newbie23
New Member
gotta say im sold-HCG desensitization-and HCG during PCT-im removing my foot from my mouth as i type
opcorn:
opcorn:
MESO-Rx
Anabolic Steroids
doc and bbc
- Thread starter newbie23
- Start date
Please clarify as I could not be sure from that sentence. You have valid concerns regarding HCG I am sure. I am pretty sure that many unknowns really remain. No one is questioning your motive to question. Keep in mind I think that Doc's whole perspective of "clinical" revolves around "correct, or unabsurd" use.... It just simply appears that really high doses have been utilized medically and clinically, with no documented adverse affects. No one says it can't hurt ya at attrocious and untested doses... And who really knows how... Perhaps the stuff could even interact with another drug or food that we have not considered for our purposes. Also be clear that the doc is also not advocating the elimination post cycle. I think he also advocates usage prior to SERM use. I am not trying to put words in his mouth. Just motivating data equillibrium, and for me to be corrected if necc.
gotta say im sold-HCG desensitization-and HCG during PCT-im removing my foot from my mouth as i type
Lizard King
New Member
But thats the whole point. If someone were to actually read them I could be found out!!!
After all I am just talking for my own mind and documentaion of thought......
After all I am just talking for my own mind and documentaion of thought......I think I would read more of your posts if they were short and to the point [)]
newbie23
New Member
basically this what i have gathered
lets say we are going to do a pct for someone who has used 500mg of test e a week--dbol at the begining.
from the realization that levels will be roughly 5-6000 ng/dl in week 12 of this cycle
here is where im still confused
he recomends 500-1000 iu E3D during cyle
then he states he uses 2-2500 EOD during PCT.
he also states with this cycle it will be at least a month before the testes begin to function.
would someone still start PCT 2 weeks after last inject-then run HCG 2 weeks in to PCT? while simultaneously stopping HCG?
PCT being a combo of clomid and nolva.
or would one wait 4 weeks after last pin to start PCT?
as far as the first comment in my thread I am refering to my prior belief in desensitization.
lets say we are going to do a pct for someone who has used 500mg of test e a week--dbol at the begining.
from the realization that levels will be roughly 5-6000 ng/dl in week 12 of this cycle
here is where im still confused
he recomends 500-1000 iu E3D during cyle
then he states he uses 2-2500 EOD during PCT.
he also states with this cycle it will be at least a month before the testes begin to function.
would someone still start PCT 2 weeks after last inject-then run HCG 2 weeks in to PCT? while simultaneously stopping HCG?
PCT being a combo of clomid and nolva.
or would one wait 4 weeks after last pin to start PCT?
as far as the first comment in my thread I am refering to my prior belief in desensitization.
I consider PCT to begin immediately after stopping AAS. This would mean the day of the last AAS whether injection or oral. To better understand PCT, disregard the hCG during AAS administration. At the end of AAS administration (actually within days), the T level will be about 6,000 ng/dL. It is better to use the higher estimate for obvious reasons.
At a half-life of 7-10 days, the serum T level will take approximately 4 half-lives to get to ~375. At this point, the HPTA will attempt to restart. It might be sooner/later, but this is a very good and reasonable T level. This is between 28-40 days! If you run SERMs before this time, they will in all likelihood not be optimally effective. It is also during this time that the testes will not be stimulated since the gonadotropins are suppressed. This is the best time to use hCG - during the expected decline of exogenous T (or other AAS). If you are being tested (the best method), if the serum T level is over 375 around week 4, prior to finishing the hCG, the value will represent endogenous production.
I am assuming you are quoting the docs protocol (just to be sure I was not misinterpreted). I do not disagree with him.
One point that we disagree on, however, is the actual levels of T that the body achieves while supplementing T. I have met enought people and done enough of my own testing to justify this statement, "you will be hard pressed to achieve a T level above 2500 or 3000 from exogenous T supplementation. Everyone is different. I think this is attributed to both actual usage rates and the body's inability to even circulate T beyond a certain level. I am not going there now.
