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Toremifene side effects

Excellent post bro!

I was on board until you said you would start an AI in week three of PCT and start it low, taper up, then taper down. Most people recommend starting the AI low in week one of PCT then tapering up and back down, or they recommend starting the AI in week three of PCT at a high dose and tapering down.

This is the first time I recall someone recommending you should start an AI in week three of PCT and taper the AI up then back down again. What is the rationale for dosing this way?

The rationale is simple: The #1 goal of PCT is re-starting the HPTA, right? Which in turn will return T and E levels to homeostasis. So, ask yourself this: if a supressive cycle has just been completed, do you think your HPTA function is fully restored by the end of PCT week 2? My opinion (and I'm sure many others would agree) - no!

So, that rules out starting a high dose of an AI in week 3. We don't want to completely crush E here, that may just further screw up the recovery process. E is important, as long as it isn't too high, and we want the body to achieve our natural levels. All we want here is just enough AI dose to keep E in check while T recovers (as explained before). We can assume that, as week 4 ends and so does the SERM, T should be at or nearly at full recovery. At this point, it makes sense to up the AI dose as explained in my last post, because messing with aromatisation now should not potentially hamper recovery; rather, it may indeed help it. Finally, it is prudent to then taper the AI back down to prevent a huge E rebound (should be self-explanatory).

As for starting an AI in week 1 of PCT - WHY?? There isn't much (if any) test to aromatise in the first place; what exactly is one hoping to accomplish? It may work for compounds that offer very little suppression (if there are any), or for very short cycles (if anyone even does that), but otherwise, it makes no sense.
 
Most of us who are opinionated on this topic have ran a few cycles. We preach what works for us and tend not to like what left us short of recovery or with side effects... so that's sort of a disclaimer that none of us have a "correct" answer that applies to everyone.

Legal designers do NOT aromatize. The majority of bloodwork that I've seen at the end of cycles shows lowered (and sometimes scary low) test AND estrogen levels. As natural test levels recover, so does the potential for natural test to aromatize.

The serm selectively prevents estrogen from binding to breast tissue even if estrogen levels are rising. Estrogen receptors in breast tissue become open game as it's tapered. So that's where some add in an AI and others (like GT) will start to ramp their AI. It's a safety net for gyno prevention.

Why you're so convinced that the AI is what causes the rebound is beyond my understanding. The only time I ever see post pct rebound occur (and with me personally) is/was with SD.

Very good post.
 
I understand that T and E will both be low at the start of PCT and will recover together, but if E is low at the beginning of PCT I don't see why it would be abnormally high be the end of your SERM run.

What I'm missing is why T is rising back to a desirable level while E is overshooting and going too high, thereby necessitating the AI?

If E isn't abnormally high at the end of SERM then won't using an AI take E back down too low? Now when you stop the AI which might be overly repressing E you're opening the door to the possibility of estro rebound. And now you don't have the SERM around to protect you from gyno.

That's my understanding of it. I am learning so I'm not saying I'm right by any means. but if I'm wrong I'm trying to understand where the flaw in my logic is.

I appreciate the time you guys are taking to help me learn.

You seem to be fixated on this "overshooting" concept. Understand that by using a SERM, you are using a strong pharmaceutical-grade drug to jumpstart T production. It may end up boosting your T to levels not naturally produced by your own body, yet obviously not to supraphysiological levels. So if your "normal" T level is maybe 600 ng/dl, and after 4 weeks of a SERM you read 800 ng/dl, E will have risen concurrently too. High T is good, obviously, but high E not so much. Again, perhaps the E level isn't clinically high, but high enough to perhaps cause problems.

There are also other growth factors to consider (prolactin for one) that I suspect may be enough to cause gyno if elevated, even in the presence of "normal" E levels. Further, there is the issue of androgen - estrogen imbalances, an issue I don't even fully understand, but suffice to say there is a theory that gyno can grow simply based on imbalances between T and E (provided the imbalance favors E) in certain individuals, even though neither level on its own would cause any alarm.

It's a very complicated issue when you get into it, but the take-home point is that it is a very real possibility that E needn't even be clinically "high" to cause a gyno flare up in the PCT environment. Controlling E is the key, hence AI use as a safeguard.
 
Everyone should state the pct philosophy that they are referring to in their post before continuing with a reply. I'm a bit slow today and it's tough to follow 4 or 5 theories at the same time :crazy:
 
As for starting ai in week on you make the ratio mucjh more favorable to test. When t levels rise around week 2 or 3 to near normal levels then stop the ai and keep the serm and watch homeostasis occur. Now u can run the ai through out pct just becareful not to let it go too low. E2 is a double edge sword too much is bad to little is bad. Its about equilibrium and the right levels for your body
 
yea im a broscientist as well my views are soo different from a lot of peopls though.

you have to realize some compounds shut you down more then others and its the ratio of T:E that will cause the problems and need to be fixed asap.

