How can your anti-e raise testosterone?

[HarryB]

Is "how is nolvadex going to help vet your test back quicker cos it's just an estrogen blocker?" A dumb question?

I'd do like realtalk.. test e 500 and I'd take the nolvadex if I started getting gyno. No harm in adding dbol but no real need to either.

Without being too dumb... my understanding is that nolvadex blocks estrogen but it doesn't have any effect on raising test levels. Neither does adex raise testosterone..

So I understand using these products to manage estrogen but I'm not clear on how they're going to raise your test levels post cycle any quicker than just waiting it out. Hcg for sure...

[maccaz]

Is "how is nolvadex going to help vet your test back quicker cos it's just an estrogen blocker?" A dumb question?

I'd do like realtalk.. test e 500 and I'd take the nolvadex if I started getting gyno. No harm in adding dbol but no real need to either.

Without being too dumb... my understanding is that nolvadex blocks estrogen but it doesn't have any effect on raising test levels. Neither does adex raise testosterone..

So I understand using these products to manage estrogen but I'm not clear on how they're going to raise your test levels post cycle any quicker than just waiting it out. Hcg for sure...

yeah my non scientific understanding was as test drops as ester tapers off, your test:estrogen ratio will go to shit as the test goes down but estro stays up, so nolvadex stops estro causing problems in this period, but doesnt actually help test increase

[Leeroid]

Excess estrogen provides negative feedback to the HPTA, inhibiting production of testosterone. In layman's term, if your estrogen is high, then your brain will think that there is no need to start making testosterone. That's why you want to control estrogen once you've finished your cycle and what makes PCT helpful in bringing testosterone production back faster than without them.

[HarryB]

But nolvadex doesn't stop production of estrogen like arimidex does so that estrogen is still in your system just not binding...and your body needs estrogen or... you can't cry..

And does it actually slow the bodies ability to get back to normal test production. I'd love to read a study

[Leeroid]

But nolvadex doesn't stop production of estrogen like arimidex does so that estrogen is still in your system just not binding...and your body needs estrogen or... you can't cry..

And does it actually slow the bodies ability to get back to normal test production. I'd love to read a study

No you're right, it doesn't stop estrogen from forming, however the nolva will bind to receptors in the pituitary (or hypothalamus, can't remember) and thus prevent estrogen from exerting it's effects there. Like I said, supraphysiological leves of estrogen will have a suppresive effect on the HPTA

[Daz69]

More on PCT: Clomiphene, stimulates the release of GnRH from the hypothalamus which then triggers release of FSH and LH from the anterior pituitary, causing the testes to produce testosterone...

This does happen even when serum testosterone levels are augmented.

However, this doesn't occur with other SERMs such as Tamoxifen, this is well documented in the literature.

 

Beyond this, however, using a SERM directly after cycle would help with, if not prevent to some degree, estrogen rebound. I understand that it is "all about the T to E ratio" but, as your testosterone levels begin to drop, that doesn't necessarily mean that your estrogen levels drop as well in a linear fashion with testosterone. In fact, it's more likely that as your testosterone levels decline, your estrogen levels, while beginning to decline, do so at a slower rate.

 

So, waiting the length of the half-life of whatever compound you're taking to begin PCT can theoretically be detrimental. Granted, your T to E ration could still be favorable, however, this doesn't negate the fact that if you're estrogen sensitive, you're still going to develop tremendous estrogenic side-effects from elevated estrogen levels.

 

Hence why I'd consider starting PCT (at least some sort of SERM or AI) directly after the end of my cycle. Testosterone is still being converted to estrogen, but estrogen levels are declining at a slower rate and as such, at a certain point, without any AI or SERMs, your estrogen levels actually end up being higher than testosterone levels after a couple of half-lives (assuming you don't start any PCT and don't cruise in-between cycles). Obviously, having your T to E ratio flipped is not desirable.

[Pseudonym]

Can someone explain the concept of the "T to E ratio"? I've never understood how this works in terms of the signals it sends to the body.

 

Testosterone functions by connecting with an androgen receptor, right? The AR receptor is switched on, and your body starts to build muscle. How does having more or less estrogen in your system affect that?

 

Similarly, if estrogen molecules are busily hooking up with their little estrogen receptors, why should they care how many testosterone molecules are around?