Regardless, and where you are confused. There is some mainstream thought out there today that would indicate a philosophy of supporting the testicles with HCG throughout a cycle will eliminate the need for post cycle usage, or more clearly, pre-serm usage. Hence you already have them up to speed, so no need. Obviously there is always the need prior to appropriate SERM start date because as long as T half-lives exist in the sustem, YOU ARE ON CYCLE. But clearly, most importantly used directly prior to SERM to ensure they are working at that point. This is also the maximum return date as the AAS related suppression is leaving thus allowing it to work more effectively.
Where will HCG effects by most pronounced? Obviously when added to the higher natural LH levels which will begin to rise with the final elimination of exogenous T. Do you want to carry HCG into SERM Therapy? NO, simply because of the fact that it stimulates T production in its self from an exogenous standpoint. I do not know if the actual application of HCG causes a negative feedback with direct regard to the hypothalmus however. But either way, the usage into SERM therapy is counter productive for return to natural states.
So why use it. The goal is to get the boys up to speed and stimulate their ability to receive and respond to natural LH signaling. Without this, it would be speculated that the return of the natural signal could be hindered by the testicles lack of proper performance. So not only is your body trying to restart from the brains perspective, it also has to now natually fire the boys up as well, and via that signal alone. You can see where this process with no HCG could prove to take 2wice as long to jumpstart. PERSONALLY, I also speculate that if the brain returns to siganling (which it will just as quickly as it shut down), and the testicles are not equipped to respond, there could be a possible re-shutdown of LH signalling. That is me, and I am soon to be convinced there is no merit there, and that any failures in PCT to complete a successful restart, are simply due to inappropriate ester timing.. This is also disproven by the fact that castrated men have higher levels of LH (I think).
So the order goes: (1) cycle, (2) lite em up, (3) brain kicks in and supports fully and naturally.
The on cycle use of HCG can be debunked simply by the fact that HCG is optimally effective near the end of the steroid's final half-lives. Considering the short lenth of cycles on a life scale, is there really any need to try to support them? I dont think there is any data out there suggesting that 8-16 week periods of testicular inactivity will cause any long term damage. HOWEVER, the use of HCG for TRT purposes, both due to permanent primary or seconary injury, as well as TRT for the aging healthy male, my be considered relevant considering the nature or the injury, or the nature of this long term eneavor. However this is unproven as well. And I do have some problems with that whole concept. Again, Later on that.
Personally I tend to subscribe to the concept of using HCG about every 8 weeks for cycling puposes, and heavily at the end and prior to SERM....
One point that we disagree on, however, is the actual levels of T that the body achieves while supplementing T. I have met enought people and done enough of my own testing to justify this statement, "you will be hard pressed to achieve a T level above 2500 or 3000 from exogenous T supplementation. Everyone is different. I think this is attributed to both actual usage rates and the body's inability to even circulate T beyond a certain level. I am not going there now.
Regardless, and where you are confused. There is some mainstream thought out there today that would indicate a philosophy of supporting the testicles with HCG throughout a cycle will eliminate the need for post cycle usage, or more clearly, pre-serm usage. Hence you already have them up to speed, so no need. Obviously there is always the need prior to appropriate SERM start date because as long as T half-lives exist in the sustem, YOU ARE ON CYCLE. But clearly, most importantly used directly prior to SERM to ensure they are working at that point. This is also the maximum return date as the AAS related suppression is leaving thus allowing it to work more effectively.
Where will HCG effects by most pronounced? Obviously when added to the higher natural LH levels which will begin to rise with the final elimination of exogenous T. Do you want to carry HCG into SERM Therapy? NO, simply because of the fact that it stimulates T production in its self from an exogenous standpoint. I do not know if the actual application of HCG causes a negative feedback with direct regard to the hypothalmus however. But either way, the usage into SERM therapy is counter productive for return to natural states.
So why use it. The goal is to get the boys up to speed and stimulate their ability to receive and respond to natural LH signaling. Without this, it would be speculated that the return of the natural signal could be hindered by the testicles lack of proper performance. So not only is your body trying to restart from the brains perspective, it also has to now natually fire the boys up as well, and via that signal alone. You can see where this process with no HCG could prove to take 2wice as long to jumpstart. PERSONALLY, I also speculate that if the brain returns to siganling (which it will just as quickly as it shut down), and the testicles are not equipped to respond, there could be a possible re-shutdown of LH signalling. That is me, and I am soon to be convinced there is no merit there, and that any failures in PCT to complete a successful restart, are simply due to inappropriate ester timing.. This is also disproven by the fact that castrated men have higher levels of LH (I think).