Agreed, trying to keep it simple by assuming a fairly severe shutdown.

its T:E ratio is sometimes shifted which is why bloodwork is and should be a must. estrogen causes negative feedback hindering recovery post cycle due to the ratio.

Provided E is high enough... but I'm not sure what your point here is?

5a reduced steriods have AI activity binding to receptors causing E2 to be lowered yet Estrone sulfate being freed from SHBG. tapering off a serm may not be nessecary its half life is around 5 days

OK, although tapering/not tapering the SERM is a different topic altogether.

"B) Introducing an AI will, of course, also boost test. As restoring natrural test is Goal #1 of PCT, this benefit is not insignificant by any means."

it will boost FHS which has a different function then LH

I've never heard of an AI's MOA being limited to boosting FHS independent of other androgens. Care to elaborate? Although, bottom line: AI use does boost absolute T levels. There is no debate on that.

EOD dosing seems to work well for me and most other people

This was suggested to me by GotTest and I found it worked well too.
 
Rebound doesn't necessarily happen to everyone. Most of the designers lower shbg which frees estrone sulfate that circulates and that may cause the rebound also upregulation of receptors after being binded to for and extended period may cause it. Its unknown
 
You seem to be fixated on this "overshooting" concept. Understand that by using a SERM, you are using a strong pharmaceutical-grade drug to jumpstart T production. It may end up boosting your T to levels not naturally produced by your own body, yet obviously not to supraphysiological levels. So if your "normal" T level is maybe 600 ng/dl, and after 4 weeks of a SERM you read 800 ng/dl, E will have risen concurrently too. High T is good, obviously, but high E not so much. Again, perhaps the E level isn't clinically high, but high enough to perhaps cause problems.

There are also other growth factors to consider (prolactin for one) that I suspect may be enough to cause gyno if elevated, even in the presence of "normal" E levels. Further, there is the issue of androgen - estrogen imbalances, an issue I don't even fully understand, but suffice to say there is a theory that gyno can grow simply based on imbalances between T and E (provided the imbalance favors E) in certain individuals, even though neither level on its own would cause any alarm.

It's a very complicated issue when you get into it, but the take-home point is that it is a very real possibility that E needn't even be clinically "high" to cause a gyno flare up in the PCT environment. Controlling E is the key, hence AI use as a safeguard.

Makes sense on paper. Problem is that a lot of the theories make sense on paper. From a noob's perspective the less popular protocols, like what you suggest, are less tested so I'd be a little more nervous to try it that way.

But with every new method that is explained (thank you for taking the time) my understanding improves.

Problem is unless you know exactly what your values are at any given time you're just guessing. Wouldn't it be nice if they had a home testing kit where you could check your values with a pin prick?

As for starting ai in week on you make the ratio mucjh more favorable to test. When t levels rise around week 2 or 3 to near normal levels then stop the ai and keep the serm and watch homeostasis occur. Now u can run the ai through out pct just becareful not to let it go too low. E2 is a double edge sword too much is bad to little is bad. Its about equilibrium and the right levels for your body
Are you suggesting you start SERM and AI together in week one then stop the AI in week 2-3 and keep the SERM going?

This is another protocol I don't recall seeing before.
 
As for starting ai in week on you make the ratio mucjh more favorable to test. When t levels rise around week 2 or 3 to near normal levels then stop the ai and keep the serm and watch homeostasis occur. Now u can run the ai through out pct just becareful not to let it go too low. E2 is a double edge sword too much is bad to little is bad. Its about equilibrium and the right levels for your body

But if we assume a very suppressive cycle... does dropping aromatase activity from next-to-nothing to microscopic levels have any real benefit? No androgens/test = no aromatase.
 
But if we assume a very suppressive cycle... does dropping aromatase activity from next-to-nothing to microscopic levels have any real benefit? No androgens/test = no aromatase.

Yes. That's how the no serm with a tapered AI pct philosophy works. It's also the basis of those who taper BOTH serm and AI at the same time.

You trick the body into elevating test. By futher lowering estrogen, the body tries to boost both test and estrogen to reach homestasis. That's how the AI only philosophy is/was marketed anyway.
 
Yes. That's how the no serm with a tapered AI pct philosophy works. It's also the basis of those who taper BOTH serm and AI at the same time.

You trick the body into elevating test. By futher lowering estrogen, the body tries to boost both test and estrogen to reach homestasis. That's how the AI only philosophy is/was marketed anyway.

See, I understand that philosophy as it relates to some designers that apparently aren't very supressive (or so some claim). If test is still being produced then an AI could have benefit.

But again, if we assume a very supressive cycle, and T and E are both in the shitter, how can we trick the body into anything if there is virtually no aromatase activity in the first place?
 
Agreed, trying to keep it simple by assuming a fairly severe shutdown.



Provided E is high enough... but I'm not sure what your point here is?



OK, although tapering/not tapering the SERM is a different topic altogether.

