalamic neurons.Cui H, Lin SY, Belsham DD.
Department of Physiology, Toronto General Hospital Research Institute, University Health Network, University of Toronto, Medical Sciences Building 3247A, 1 King's College Circle, Toronto, ON, Canada M5S 1A8.
Dehydroepiandrosterone (DHEA) has been reported to have diverse effects on overall physiology, although its mechanism of action and specific receptor are not yet known. We have used the immortalized, clonal GT1-7 hypothalamic neurons to study DHEA effects on gonadotropin-releasing hormone (GnRH) gene expression. DHEA (10(-4) M) downregulates GnRH transcription by 39, 70 and 83% at 24, 36, and 48 h, respectively, while DHEA-sulphate had no effect. Hydroxyflutamide a specific androgen receptor (AR) antagonist, and cyproterone acetate or trilostane, both inhibitors of 3 beta-hydroxysteroid dehydrogenase/delta 4,5 isomerase, the rate-limiting enzyme for the conversion of DHEA to sex steroids, did not affect the ability of DHEA to downregulate GnRH gene expression. We found that GT1-7 cells did not express aromatase, thereby precluding conversion to estrogen. Analysis of [(14)C] DHEA metabolism by thin layer chromatography indicates that the main metabolites produced are 7 alpha- and 7 beta-hydroxy DHEA, and 7-oxo DHEA, although these steroids were not able to repress GnRH gene expression alone. Cell viability studies indicated that the transcriptional repression observed is not due to GT1-7 cell death. Interestingly, SV40 T-antigen mRNA levels, under the control of 2.3 kb of the rat GnRH gene 5' regulatory region, are also repressed by DHEA. Our studies indicate that DHEA has direct effects on GnRH transcription that appear to be unique from those observed after conversion to other steroidogenic compounds.
PMID: 12782399 [PubMed - indexed for MEDLINE]
Personally I don't listen to someone giving advice without ever having used an anabolic substance. First hand experience is worth 10x more than text book preachers. Anyone can read a book and say do this or don't do that, does that mean they're knowledgeable or that they can read out of a book?
Dr.D FTW
Patrick Arnold (knows his ****) basically laid out a pct protocol for superdrol in an MD mag just a few issues ago,I recall Dr.D saying around week 3 its ok to start activate, but im not sure how this stands today though.
Pat is a smart guy, and I like reading his articles. That pct idea looks like a great method.Patrick Arnold (knows his ****) basically laid out a pct protocol for superdrol in an MD mag just a few issues ago,
Week 1,2,3 - a "good dose" of a serm (tamox)
Week 4 - serm, plus an AI
Week 5,6,7 - AI, plus a SHBG binding compound
I had used Activate before for pct and had so-so results until the end of the bottle. But i figure i had so-so results because I used it right away post cycle, and like I said it worked better near the end of the bottle, it makes sense
You should probably actually know who your talking about without making generalizations.Personally I don't listen to someone giving advice without ever having used an anabolic substance. First hand experience is worth 10x more than text book preachers. Anyone can read a book and say do this or don't do that, does that mean they're knowledgeable or that they can read out of a book?
Dr.D FTW
Sorry to diss your boyfriend bro, I didnt think you'd take it that hard....:toofunny:You should probably actually know who your talking about without making generalizations.
Most if not all "cycle" planning is built off bits and pieces from studies completed by individuals who likely dont even weight train. So even though you "think" your not listening to someone who has never used an anabolic substance you are essentially following a cycle outlined by the same people.
Its okay though the corn people stilll love you. :hammer:
I saw it, pretty good read.Patrick Arnold (knows his ****) basically laid out a pct protocol for superdrol in an MD mag just a few issues ago,
Week 1,2,3 - a "good dose" of a serm (tamox)
Week 4 - serm, plus an AI
Week 5,6,7 - AI, plus a SHBG binding compound
I had used Activate before for pct and had so-so results until the end of the bottle. But i figure i had so-so results because I used it right away post cycle, and like I said it worked better near the end of the bottle, it makes sense
I'm not comparing anyone to anything, the topic kinda branched to "modern guru's" and I ran into that article. Take it or leave it I don't really care either way.Damn Trip. I have read some pretty good post from you before but are you seriously gonna try to compare Dana Houser (dinoiii) to Anthony Roberts? Thats just rediculous.