 

(I realise more test = more aromatisation = more estrogen, but that's not what the ratio is about, is it?)

[HarryB]

Ok so clomid use makes complete sense.. nolvadex to reboot test doesn't nor does the use of arimidex and yet these are the 2 things people seem to refer to most often when describing what they're going to implement post cycle to quick start their bounce back.

Yes managing your estrogen is desirable but it's the premis that using estrogen blockers (clomid isn't one is it?) is going to speed up test level return to pre cycle levels that I don't really agree with. Yeah so test to estrogen levels might be better quicker through using anti e. Although nolva doesn't actually shut production down so.... that estrogen is still getting produced and in your system. Then when you stop taking the nolva... there's all this unbound estrogen looking for manboobs to attach to

So perhaps an anti e with clomid or hcg... but an anti e on its own as a means for kick starting... I don't get it at all.

[yeelang]

More on PCT: Clomiphene, stimulates the release of GnRH from the hypothalamus which then triggers release of FSH and LH from the anterior pituitary, causing the testes to produce testosterone...

This does happen even when serum testosterone levels are augmented.

However, this doesn't occur with other SERMs such as Tamoxifen, this is well documented in the literature.

 

Beyond this, however, using a SERM directly after cycle would help with, if not prevent to some degree, estrogen rebound. I understand that it is "all about the T to E ratio" but, as your testosterone levels begin to drop, that doesn't necessarily mean that your estrogen levels drop as well in a linear fashion with testosterone. In fact, it's more likely that as your testosterone levels decline, your estrogen levels, while beginning to decline, do so at a slower rate.

 

So, waiting the length of the half-life of whatever compound you're taking to begin PCT can theoretically be detrimental. Granted, your T to E ration could still be favorable, however, this doesn't negate the fact that if you're estrogen sensitive, you're still going to develop tremendous estrogenic side-effects from elevated estrogen levels.

 

Hence why I'd consider starting PCT (at least some sort of SERM or AI) directly after the end of my cycle. Testosterone is still being converted to estrogen, but estrogen levels are declining at a slower rate and as such, at a certain point, without any AI or SERMs, your estrogen levels actually end up being higher than testosterone levels after a couple of half-lives (assuming you don't start any PCT and don't cruise in-between cycles). Obviously, having your T to E ratio flipped is not desirable.

 

heh seems we constantly have this debate, heaps of research showing nolva just as effective if not more than clomid, I posted this last time it was discussed.

 

Nolva and other serms just cause you to produce more test by stimulating/amplyfing LH.

 

Nolva is only going to work when you aren't taking AAS.

 

you can also boost test by lowering estrogen, the feedback loop for your HPTA factors in estrogen, so if estrogen is low you will produce more LH which = more test.

 

Test Estogen ratio isn't that important because it very personal, however general a lower body fat will = less test to estrogen ratio

[Riccardo]

Tamoxifen does increase testosterone levels, presumably by inhibiting the negative feedback loop at the level of the hypothalamus. Aromatase inhibitors also increase testosterone, if you are preventing the conversion of testosterone to estrogen then it is only logical that there will be more testosterone available.

http://press.endocrine.org/doi/abs/10.1210/jc.2003-031467

I still maintain that all these anti estrogens are superfluous if you taper off testosterone. They bring their own set of side effects and we don't fully understand the effects of their use in this context.

[jimmybro1]

Tamoxifen does increase testosterone levels, presumably by inhibiting the negative feedback loop at the level of the hypothalamus. Aromatase inhibitors also increase testosterone, if you are preventing the conversion of testosterone to estrogen then it is only logical that there will be more testosterone available.

http://press.endocrine.org/doi/abs/10.1210/jc.2003-031467

I still maintain that all these anti estrogens are superfluous if you taper off testosterone. They bring their own set of side effects and we don't fully understand the effects of their use in this context.

If you taper off at what rate would you taper? 

 

For example would you reduce the mg supplemented every half live on the compound by half.

 

If estrogen was to deplete slower than estrogen you wouldn't want to be dropping testosterone levels to fast.

 

I think tapering off does sound like a more practicable approach (less additional factors) although I am not experienced in this field. I know people that have tapered off an seem to have no re-bound issues nor estrogen issues but these things can be very individual I  would imagine.  