"B) Introducing an AI will, of course, also boost test. As restoring natrural test is Goal #1 of PCT, this benefit is not insignificant by any means."


your right provided E is high enough but homeostasis occurs with a ratio of T:E


I've never heard of an AI's MOA being limited to boosting FHS independent of other androgens. Care to elaborate? Although, bottom line: AI use does boost absolute T levels. There is no debate on that.
no its not limiting to that LH boost isnt as much as lets say an anti androgen like ATD. plus yes it DOES increase Test the most ive seen an increase is 60 % but thats only with aromasin, i have not seen an actuall percentage of test increase with any other AI.


This was suggested to me by GotTest and I found it worked well too.

kk...
 
See, I understand that philosophy as it relates to some designers that apparently aren't very supressive (or so some claim). If test is still being produced then an AI could have benefit.

But again, if we assume a very supressive cycle, and T and E are both in the shitter, how can we trick the body into anything if there is virtually no aromatase activity in the first place?

Even if you took nothing in general, once your exogenous circulating androgen levels drop off to a certain point your body kicks in its upregulation mechanism fairly swiftly (GnRH, LH and FSH secretion). I just think that so many guys are having issues with PCT because of the aggressive nature in mitigation of some of these PCT protocols. Hormonal balance is so fragile in nature that even mild alterations can/will be very significant.

There are many other cofactors that potentially play a role in the equation as well (i.e, SHBG, Prolactin, Progesterone). Without blood work to follow each individual case, there is no way to say for certain how to formulate a truly effective individual treatment modality.
 
This is some of the best posting about this subject I've ever seen. And I've been looking for a long time now.

Two things I think I've settled on. I will for sure use an AI (Formex) along with Torem in my PCT and I will not use the AI in week one of PCT.

So I need to settle on my Torem dosing. I'm thinking something like 120x2, 90, 60x4/60/60-or-30/30.

And I need to figure out when to introduce the Formex. I'm thinking 0/25/50/50/25/25.

I also ordered some I3C. Is 400 ED for the first four weeks good or should I run it for all six weeks until I'm done with the AI?

Wish I could give more rep :)
 
See, I understand that philosophy as it relates to some designers that apparently aren't very supressive (or so some claim). If test is still being produced then an AI could have benefit.

But again, if we assume a very supressive cycle, and T and E are both in the shitter, how can we trick the body into anything if there is virtually no aromatase activity in the first place?

its not just aromatase activity that we are talking about ...

yea there wont be much T aromatising in the beggining but E2 is probably in the 20's which is normal when your T levels are 200-800ng but that isnt the case when you come off cycle,

my t and e levels were 36 and 22 respectivly, so i included a SERM which would bring up test (and in some cases it CAN bring up e2 levels) and i incorperated an AI EOD to make sure it stays in normal levels. once T levels return to normal there is always natural aromatization occuring how much? im unsure, but i would like to keep most of my T as T and make sure minimum amounts of t are lost due to aromatization.

You haver to be aware of how your bodsy reacts, Im not saying kill E2 in the begining im saying control it lower it a little, make the ratio more favorable until T rises and then let E2 return to normal while continueing the SERM, OR you can run it throughout the PCT with the SERM and it all depends on how you feel

i like aromasin but last time i used Adex, i really was not a fan of how it mad me feel, id rtather use adex on cycle then pct, but either at certain doses will do the trick. it comes down to kmnowing your body as ive said earlier of course your not gunna say "hey i feel like **** today it must be my e2 levels" but you have to know how these things work and BLOODWORK is the best way to do that.

as far as this statement is conserned...

There are also other growth factors to consider (prolactin for one) that I suspect may be enough to cause gyno if elevated, even in the presence of "normal" E levels. Further, there is the issue of androgen - estrogen imbalances, an issue I don't even fully understand, but suffice to say there is a theory that gyno can grow simply based on imbalances between T and E (provided the imbalance favors E) in certain individuals, even though neither level on its own would cause any alarm

prolactin being hiugh and causing gyno is usually only the case with elevated E2 levels. Prolactin is a peptide hormone that needs other growth factors concurrently to function (IGF1, GH) so you will most likely not leak if the other growth factors are present.

Even if the balance is in favor of t, gyno can occur. it comes down to how your own body reacts to those levels. some people will not experience gyno at higher e2 levels because they arent prone to it. some will even at normal levels.
 
Torem has AI properties according to one study i saw which means formex may not even be neccessary but dont rule it out as of yet.

I'd love to save the Formex for a standalone run because I hear it works well alone.

But the vast majority of people recommend using an AI. Maybe they just aren't as knowledgeable about Torem. As always I'm all ears to anyone who can intelligently comment about this.

Did I mention how great this thread is? ;)
 
See, I understand that philosophy as it relates to some designers that apparently aren't very supressive (or so some claim). If test is still being produced then an AI could have benefit.

But again, if we assume a very supressive cycle, and T and E are both in the shitter, how can we trick the body into anything if there is virtually no aromatase activity in the first place?