Unsubscribed to try to save myself from losing anymore IQ points.
Personally I don't listen to someone giving advice without ever having used an anabolic substance. First hand experience is worth 10x more than text book preachers. Anyone can read a book and say do this or don't do that, does that mean they're knowledgeable or that they can read out of a book?
Well, I apologize for that - this is NOT as easy a topic set as is often attempted to suggest as well. I ALWAYS ask for people to ask questions when they don't get something suggested however. Funny many may not ask, but will later suggest they have no idea what the hell I am talking about.D -
thanks for showing up over here. i enjoy reading your stuff....even though i don't understand most of it. lol.
Possibly, but I don't recommend DHEA in any event for many reasons - and I wouldn't be doing my job if I was merely offering experimental protocol to clients/patients now would I? But, hold on a second, I will expand upon this momentarily.would you say dhea + any serm = bad?
Again, possibly, but it is unnecessary.wouldn 't a smaller dose of dhea spaced between serm dosing help minimize interference?
Let's figure out what the hell is happening, shall we?HPTA-suppression typically leads to low levels of dhea. it seems like a perfect time to supplement with it.
it's just hard to ignore the hundreds of studies with millions of improved patcients backing up dhea supplementation.
and serum DHEA levels correlate better with sexual function in adult men better than any other homrone we mesure.
i personally feel much better using dhea in pct.
but if it really is bad i will change my ways.
You know the only theoretic suggestion that I could contribute here is that trib does, to some degree, promote elevations in DHEA (which is thought to be an alternative mechanism of action of the herbal favorite).What about Trib and Nolvadex?
funny, i'm one of those who has not asked but later admitted i had no idea what you were saying.I ALWAYS ask for people to ask questions when they don't get something suggested however. Funny many may not ask, but will later suggest they have no idea what the hell I am talking about.
experimental because it has not been published in a medical document?Possibly, but I don't recommend DHEA in any event for many reasons - and I wouldn't be doing my job if I was merely offering experimental protocol to clients/patients now would I?
i think i understand you here.Of course, cortisol is also LOW (contrary to the abuse of anti-cortisol agents due to lack of understanding of these pathways in the immediate post-cycle timeframe), but alas I digress...this is supplement advertising at its finest.
i thought only excess dhea in your system has the potential to convert to estrogen.Still, if you weigh out this adrenal compensation (ie. - supply of exogenous DHEA, et al) vs. estrogenic control (and the side effects that may result - ie. - gyno, et al), I would bet sacrificing the use of the SERM is NOT something many would be willing to become a test subject for.
Nope, but experimental because a controlled setting has not established adequate rationale for me to consider changing what I too have found to work just find with said individuals.experimental because it has not been published in a medical document?
Nothing is "proven" in science, merely "supported." But - sure there are no adequate labs comparatively supporting DHEA vs. placebo to merit people who didn't use DHEA would be any worse off.or experimental because you have never seen any lab results to prove benefitial or negative?
I said that they DID have effects - just NOT on the HPTA directly - Indirectly at best through the HPAA. Now, we also acknowledged in the above that a hypOadrenal state would experience improved mood overall - hence even recovery in depressed patients, HOWEVER, the trade-off when comparing anti-E (provided you are going to resort to SERM use) isn't worth it.Swale perscribes dhea to a lot of his hpta patcients.
he also seems to get favorable lab results showing significant improvement from his patcients. probably not a controlled setting, but i wouldn't think he wouldn't keep experimenting w/dhea if it didn't show some signs of benefit to his patcients.
Perhaps, because the protocol I'd employ is a reverse ramp with lowering the SERM while increasing the AI simultaneously. I know of no such studies suggesting interference between an AI and DHEA. Still, one could also suspect that the use of DHEA with adrenal recovery (about 2.5 weeks post-cycle in rather indiscriminate fashion verified by 24-hour urinary cortisol amongst a battery of challenge tests) would offer minimal in the realm of added benefit at that time also.i think i understand you here.
you are saying dhea use for cortisol suppression in the early stages of pct is unnecessary since cort levels are initially low?
what about later on when cort levels begin to climb?