So the order goes: (1) cycle, (2) lite em up, (3) brain kicks in and supports fully and naturally.
The on cycle use of HCG can be debunked simply by the fact that HCG is optimally effective near the end of the steroid's final half-lives. Considering the short lenth of cycles on a life scale, is there really any need to try to support them? I dont think there is any data out there suggesting that 8-16 week periods of testicular inactivity will cause any long term damage. HOWEVER, the use of HCG for TRT purposes, both due to permanent primary or seconary injury, as well as TRT for the aging healthy male, my be considered relevant considering the nature or the injury, or the nature of this long term eneavor. However this is unproven as well. And I do have some problems with that whole concept. Again, Later on that.
Personally I tend to subscribe to the concept of using HCG about every 8 weeks for cycling puposes, and heavily at the end and prior to SERM....
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newbie23
New Member
so to me im getting that 4 weeks is a good estimate without bolod tests
Im also getting that truly testing is the only way to know when the best time to stop HCG is-otherwise we will not know for sure that the testes are producing endogenous test.
so if one had to guess-or i was making a recomendation and the OP did not have the luxury of blood test-this is a good guess
1-4 dbol
1-12 test E
13-16 HCG 2000 iu EOD or E3D
17-20 clomid nolva combo
I posted this before i read your post BBC-so gimme a min to comprehend
Im also getting that truly testing is the only way to know when the best time to stop HCG is-otherwise we will not know for sure that the testes are producing endogenous test.
so if one had to guess-or i was making a recomendation and the OP did not have the luxury of blood test-this is a good guess
1-4 dbol
1-12 test E
13-16 HCG 2000 iu EOD or E3D
17-20 clomid nolva combo
I posted this before i read your post BBC-so gimme a min to comprehend
newbie23
New Member
great post BBC and DOC
it seems I am stuck at a crossroad here-many of the guys i know simply do not get bloodtests-and no matter how easy it would be-they just prolly wont do it. I could get them-i think there is home kit for 35 bucks. But hopefully we can continue this discussion with the assumption that the majority of users just wont get tested...........because the majority just wont
so what am i to do about SERM timing if i can not get you guys to agree on T levels while on cycle?
it seems I am stuck at a crossroad here-many of the guys i know simply do not get bloodtests-and no matter how easy it would be-they just prolly wont do it. I could get them-i think there is home kit for 35 bucks. But hopefully we can continue this discussion with the assumption that the majority of users just wont get tested...........because the majority just wont
so what am i to do about SERM timing if i can not get you guys to agree on T levels while on cycle?
newbie23
New Member
i guess it could be done like this
1-4 dbol
1-12 test e
13-16 HCG
15-20 SERM
but seeing as how running the SERM with HCG is pointless-it would make me think to use the DOC's theory that waiting longer to start the SERM is the ony logical way to do it without testing.
so my prior post for timing seems more correct if one were to guess without testing
1-4 dbol
1-12 test e
13-16 HCG
15-20 SERM
but seeing as how running the SERM with HCG is pointless-it would make me think to use the DOC's theory that waiting longer to start the SERM is the ony logical way to do it without testing.