You're probably right. Based on the scenario you described, I would start with a more aggressive dose of clomid to stimulate hpta activity. In which case, I'd follow the AI ramp method starting day 1, peak dosage at week 4 and taper for 2-3 more weeks depending on which AI. In my opinion, Clomid has the potential to boost test quickly since it has a higher affinity for E receptors in the brain. So ya man, i'd have a low dose AI in there right away.

With other serms (nolva, torem) wich have a higher affinity for breast tissue, I'd like to think I could introduce an AI taper at week 2 or 3 or even 4ish of pct.

Edit: typo corrected. Thanks Dragon :study:
 
i may have posted the study on torem in this thread

ive only found like 3-4 abstracts on torem and HPGA recovery. which IMO isnt enough so i dont use it. even though its SIMILAR to nolva its NOT nolva
 
i may have posted the study on torem in this thread

ive only found like 3-4 abstracts on torem and HPGA recovery. which IMO isnt enough so i dont use it. even though its SIMILAR to nolva its NOT nolva

You're not saying Torem is not advised are you?

I don't know about the studies but wouldn't you agree that there is overwhelming anecdotal evidence supporting Torem's efficacy in PCT?
 
You're not saying Torem is not advised are you?

I don't know about the studies but wouldn't you agree that there is overwhelming anecdotal evidence supporting Torem's efficacy in PCT?

it is advised, but for me to use it there isnt enouygh studies done on it.

its more potent then nolva and less toxic (toxicity is blown outta proportion on the length we use it though)
 
You're probably right. Based on the scenario you described, I would start with a more aggressive dose of clomid to stimulate hpta activity. In which case, I'd follow the AI ramp method starting day 1, peak dosage at week 4 and taper for 2-3 more weeks depending on which AI. In my opinion, Clomid has the potential to boost test quickly since it has a higher affinity for E receptors in the brain. So ya man, i'd have a low dose AI in there right away.

With other AI's (nolva, torem) wich have a higher affinity for breast tissue, I'd like to think I could introduce an AI taper at week 2 or 3 or even 4ish of pct.

Celc I think you got mixed up? Clomid, Nolva, and Torem are all SERMs, not AIs.

Edit - CrazyFool I will reply again tomorrow. Gotta run.
 
Reading this thread makes my head explode with different ideas and knowledge. I would like to see what everyone thinks of PP's plan to run a low dose SERM and their PP recovery stack together. Not necessarily just PP reps either ;). Im curious with the whole AI-SERM relationships I keep reading about. Facinating stuff, I hope posting doesnt stop anytime soon.
 
I think its good. But low dosed serms (ie 25mg clomid) hasn't been used in recovery. 50+ mg have neen used and shown effective. I also don't know much on gabaergic modulation I can't find enough about it that I understand
 
Its probably the hypothetical route I would go if I ever cycle anything.

I mean, I read up on HCG, and no, Im not getting all my info from that PP post about PCT, and it seems like a Godsend. I mean, keeping your testes large and active throughout the cycle and makign PCT a breeze no? Whats the deal? It says its not needed in stacks shorter than 8 weeks but need is relative. Id rather be more aggressive and make sure it goes well.

Clomid seems better suited to a non aromatizing PH since E can be monitored with an AI if needed once levels return and it seems to be more popular for bringing sexy/nuts back faster. Thats how Ive seen it but I also notice PP lists this one last in the desireable category? Reasons? Ive heard it makes people extremely emotional, which would suck ass to say the least.

And finding a reliable online source sucks ass.
 
Reading this thread makes my head explode with different ideas and knowledge. I would like to see what everyone thinks of PP's plan to run a low dose SERM and their PP recovery stack together. Not necessarily just PP reps either ;). Im curious with the whole AI-SERM relationships I keep reading about. Facinating stuff, I hope posting doesnt stop anytime soon.

It's really far more complicated than most people think. I've recommended that PCT stack before, and i like the dynamic it provides. I'm not a clomid fan, and i'm not going to get into why because it's been discussed a million times before. Torem or Nolva would work well with the stack.

The bottom line here is this. We can sit here all day long and speculate about what modality to use, but in reality, it's completely irrelevant without blood work to support it; every situation is very much unique, and this is why results with the same protocol can and will vary. I think there can be a general guideline that people should follow to cover the basics (which i think is what we're eventually getting at here), but there are so many unknown variables that can be part of the equation. Part of the problem i see all the time is people that attempt to mitigate every potential aspect even when it's not warranted during PCT.

I do like the role of SERM during PCT; especially if you're very suppressed to begin with. The dosing guidelines i see people recommend sometimes though are ridiculous. I used fareston (Toremifene) myself (not going higher than 60mg/day even in the beginning) during my last PCT. It was probably the best PCT i've had to date.
 
It's really far more complicated than most people think. I've recommended that PCT stack before, and i like the dynamic it provides. I'm not a clomid fan, and i'm not going to get into why because it's been discussed a million times before. Torem or Nolva would work well with the stack.