Again, keep in mind this is an adrenal-predominate. The levels required and length of cycle for DHEA (especially for someone in an age less-than 65-70 years) has not nearly been scrutinized enough. In order to see significant effect, your oral dose has to be up there, but then consider blood sugar regulation, et al issues which would contribute to problems keeping gains into post-cycle as well.i thought only excess dhea in your system has the potential to convert to estrogen. if you are hpta suppressed with low dhea levels, wouldn't supplementing w/dhea (using only engough to bring levels up to normal) not directly translate to elevated estrogen levels?
What about transdermal DHEA where you get closer to 30-40% availability vs. oral (~3%)?Again, keep in mind this is an adrenal-predominate. The levels required and length of cycle for DHEA (especially for someone in an age less-than 65-70 years) has not nearly been scrutinized enough. In order to see significant effect, your oral dose has to be up there, but then consider blood sugar regulation, et al issues which would contribute to problems keeping gains into post-cycle as well.
D_
Usually just you and thesinner. And I guess me at your nerdly back and forth banter. lol jkMind you, my humor is pretty "raw" as I have been told, so you may not be dropping dead in laughter - but somewhere someone is laughing - probably me?!?
Why then the recommendation of dyslipidemia modifying agents in your PCT series?What's one of the sure-fire things we know about lipids during cycle? The quoted "deleterious" effects include: decreased HDL, increased LDL, increased Tot. Cholesterol, etc... However, knowing too that 99% of dyslipidemia is found at the level of the liver - meaning if we try and "treat" cholesterol issues, we are screwing up the fundamental endogenous correction factor put in place by the body to supply androgen substrate. IT IS THAT WAY FOR A REASON...high cholesterol is the origin of increased test - leave it alone, or you will have difficulty re-gaining control of endocrinologic balance -
No controlled setting under the same set of conditions unfortunately. Even the patent that exists for TD DHEA doesn't consider any condition that closely approximates post-cycle.What about transdermal DHEA where you get closer to 30-40% availability vs. oral (~3%)?
:fool2:Usually just you and thesinner. And I guess me at your nerdly back and forth banter. lol jk
Great question!Why then the recommendation of dyslipidemia modifying agents in your PCT series?
In saying that, are you saying that there are some people that have no apparent negative effects and are, basically, not affected by running cycles, no matter the toxicity of the "supp"?There are, for whatever reason, many people suffering from one of the inhereted five most clinically-significant dyslipidemia categorizations that opt to run cycles. For someone in this instance, keeping a close watch on said issues is and will forever be pertinent.
I was actually referencing that someone with one of these disorders is actually further burdened by the addition of PH/PS/DeS/AAS.In saying that, are you saying that there are some people that have no apparent negative effects and are, basically, not affected by running cycles, no matter the toxicity of the "supp"?
Dinoiii, I think it is fantastic to have an actual medical professional dispensing careful analysis instead of the kind of anecdotes that are the usual stock in trade. But I have to add something here and pardon me if I offend. I understand that one of your paramount messages is that the science is often far more complicated and nuanced than people in the AAS culture assume. I also am not surprised to read in threads such as this that people have a hard time understanding your postings. I have to tell you, as a person with 5 years of post-BA education (including an MA in linguistics), your writing is often d@mn-near impenetrable. And I don't believe it is only because the science is complicated. Your sytax is sometimes hard to follow, like someone who learned German before English.
I feel frustrated because I know that buried in the text is the gem of biochemical knowledge that is going to save my testicles, but it is buried.
Nome sayn?
Yeah, I get what your saying now...matter of a fact, if I had actually took time to read it again, i would have seen what you were conveying the first time....go figure on me, haha.I was actually referencing that someone with one of these disorders is actually further burdened by the addition of PH/PS/DeS/AAS.
In other words, they were already "screwed" and victims of their own pathology and the use of aides to keep these guys more in the normal range (whatever "normal" means) may be of benefit.
To the rest, probably no need for employment.
D_