AI's and Tren...Anthony Roberts?...Please Help...

[MrKadugen]

I am looking for a definitive answer on what to take with Tren ; which seems to be very hard to get.

I am prone to gyno, so I am cautious and during a cycle I normally take either an SERM or AI...

In a thread I read a post by Anthony Roberts (http://67.18.108.244//showthread.php...+arimidex+tren) on SERMs and AI's. In his post I read that he said Nolva will actually increase progesterone receptors (which would be very bad while taking tren), and that exemestane is the best AI to take. But I can only get Letro or Arimidex ...

Here is a quote by Anthony Roberts from the thread “Too much letro in Cycle?”:

“I also feel that some of the advice given in this thread (use of nolvadex with a Type-II AI) is less than optimal or well researched. In addition, since nolvadex increases progesterone receptors, using it along with a progestin like Tren is also less than optimal..in fact...it's plain horrible advice, in my opinion.

Ergo, based on the available research, I now feel the best single compound to run on a cycle for Aromatase Inhibition, is exemestane. This is all through alot of very recent research I'm doing on exemestane…”


So would it make sence to just take an AI (letro or arimidex) without Nolva while on Tren.

Here this might help too, my cycle is going to be as follows:

Week 1-4 - Dbol (35-45mg/ED)
Week 1-8 - Tren A (50 - 75 mg/ED)
Week 1-13 - Eq (400mg/wk)
Week 1-14 - Test-e (700mg/wk)

Would it be best to take letro (.25-.5mg ED) or Arimidex (.5-1mg ED) for the first 8 weeks while on tren, then switch over to nolva (10mg ED) and keep on letro (.25mg ED) or arimidex (.5mg ED) until my PCT (obviously taper off letro prior to PCT)?

I'm just trying to figure out ancillaries, so any help would be appreciated.

Thanks

[C_Bino]

I personally really like letro, you seem to know what you are doing. .25-.5mg ED letro is a good dose. There is no need to run Nolva at the same time as this as it will be pointless. Definitely taper off when coming into PCT and you are set.

-Bino

[Swifto]

I personally really like letro, you seem to know what you are doing. .25-.5mg ED letro is a good dose. There is no need to run Nolva at the same time as this as it will be pointless. Definitely taper off when coming into PCT and you are set.

-Bino

Enough said.

I'll add that you can run an AI/SERM but if its Arimdex/Letro with Nolva it isnt optimal. It will, however, cover every base and reduce the chances of estrogen related gyno greatly.

Progesterone related gyno can only arise when estrogen is present. So...Run an effective AI, one that is good at reducing estrogen, such as Aromasin /Letro/Arimidex and you'll reduce progesterone related gyno too. If I were to suggest a protocol to combat progesterone gyno it would be an AI in conjuction with Vit-B6 100-200mg/ED with Nolva on hand for estrogen related sides and covering every base, as above.

[C_Bino]

Enough said.

I'll add that you can run an AI/SERM but if its Arimdex/Letro with Nolva it isnt optimal. It will, however, cover every base and reduce the chances of estrogen related gyno greatly.

Progesterone related gyno can only arise when estrogen is present. So...Run an effective AI, one that is good at reducing estrogen, such as Aromasin/Letro/Arimidex and you'll reduce progesterone related gyno too. If I were to suggest a protocol to combat progesterone gyno it would be an AI in conjuction with Vit-B6 100-200mg/ED with Nolva on hand for estrogen related sides and covering every base, as above.

Great Post Swifto. In what scenario would you suggest running a SERM when you are already using an AI such as Letro? I have always gone by the idea that it is near pointless, not only will Nolva reduce the effectiveness of Letro but also since letro destroys 98+% of Estro, why would you need to block estrogen receptors if there is essentially no free floating estrogen in your system?

I would love to hear what you know about this, you always seem to know your stuff really well, good member.

-Bino

[velvetlion]

Let me make sure that I am getting this straight since I sometimes have a hard time seeing exactly how each of these works.