so my prior post for timing seems more correct if one were to guess without testing
Home test kits will be worthless considering methods, and time for results. The bottom line is that a month is a strong and safe figure for esters with 7 day half-lives. To begin earlier will not destroy the PCT,but it could hinder the effectiveness on paper. HCG will still stimulate the testicles in lieu of an exogenous steroid. IF the method of operation for a SERM to stimulate, is to block the hypothalmus's abiiity to see estrogen in the system, then even a Serm will have a strong effect on in the presence of, or even on cycle. The issue is the effectiveness of the blocking action with regard to circulating hormones, and what will happen once the serm is removed. Also consider that HCG has a 2 day half-life and that clomid and Nolva is more like 6 days. So they have some hang time of their own. Nolve also takes almost a week to reach steady plasma concentrations ( I think). It boils down to two things: How important it is to you to return quickly. And what your goals are. I personally have a few hang ups with using a SERM for the layman's purpose with regard to a need for PCT. PCT was initially designed to limit a professional body builder's time down. I remain pretty convinced that, considering a 16 week cycle, equal time off always, and the body's ability to start signaling again, does and average guy want to do it. Should HCG be enought? Consider that many of the steroid patients needing a PCT type treatment for long term unresponsiveness naturally, were also certain cuprets of breaking the time on = time off rule. And they continued to do this thus compounding to their current problems that Dr Scalley has helped them with. Life is a zero sum game. So this continiues imbalance of the natural demand in place adds up. I have proven myself to return naturally in 6-8 weeks from an 8 month session of exogenous T application with HCG alone. Why? I just answered the question. One of the primary problems that necessitates the need for PCT in AAS is the fact that it provides a false sense of normalcy. The bottom line is that once the brain has been told it does not need to make T for 3 months straight (or whatever), it needs at least 3 months to learn back "normal" behaviour. Just because ones HPTA restored in as little as a month, HAS NOTHING TO DO WITH THE BEHAVIOR THAT THE BRAIN JUST LEARNED!!!!.
Splitting hairs over two weeks is too technical. From this standpoint, you could go ahead and take everyone in the first 16 week scenario I mentioned up top and throw out their first two weeks of SERM usage. Because technically, if they began prior to the one month mark, they were wasting their time, at least partially, and not to create an argument for the validity of SERM use on cycle. If their PCT started say 2 weeks post cycle, wouldn't that prove that they never needed more than two weeks anyway? But no, even the use of the SERM while still having metabolites in the system facilitating shutdown, has benefitted them by the time if had the HPTA running as contributed. Again, the effectiveness of a serm as related to the amount of hormones circulating, and their actual actions, is far from proven. After all, if the action of the SERM was to stimulate T production via TOTALLY blocking estrogen from the hypothalmus, then why would a would it not be a good idea to run a SERM even while on an extremely extended cycle, as a method of keeping the hypothalmus up to speed? Who know if the action of a serm is not just a reaction to a particulat drug at the brain, and not a relation of hormone perception at all? I am not say it does not do what it does. I am just saying who really knows how. The body is a complex simphony. You dont think it will shut down t production at the sight of too much DHT? So could it be possible that natural restart is related to the brains interpretation of a simple lack of DHT could be an operational factor? Or maybe it does not even need metaobolites as it could possibly even sence the general lack of T as a motive to restart. I wager that any and all could have an effect either way. I also think that a serm is probably only one road explored on this new frontier....opcorn:
Splitting hairs over two weeks is too technical. From this standpoint, you could go ahead and take everyone in the first 16 week scenario I mentioned up top and throw out their first two weeks of SERM usage. Because technically, if they began prior to the one month mark, they were wasting their time, at least partially, and not to create an argument for the validity of SERM use on cycle. If their PCT started say 2 weeks post cycle, wouldn't that prove that they never needed more than two weeks anyway? But no, even the use of the SERM while still having metabolites in the system facilitating shutdown, has benefitted them by the time if had the HPTA running as contributed. Again, the effectiveness of a serm as related to the amount of hormones circulating, and their actual actions, is far from proven. After all, if the action of the SERM was to stimulate T production via TOTALLY blocking estrogen from the hypothalmus, then why would a would it not be a good idea to run a SERM even while on an extremely extended cycle, as a method of keeping the hypothalmus up to speed? Who know if the action of a serm is not just a reaction to a particulat drug at the brain, and not a relation of hormone perception at all? I am not say it does not do what it does. I am just saying who really knows how. The body is a complex simphony. You dont think it will shut down t production at the sight of too much DHT? So could it be possible that natural restart is related to the brains interpretation of a simple lack of DHT could be an operational factor? Or maybe it does not even need metaobolites as it could possibly even sence the general lack of T as a motive to restart. I wager that any and all could have an effect either way. I also think that a serm is probably only one road explored on this new frontier....