[Riccardo]

Arguably test E and the longer esters provide enough of a taper anyway so you could just stop cold turkey so long as your at least four half lifes deep sunce stopping any other compounds. But I don't think thats very sensible unless you're on a basic as shit <500mg per week test only. So i would say continue with normal frequency of pin and just decrease dose by half each time

[maccaz]

 

 

I think tapering off does sound like a more practicable approach (less additional factors) although I am not experienced in this field. I know people that have tapered off an seem to have no re-bound issues nor estrogen issues but these things can be very individual I  would imagine.  

 

this whole subject is super individual in my experience. I know heaps of people that just have no clue, stop cycle, no pct, and no negative effect whatsoever. some of them dont even lose much or any of the gains (go figure), I reckon this is just because of ester tapering down for them.

 

i think in a lot of cases, pct (and probably even tapering off) mitigates worse case kind of scenarios but isn't 100% necessary, good insurance but.

 

i would say to get back to a happy natural state, whatever way you can do it with the least drugs possible is ideal, so taper vs pct better if possible.

 

im talking real world results and best practice, not necessarily medically approved or daz science approved, just from people i know and what they have done.

 

inb4 big pharma and big UGL create myth of PCT to sell drugs, tinfoil hat, 9/11 was an inside job etc

[HarryB]

Studied group ranged from 67 to 74. Anything relevant to bodybuilders and steroid use?

Interesting read though and no doubt a whole lot of it applies but it's top many other variables for me to think it's conclusive. As for the tamoxifen test boosting .. anything I can read up on there?

[yeelang]

Studied group ranged from 67 to 74. Anything relevant to bodybuilders and steroid use?

Interesting read though and no doubt a whole lot of it applies but it's top many other variables for me to think it's conclusive. As for the tamoxifen test boosting .. anything I can read up on there?

 

Just search tamoxifen + LH it has been researched a lot. It's actually stronger than clomid in it's effect on LH

I taper most cycles out with a DHT drug to finish, no conversion so 2-3 weeks (4-5 weeks for tren) and any conversion/metabolites have cleared the system before you make the next move. I personally like to go up and down 250mg per 2 weeks you feel shitter for longer (general mood) but you can hold a lot more imo. It's basically the same approach to cutting/reverse dieting

[HarryB]

Just search tamoxifen + LH it has been researched a lot. It's actually stronger than clomid in it's effect on LH

I taper most cycles out with a DHT drug to finish, no conversion so 2-3 weeks (4-5 weeks for tren) and any conversion/metabolites have cleared the system before you make the next move. I personally like to go up and down 250mg per 2 weeks you feel shitter for longer (general mood) but you can hold a lot more imo. It's basically the same approach to cutting/reverse dieting

No offence intended here.. but are you very big?

[Riccardo]

Older gents with moderate hypogonadism are probably physiologically similar to bodybuilders off cycle hahahaha but in all seriousness, there is not a lot of individual variation here and you can't cheat human biology so I think its reasonable to extrapolate the literature to bodybuilders. There is plenty of other research showing the effects of serms and AIs on testosterone just search in google scholar. But you're right in the same vain as my previous comment about not knowing enough about these compounds in this particular context so while we can extrapolate a reasonable hypothesis, its better to take a conservative approach.

[Daz69]

heh seems we constantly have this debate, heaps of research showing nolva just as effective if not more than clomid, I posted this last time it was discussed.

 

Nolva and other serms just cause you to produce more test by stimulating/amplyfing LH.

 

Nolva is only going to work when you aren't taking AAS.

 

you can also boost test by lowering estrogen, the feedback loop for your HPTA factors in estrogen, so if estrogen is low you will produce more LH which = more test.

 

Test Estogen ratio isn't that important because it very personal, however general a lower body fat will = less test to estrogen ratio

 

You could be correct....  :smackbottom:

 

Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.

Vermeulen A, Comhaire F.

Abstract

The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.

[yeelang]

No offence intended here.. but are you very big?

 

No I'm 176 88-90kg 7-8% on 250mg/w 2iu/d.

[Daz69]

This is a link to the paper I was referencing, in my earlier post it is a direct comparison of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.

 

When the effect of clomiphene and tamoxifen on pituitary gonadotropin release was studied, it was found that clomiphene, "unlike tamoxifen, exert[ed] a direct estrogenic rather than antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin."1

 

1 Disparate Effect of Clomiphene and Tamoxifen on Pituitary Gonadotropin Release In Vitro http://www.ncbi.nlm.nih.gov/pubmed/6781360

 

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.