Nolva won't help because it only blocks the estrogen receptors, but you will still have free floating estrogen which is needed to cause progesterone gyno?

Is that statement correct or am I completely f***ed up on it.

[Swifto]

Great Post Swifto. In what scenario would you suggest running a SERM when you are already using an AI such as Letro? I have always gone by the idea that it is near pointless, not only will Nolva reduce the effectiveness of Letro but also since letro destroys 98+% of Estro, why would you need to block estrogen receptors if there is essentially no free floating estrogen in your system?

I would love to hear what you know about this, you always seem to know your stuff really well, good member.

-Bino

You've answered your own question. Letro does reduce estrogen levels by 98%, not 100%. Their is still free floating estrogen that may cause a problem, doubtful, but a reality IMO. So as you can see, running a SERM, like Nolva should cover every base. It all depends on how prone you are. I'm lucky.

Running an AI/SERM isnt optimal as using Nolva with Arimidex /Letro will reduce their effectiveness. Not much but its not optimal. Run an AI with a SERM on hand and use if needed.

Cheers bro.

[Swifto]

Let me make sure that I am getting this straight since I sometimes have a hard time seeing exactly how each of these works.

Nolva won't help because it only blocks the estrogen receptors, but you will still have free floating estrogen which is needed to cause progesterone gyno?

Is that statement correct or am I completely f***ed up on it.

That is, I believe, correct.

Reduce estrogen, using an AI and reduce the chances of estrogen AND progesterone related gyno. A SERM will block the estrogen at the receptor site, but the elevated estrogen is still evident.

[powerliftmike]

I like 0.2-.25mg ldex myself. I use nolva for pct.

[Swifto]

'powerliftmike' is floating about. He may be able to shed some light on it.

Please correct me if I'm wrong...? But thats my understanding.

[Matt2499]

How much exemestane would be needed if you are gyno prone while on a cycle with Tren ?? Any help here??

[C_Bino]

How much exemestane would be needed if you are gyno prone while on a cycle with Tren?? Any help here??

You should probably start your own thread about this. But since this one is done anyways I gues it doesnt matter. I think most people go with 25mg ED, up to 50mg. But I have never used it so I could be off.

-Bino

[Swifto]

From what I've seen reported, I'd start on 20mg/ED.

[Matt2499]

Sorry had no means in hijacking, its just it all relates to the broad topic and I am sure he wants to know as well..
So 20-25 mg ED...Wow, that would cost you a couple hundred dollars just for the Aromasin ..
Is there an EQUAL amount you could run with something like L-Dex??? How much L-Dex would it take to get similar results??
Swifto?? CBino???

[C_Bino]

From what I've seen reported, I'd start on 20mg/ED.

Swifto *cough* soon to be green *cough* always has to correct my newb ass. LOL, yes you should be ok with 20mg, I was merely saying anywhere from 25-50 is standard, you would not need more than that. Good luck. But honestly from my experience, I have said it many times I find Letro to be an amazing compound, I wouldnt be without it on a cycle, plus its cheap.

-Bino

[Rickson]

I am not sure if Hooker showed this in his discussion but I lifted this from Macro at AF.



was browsing s'ology and came across a thread with this study, it is quite interesting. and indicates that with progestin AI's alone are probably a far better choice than SERM or SERM+ AI.

J Steroid Biochem Mol Biol. 2005 May;95(1-5):83-9.

Aromatase inhibitors: cellular and molecular effects.

Miller WR, Anderson TJ, White S, Larionov A, Murray J, Evans D, Krause A, Dixon JM.