The bottom line here is this. We can sit here all day long and speculate about what modality to use, but in reality, it's completely irrelevant without blood work to support it; every situation is very much unique, and this is why results with the same protocol can and will vary. I think there can be a general guideline that people should follow to cover the basics (which i think is what we're eventually getting at here), but there are so many unknown variables that can be part of the equation. Part of the problem i see all the time is people that attempt to mitigate every potential aspect even when it's not warranted during PCT.

I do like the role of SERM during PCT; especially if you're very suppressed to begin with. The dosing guidelines i see people recommend sometimes though are ridiculous. I used fareston (Toremifene) myself (not going higher than 60mg/day even in the beginning) during my last PCT. It was probably the best PCT i've had to date.

Good post.

From what I gather it seems like 60 is the sweet spot for Torem. But quite a few people advise elevated doses for the first 2-4 days. Whether or not you think it's good/bad advice, do you think there's any downside to starting Torem with something like 120x2 + 90x2 before you drop down to 60?
 
i have major shut down im running hcg 2500iu,nolva 10mg,and clomid at 50mg twice a day. is it safe to break nolva and clomid in half?
 
Good post.

From what I gather it seems like 60 is the sweet spot for Torem. But quite a few people advise elevated doses for the first 2-4 days. Whether or not you think it's good/bad advice, do you think there's any downside to starting Torem with something like 120x2 + 90x2 before you drop down to 60?

Yeah - You could start it a bit higher for the first day or two in an attempt to boost serum concentration.
 
Celc I think you got mixed up? Clomid, Nolva, and Torem are all SERMs, not AIs

typo fixed. Good catch :cheers:

ive only found like 3-4 abstracts on torem and HPGA recovery. which IMO isnt enough so i dont use it. even though its SIMILAR to nolva its NOT nolva

Agreed. Also, the Fareston home page actually sites GREATER toxicity than Nolva. Go figure, since the broskis say how much more liver friendly Torem is than Nolva. But the people who are selling Torem show us plain as day that it's more toxic. Fareston.com I believe.

wouldn't you agree that there is overwhelming anecdotal evidence supporting Torem's efficacy in PCT?

I wouldn't agree. IMO most of what you hear is parroting. I won't use Torem again as it's not that great for testicular recovery (although I think it did help to a certain extent), it kills my libido (opposite of the hype), and affects my mood until I get deeper into the taper. I do think that it should potentially help as part of a gyno treatment plan, although I haven't used it that way myself. I also strongly suspect RC Torem quality varies substantially among popular vendors (obviously there's no way I'm going to name names).
 
its not just aromatase activity that we are talking about ...

yea there wont be much T aromatising in the beggining but E2 is probably in the 20's which is normal when your T levels are 200-800ng but that isnt the case when you come off cycle,

my t and e levels were 36 and 22 respectivly, so i included a SERM which would bring up test (and in some cases it CAN bring up e2 levels) and i incorperated an AI EOD to make sure it stays in normal levels. once T levels return to normal there is always natural aromatization occuring how much? im unsure, but i would like to keep most of my T as T and make sure minimum amounts of t are lost due to aromatization.

OK, I understand what you're saying now I think. You are espousing using an AI right away to suppress E even though there is little T being produced in order to get the ratio back to normal levels, correct? However, I have 2 issues with the above:

1) The estrogen-lowering capabilities of AIs are due to their blocking of the aromatase enzyme, which as we all know converts androgens to estrogens. Unless there is a MOA I am unaware of, how can an AI work as it's supposed to if there are no androgens being produced? The rationale that you want to re-establish a proper T/E ratio ASAP is fine, but the method doesn't make sense IMO. I suppose the discussion could veer towards how quickly SERMs boost T levels to the point that including an AI would be of benefit, but I don't have that data offhand.

2) I was always working here under the assumption that end-of-cycle T and E levels would both be low. Now, everyone is different, and different AAS do different things, but all that being said, your results seem to fly in the face of "conventional wisdom" (FWIW) in that E should be very low post-cycle too. I think you said it was a SD cycle on another thread? Am I right?

You haver to be aware of how your bodsy reacts, Im not saying kill E2 in the begining im saying control it lower it a little, make the ratio more favorable until T rises and then let E2 return to normal while continueing the SERM, OR you can run it throughout the PCT with the SERM and it all depends on how you feel

Again, starts to make sense as T rises, but not right away IMO.

i like aromasin but last time i used Adex, i really was not a fan of how it mad me feel, id rtather use adex on cycle then pct, but either at certain doses will do the trick. it comes down to kmnowing your body as ive said earlier of course your not gunna say "hey i feel like **** today it must be my e2 levels" but you have to know how these things work and BLOODWORK is the best way to do that.

as far as this statement is conserned...

