crazyfool405
Banned
with or without food is fine you may wanna take it with food to avoid the numbness on your tongue.
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?
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.
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.
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.
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.
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
it will boost FHS which has a different function then LH
EOD dosing seems to work well for me and most other people
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.
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?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
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.
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.
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.
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?
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?
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.
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?
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 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.
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.
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?
Celc I think you got mixed up? Clomid, Nolva, and Torem are all SERMs, not AIs
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
wouldn't you agree that there is overwhelming anecdotal evidence supporting Torem's efficacy in PCT?
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.
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?
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.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?
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
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.
I may be jumping in too quick but I didn't think I could finish the thread without commenting on this.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.