Breast Unit, Western General Hospital, Edinburgh, Scotland, UK. [email protected]

Marked cellular and molecular changes may occur in breast cancers following treatment of postmenopausal breast cancer patients with aromatase inhibitors. Neoadjuvant protocols, in which treatment is given with the primary tumour still within the breast, are particularly illuminating. In Edinburgh, we have shown that 3 months treatment with either anastrozole, exemestane or letrozole produces pathological responses in the majority of oestrogen receptor (ER)-rich tumours (39/59) as manifested by reduced cellularity/increased fibrosis. Changes in histological grading may also take place, most notably a reduction in mitotic figures. This probably reflects an influence on proliferation as most tumours (82%) show a marked decrease in the proliferation marker, Ki67. These effects are generally more dramatic than seen with tamoxifen given in the same setting. Differences between aromatase inhibitors and tamoxifen are also apparent in changes in steroid hormone expression. Thus, immuno-staining for progesterone receptor (PgR) is reduced in almost all cases by aromatase inhibitors, becoming undetectable in many. This contrasts with effects of tamoxifen in which the most common change on PgR is to increase expression. Changes in proliferation occur rapidly following the onset of exposure to aromatase inhibitors. Thus, neoadjuvant studies with letrozole in which tumour was sampled before and after 14 days and 3 months treatment show that decreased expression of Ki67 occur at 14 days and, in many cases, the effect is greater at 14 days than 3 months. These early changes precede evidence of clinical response but do not predict for it. However, this study design has allowed RNA analysis of sequential biopsies taken during the neoadjuvant therapy. Based on clustering techniques, it has been possible to subdivide tumours into groups showing distinct patterns of molecular changes. These changes in tumour gene expression may allow definition of tumour cohorts with differing sensitivity to aromatase inhibitors and permit early recognition of response and resistance

MP

[C_Bino]

I am not sure if Hooker showed this in his discussion but I lifted this from Macro at AF.



was browsing s'ology and came across a thread with this study, it is quite interesting. and indicates that with progestin AI's alone are probably a far better choice than SERM or SERM+ AI.

J Steroid Biochem Mol Biol. 2005 May;95(1-5):83-9.

Aromatase inhibitors: cellular and molecular effects.

Miller WR, Anderson TJ, White S, Larionov A, Murray J, Evans D, Krause A, Dixon JM.

Breast Unit, Western General Hospital, Edinburgh, Scotland, UK. [email protected]

Marked cellular and molecular changes may occur in breast cancers following treatment of postmenopausal breast cancer patients with aromatase inhibitors. Neoadjuvant protocols, in which treatment is given with the primary tumour still within the breast, are particularly illuminating. In Edinburgh, we have shown that 3 months treatment with either anastrozole, exemestane or letrozole produces pathological responses in the majority of oestrogen receptor (ER)-rich tumours (39/59) as manifested by reduced cellularity/increased fibrosis. Changes in histological grading may also take place, most notably a reduction in mitotic figures. This probably reflects an influence on proliferation as most tumours (82%) show a marked decrease in the proliferation marker, Ki67. These effects are generally more dramatic than seen with tamoxifen given in the same setting. Differences between aromatase inhibitors and tamoxifen are also apparent in changes in steroid hormone expression. Thus, immuno-staining for progesterone receptor (PgR) is reduced in almost all cases by aromatase inhibitors, becoming undetectable in many. This contrasts with effects of tamoxifen in which the most common change on PgR is to increase expression. Changes in proliferation occur rapidly following the onset of exposure to aromatase inhibitors. Thus, neoadjuvant studies with letrozole in which tumour was sampled before and after 14 days and 3 months treatment show that decreased expression of Ki67 occur at 14 days and, in many cases, the effect is greater at 14 days than 3 months. These early changes precede evidence of clinical response but do not predict for it. However, this study design has allowed RNA analysis of sequential biopsies taken during the neoadjuvant therapy. Based on clustering techniques, it has been possible to subdivide tumours into groups showing distinct patterns of molecular changes. These changes in tumour gene expression may allow definition of tumour cohorts with differing sensitivity to aromatase inhibitors and permit early recognition of response and resistance

MP

Thanks Rickson, I find some of it a little hard to understand, but I am always one to love reading new things. Appreciate it.

-Bino