There are also other growth factors to consider (prolactin for one) that I suspect may be enough to cause gyno if elevated, even in the presence of "normal" E levels. Further, there is the issue of androgen - estrogen imbalances, an issue I don't even fully understand, but suffice to say there is a theory that gyno can grow simply based on imbalances between T and E (provided the imbalance favors E) in certain individuals, even though neither level on its own would cause any alarm

prolactin being hiugh and causing gyno is usually only the case with elevated E2 levels. Prolactin is a peptide hormone that needs other growth factors concurrently to function (IGF1, GH) so you will most likely not leak if the other growth factors are present.

I disagree with this one. I believe you were in that thread Seth Roberts started re: prolactin and progesterone. I have a rather long-winded post refuting Seth's claim that prolactin is only a growth factor if E is elevated. He sort of agreed with me but never revisited it after that. I do agree other growth factors must be present for gyno (this is always true), but my current line of thought focuses on this relationship: normal E, elevated secondary growth factor(s) (i.e. prolactin). Can such a situation induce gyno? I believe it can.

Even if the balance is in favor of t, gyno can occur. it comes down to how your own body reacts to those levels. some people will not experience gyno at higher e2 levels because they arent prone to it. some will even at normal levels.

Which is why "normal" is all relative, although not sure what you are saying re: the ratio favoring T. I assume you mean you can establish a ratio in favor of T (higher than your individual norm), yet still get gyno, as high T will result in a concurrent rise in E above "normal" levels (yet still, the ratio favors T more than usual). I agree completely, although - if you believe this, you said in a previous post it was all about the ratio. That thinking would seem to contradict the previous post.

Anyway, good discussion and your input is appreciated.
 
I wouldn't agree. IMO most of what you hear is parroting. I won't use Torem again as it's not that great for testicular recovery (although I think it did help to a certain extent), it kills my libido (opposite of the hype), and affects my mood until I get deeper into the taper. I do think that it should potentially help as part of a gyno treatment plan, although I haven't used it that way myself. I also strongly suspect RC Torem quality varies substantially among popular vendors (obviously there's no way I'm going to name names).

There is a lot of parroting but I have read many positive first hand experiences with Torem. From people who have used other SERMs and liked their results from Torem best.

What dose(s) did you use when you ran Torem in your PCT?
 
There is a lot of parroting but I have read many positive first hand experiences with Torem. From people who have used other SERMs and liked their results from Torem best.

What dose(s) did you use when you ran Torem in your PCT?

How about the positive first hand experiences with AI and NO SERMs?
 
There is a lot of parroting but I have read many positive first hand experiences with Torem. From people who have used other SERMs and liked their results from Torem best.

What dose(s) did you use when you ran Torem in your PCT?

Torem got popular right around the time mild epithio compounds showed up. People ran the new mild compound after having been wrecked by superdrol and having miserable pcts in the past. Roll the dice pick your serm, sd pct is a miserable endeavor for most. Do the same following 4 weeks of 40mg epithio and you'll fall in love with whatever serm showed up in your plan because the recovery is so much smoother. Torem was the benefactor. It has it's pros and cons but doesn't warrant the hype.

I've ran the broski dose and i"ve ran 1/2 of that as well. Both had pros and cons as previously discussed over and over.
 
How about the positive first hand experiences with AI and NO SERMs?

There are lots of them. No question about it. You've never heard me say that OTC PCT won't work or that it is bad.

All I've ever said is that when you compare OTC vs Torem (specifically Torem) head-to-head, by my analysis Torem comes out on top.

The number one argument against using Torem for h-drol (which I assume is what you are referring to) is that "SERMs are overkill." But it's not overkill in the same way that using a fire hose to put out a match is, where there is going to be collateral damage. It's like making toast in a commercial oven. The oven can handle big jobs and small, but you're no worse off for using the oven to make your toast than making it with a toaster. And for this example the oven is better than the toaster in some ways.

So far just about all the arguments I've heard against Torem can be classified as "overkill."
 
So if this is allowed...can I ask for some input on a hypothetical PCT for Havoc?

Based on the reading in this thread, I would start with

Week 1
Sustain Alpha
I3C
DTH
Week 2
Sustain Alpha
I3C
DTH
Week 3
Sustain Alpha
I3C
TD Form
Divanex (I only have 12 days worth of DTH)
Week 4
Ditto

Im trying to get a SERM (nolva) and would run at 10/mg day or maybe 20mg EOD?
Maybe blow off some of these things and use the Test Recovery Stack?

Again, Im not trying to rain on your good discussion parade but these are the people Id like to ask.
 
So if this is allowed...can I ask for some input on a hypothetical PCT for Havoc?

Based on the reading in this thread, I would start with

Week 1
Sustain Alpha
I3C
DTH
Week 2
Sustain Alpha
I3C
DTH
Week 3
Sustain Alpha
I3C
TD Form
Divanex (I only have 12 days worth of DTH)
Week 4
Ditto

Im trying to get a SERM (nolva) and would run at 10/mg day or maybe 20mg EOD?
Maybe blow off some of these things and use the Test Recovery Stack?

Again, Im not trying to rain on your good discussion parade but these are the people Id like to ask.