Adashi EY, Hsueh AJ, Bambino TH, Yen SS.

Abstract

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.

 

http://www.ncbi.nlm.nih.gov/pubmed/6781360

[Daz69]

Also in this study, "Off-label use of SERMs, such as clomiphene citrate, are effective for maintaining testosterone production long-term and offer convenience of representing a safe, oral therapy. At present, routine use of aromatase inhibitors is not recommended based on a lack of long-term data."1 2

 

1Treatment of Hyopgonadotropic Male Hyopgonadism: Case-Based Scenarios - http://www.ncbi.nlm.nih.gov/pubmed/25949938

2 Effect of Rejuvenation Hormones on Spermatogenesis - http://www.ncbi.nlm.nih.gov/pubmed/23663992

 

Here is another looking at Tamoxifens negative effects on IGF-1:

 

"Tamoxifen, a selective estrogen receptor modulator (SERM), possesses central estrogen antagonistic effect but peripheral hepatic agonist effect, lowering IGF-1. Thus, tamoxifen is likely to perturb the neuroendocrine regulation of GH and gonadal axes." The study found that Tamoxifen, but not raloxifene, significantly reduced IGF-1 levels by 25+/-6% and increased SHBG levels by 20+/-7% at a therapeutic dose. Tamoxifen did, however, increase Testosterone (40%) and LH (70%) levels.1

 

Moral of this is that an increase in testosterone production is good, yes. However, an increase in testosterone production with an even more dramatic increase in SHBG actually could reduce free testosterone levels... which is important as this is what has the highest bioavailability (what your body can actually use). If more testosterone is bound to SHBG in the blood then it isn't binding to and activating the AR, which means the activated AR complex isn't translocating to the nucleus where it can influence gene transcription and protein synthesis. So, an increase in total testosterone may sound great, but unless they provided information on the levels of free testosterone in relation to total serum testosterone and showed a significant increase in free testosterone in response to the tamoxifen treatment despite the increase in SHBG, one must be left to assume that there was a negligible change, if not decrease, in the amount of usable (free) testosterone. Also of note, IGF-1 levels declined by 19-31%! This is a huge factor to consider. Insulin is THE MOST anabolic hormone known to man, of which IGF-1 (insulin like growth factor 1) shares a very similar molecular structure. Such a large reduction in IGF-1 levels are certainty not going to be beneficial to maintaining an anabolic state.

 

Too many people like to oversimplify how testosterone works in the body and automatically assume that more testosterone is better. As a matter of fact, this is most definitely not the case. The level of free testosterone is a very different thing than the level of bound testosterone and total serum testosterone. Other factors that must be taken into account are AR expression, protein content, mRNA etc. Even if all factors are perfectly accounted for, there's still the possibility that an induction of gene transcription isn't taking place.. fact of the matter is that without this induction, you won't see diddly squat happen on a macro level. Just because an increase exists in any one of these or even all of these doesn't necessarily mean that you're going to experience gains. In actuality, there is far more to how our bodies grow than what we currently understand - just to throw this whole thing on its head, there was a study where it was shown that testosterone isn't even necessary for muscle growth..

 

1 Neuroendocrine Regulation of Growth Hormone and Androgen Axes by Selective Estrogen Receptor Modulators in Healthy Men -http://www.ncbi.nlm.nih.gov/pubmed/20843951

[Daz69]

MPS and mTOR signalling (among other pathways) isn't only stimulated by testosterone and/or AR-mediation, but by a whole variety of things from amino acids, medicinal pharms, nutritional supplements to the various growth hormones (MGF, insulin etc) and myostatin blockers. And of course we now know that many (perhaps all) AAS mediate some of their effect without interacting with the AR at all.

 

It's one reason getting bogged down in discussion of the 'perfect cycle' and the 'perfect steroid' - the often rather one-dimensional detail of AAS and their AR effect - as they do on most boards, is so myopic and uninteresting. It's why we need to focus on the whole range of dietary, hormonal and supplement strategies when optimising for maximal muscle growth (ie the big picture).

[HarryB]

Yeah I took yeelangs advice and Googled it. Interesting reading