It looks good to me, but assuming you don't get a SERM what would people think about starting the form in week one and dropping SA?

I still can't figure out what SA is. An AI? A test booster? Seems like you can drop SA and still have all your bases covered.

You might consider adding cort control in week 3 if you're on a cut.

How do you plan to dose the I3C?
 
So if this is allowed...can I ask for some input on a hypothetical PCT for Havoc?

Based on the reading in this thread, I would start with

Week 1
Sustain Alpha
I3C
DTH
Week 2
Sustain Alpha
I3C
DTH
Week 3
Sustain Alpha
I3C
TD Form
Divanex (I only have 12 days worth of DTH)
Week 4
Ditto

Im trying to get a SERM (nolva) and would run at 10/mg day or maybe 20mg EOD?
Maybe blow off some of these things and use the Test Recovery Stack?

Again, Im not trying to rain on your good discussion parade but these are the people Id like to ask.
That looks pretty solid to me if you dose Havoc 40mg/day or less and run it for a typical 4 week cycle.
I like to taper up then down with Formestane/AI's, and adjust Natty boosters according to libido. If I have a solid libido, I ride out at that dose then taper it down too, just to avoid a "crash". The I3C taper was a protocol I read from dinoiii...and what I've used for EVERY PCT.
Sustain Alpha was just "OK" for me, some guys love it. I say taper just to get the full 4 weeks out of it if you can.
EXAMPLE (adjust accordingly as you feel fit)...

WEEK 1
Sustain Alpha--couple pumps AM/PM
I3C--600mg/day
DTH--4/day

WEEK 2
Sustain Alpha--couple pumps AM/PM
I3C--400mg/day
DTH--3/day
Form--2pumps/day

WEEK 3
Sustain Alpha--couple pumps AM
I3C--200mg/day
DTH--3/day or Transition to Divanex (500mg/day)
Form--4pumps/day

WEEK 4
Sustain Alpha--couple pumps AM
I3C--200mg/day
DTH--3/day or Transition to Divanex (500mg/day)
Form--3pumps/day

WEEK 5
I3C--200mg/day
DTH--Divanex (500mg/day)
Form--2pumps/day
 
It looks good to me, but assuming you don't get a SERM what would people think about starting the form in week one and dropping SA?

I still can't figure out what SA is. An AI? A test booster? Seems like you can drop SA and still have all your bases covered.

You might consider adding cort control in week 3 if you're on a cut.

How do you plan to dose the I3C?

Im basically on a permanent bulk. Im trying to play football again.

Im 5'5'' (yes, laugh) but am trying to hit 185. Coach told me if I was 6 inches taller, I could have played football anywhere Id ever wanted. Not willing to let that go yet.

SA helps boost test basically. Im sure you have read this.




That looks pretty solid to me if you dose Havoc 40mg/day or less and run it for a typical 4 week cycle.
I like to taper up then down with Formestane/AI's, and adjust Natty boosters according to libido. If I have a solid libido, I ride out at that dose then taper it down too, just to avoid a "crash". The I3C taper was a protocol I read from dinoiii...and what I've used for EVERY PCT.
Sustain Alpha was just "OK" for me, some guys love it. I say taper just to get the full 4 weeks out of it if you can.
EXAMPLE (adjust accordingly as you feel fit)...

WEEK 1
Sustain Alpha--couple pumps AM/PM
I3C--600mg/day
DTH--4/day

WEEK 2
Sustain Alpha--couple pumps AM/PM
I3C--400mg/day
DTH--3/day
Form--2pumps/day

WEEK 3
Sustain Alpha--couple pumps AM
I3C--200mg/day
DTH--3/day or Transition to Divanex (500mg/day)
Form--4pumps/day

WEEK 4
Sustain Alpha--couple pumps AM
I3C--200mg/day
DTH--3/day or Transition to Divanex (500mg/day)
Form--3pumps/day

WEEK 5
I3C--200mg/day
DTH--Divanex (500mg/day)
Form--2pumps/day

I already have the SA, frankly it did great stuff for me just trying to stay natty coupled with DTH. The only reason Im considering havoc is Im running out of time to get back into a program to play.

I like the I3C taper and the AI tapering as well. I wonder why the natty test boosters are dosed fairly low?

And how did you feel about 10mg novla daily vs 20 EOD?


Im still not resolved on a havoc cycle. I mean, I wonder if I could do some natty things like Divanex and SA or T911 and gain like...say 4-5lbs and do it again the next month for another 4-5. Then it would defeat the purpose of a cycle to gain like 12, lose 2-3, and etc etc. I dont know, still not resolved.


Lastly, thank yall both for the input.
 
What's logic behind using SA and DTH? SA is expensive and you already have a test booster in DTH.

Also, if he doesn't use nolva shouldn't the form be started in week one of PCT?
 
OK, I understand what you're saying now I think. You are espousing using an AI right away to suppress E even though there is little T being produced in order to get the ratio back to normal levels, correct? However, I have 2 issues with the above:

1) The estrogen-lowering capabilities of AIs are due to their blocking of the aromatase enzyme, which as we all know converts androgens to estrogens. Unless there is a MOA I am unaware of, how can an AI work as it's supposed to if there are no androgens being produced? The rationale that you want to re-establish a proper T/E ratio ASAP is fine, but the method doesn't make sense IMO. I suppose the discussion could veer towards how quickly SERMs boost T levels to the point that including an AI would be of benefit, but I don't have that data offhand.

makes sense what your saying but if that were the case then your e2 wont lower at all implementing an AI in PCT. SERMs may work pretty fast i believe however im not saying slam an AI dose im staying small doses here and there.

2) I was always working here under the assumption that end-of-cycle T and E levels would both be low. Now, everyone is different, and different AAS do different things, but all that being said, your results seem to fly in the face of "conventional wisdom" (FWIW) in that E should be very low post-cycle too. I think you said it was a SD cycle on another thread? Am I right?

i never know what FWIW means or conventional wisdom haha. yes my e2 got lowered while prolactin raised a tad however didnt bring it out of the physiological range. you cant always work over an assumtion although thats usually all we have to work with.

Again, starts to make sense as T rises, but not right away IMO.

very true


I disagree with this one. I believe you were in that thread Seth Roberts started re: prolactin and progesterone. I have a rather long-winded post refuting Seth's claim that prolactin is only a growth factor if E is elevated. He sort of agreed with me but never revisited it after that. I do agree other growth factors must be present for gyno (this is always true), but my current line of thought focuses on this relationship: normal E, elevated secondary growth factor(s) (i.e. prolactin). Can such a situation induce gyno? I believe it can.


yea ive leanred quite a bit from that thread, i still believe it is possible however its not as likley if e2 isnt elevated. also the gyno with high prolactin will mostly show signs (i beilieve) when other growth factors are high. i dont think anyone can say with 100% certainty that it always happens only one way. but secondary growth factors you have only mentioned Prolactin, not GH or IGF1 which play a HUGE role in it as well. Why do you think you MAY notice reduced gyno with nolva in some instances? i believe its dues to lowering IGF1, because it doesnt lower E2

Which is why "normal" is all relative, although not sure what you are saying re: the ratio favoring T. I assume you mean you can establish a ratio in favor of T (higher than your individual norm), yet still get gyno, as high T will result in a concurrent rise in E above "normal" levels (yet still, the ratio favors T more than usual). I agree completely, although - if you believe this, you said in a previous post it was all about the ratio. That thinking would seem to contradict the previous post.

i think we are mis communicating and decifering posts in the wrong context.

Anyway, good discussion and your input is appreciated.


...
 
im also thinking about using Toremifene for PCT after a 6 week cycle of H-Drol at 50mg a day. my question is how would i dose it?

PCT:
Formex by IBE
Cycle Assist by CEL
maybe Toremifene? or should i stick with CEL PCT Assist?
and a cort control at week 3.

Would def appreciate how to go about dosing the above compounds.
 
im also thinking about using Toremifene for PCT after a 6 week cycle of H-Drol at 50mg a day. my question is how would i dose it?

PCT:
Formex by IBE
Cycle Assist by CEL
maybe Toremifene? or should i stick with CEL PCT Assist?
and a cort control at week 3.

Would def appreciate how to go about dosing the above compounds.

Check out my log (in my sig) to see how I dosed Torem and everything else in PCT -- it's in the first post. This was after extensive, painstaking research. I ran h-drol for five weeks and my PCT is going smoothly, I'm at the end of week #2 right now.
 
hey just wondering why u started ur Post Cycle Support on week 8? And why did u keep it in the PCT if u already had Torem?
 
w
hat people need to understand is that theres a higher amount of estrogen to testosterone when you come off cycle, which is why its important in the beginning to lower it a little while allowing the SERM to do its job, it will help your body recover faster, remember estradiol is responsible for the negative feedback loop.

but too low of estrogen will lower libido, so dose accordingly.

AIs arent just for blocking estrogen rebound after PCT they are for increasing LH and FSH in conjunction with the serm.
I may be jumping in too quick but I didn't think I could finish the thread without commenting on this.
Ok, from what I have learned is that the "SERM" is created to stop the "bad" estrogen. Not all estrogen is bad, your body has so much more at the end of a cycle because the cycle has your levels all out of whack and your body is trying to compensate for the elevated "fake" test levels your body has been getting. NOW what we want from the serm is too allow the estrogen to remain HIGH but not the estrogen that causes us to grow boobies but all other estrogen so that our bodies will see the levels of estrogen being high and counter react by NATURALLY elevating our test levels.
I too have been toying around with the idea of using a serm around the last couple of weeks of being on my cycle as to go ahead and stop the bad estrogen and allow me to not worry about my levels being off. This way there is no lapse because gyno can hit during your cycle not just after.
 
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