opcorn:Fascinatig read guys, probably the most informative post I've ever read for real world applications...I also have been confused about HCG vs SERM timing with longer esthers. Not to confuse the issue, but what are your thoughts abut using an AI (like Aromasin) along with the HCG and prior to SERM application? This is the way I've done it in the past, and I've been pleased with the results: ie never had any prononced sides or issues...but if I'm reading this correcty I have been starting the Nolva and Clomid too soon...with test E I have done it as follows:
wk 1-14 Test E 500mg/wk
wk 1-4 Test P 100 mg EOD
wk 14-16 test p 100 mg EOD
Wk 4-16 500 iu's HCG E3D
wk 17-19 500 iu's HCG ED
wk 17-19 Aromasin 20mg ED
wk 20-25 nolva @ 40/20/20/20/20 ED
wk 20-22 Clomid @ 100/50 ED
So if I'm reading this correctly, I'm starting SERM's a week earlier than it would be most effective to start...is that right?
wk 1-14 Test E 500mg/wk
wk 1-4 Test P 100 mg EOD
wk 14-16 test p 100 mg EOD
Wk 4-16 500 iu's HCG E3D
wk 17-19 500 iu's HCG ED
wk 17-19 Aromasin 20mg ED
wk 20-25 nolva @ 40/20/20/20/20 ED
wk 20-22 Clomid @ 100/50 ED
So if I'm reading this correctly, I'm starting SERM's a week earlier than it would be most effective to start...is that right?
AIs will increase overall T levels simply because of the fact that they are preventing the metabolization of Free T, to E2. Therefore the Total T levels will go up as less is used for E2 manufacture. This has also been studied and I believe that the body quickly compensates ly further lower TT levels back to previous values as it becomes more astute and precise with its use of E2 remaining available (last part is my personal guess). This does not AI's stimulate the HPTA. In fact, I believe they are reported to barely stimulate the HPTA if at all. ( by the way, this tends to give credence to my hypothesis that the serms action as a drug in its self causes the stimulation, and not the blockage of E2 at the Hypothalmus)
To throw an AI in the mix would seem to me to simply confuse matters more. IF there is anything to the theory that a SERMS blockade of E2 at the hypo being the cause of the restart, one might think it could help if: There is no rebound affect once the AI halflife is spent, and if the blockage the SERM creates is not 100% and complete. Overall I have read not a good idea. I would not use it myself. But who knows. It just seems like generally not necessary and unwlecomed variable considering what is proven today.
To throw an AI in the mix would seem to me to simply confuse matters more. IF there is anything to the theory that a SERMS blockade of E2 at the hypo being the cause of the restart, one might think it could help if: There is no rebound affect once the AI halflife is spent, and if the blockage the SERM creates is not 100% and complete. Overall I have read not a good idea. I would not use it myself. But who knows. It just seems like generally not necessary and unwlecomed variable considering what is proven today.
newbie23
New Member
K BBC im with you.......HCG is king to PCT-and a SERM helps but maybe it is not necessary.
if you have time i would like you to bring the calculation of half lives by hand down to my level.
I remember the DOC saying at a 6000ng/dl the half lives would have to be reuced 4 times in order to bring serum t levels to a range in which the HPTA is willing to activate naturally. since we are going to use a month's timeframe as a safe estimate for a 7-10 day half life. how do i figure out test prop?
why 4 times with test e? please enlighten
and as far as you running for 8 months and successfully restarting-i to am considering continuing my cycle that im currently on for about the long-even before your remark that you have done it successfully-i too have wondered if it is really that bad-and if i could restart after such a time. thoughts? i appreciate your time
if you have time i would like you to bring the calculation of half lives by hand down to my level.
I remember the DOC saying at a 6000ng/dl the half lives would have to be reuced 4 times in order to bring serum t levels to a range in which the HPTA is willing to activate naturally. since we are going to use a month's timeframe as a safe estimate for a 7-10 day half life. how do i figure out test prop?
why 4 times with test e? please enlighten
and as far as you running for 8 months and successfully restarting-i to am considering continuing my cycle that im currently on for about the long-even before your remark that you have done it successfully-i too have wondered if it is really that bad-and if i could restart after such a time. thoughts? i appreciate your time
I agree with at least some of what you said BBC, but the addition of the A-sin is primarily to control both Cortisol and E, especially since HCG is known to be estrogenic. So while re-start is the ultimate goal, the addition of the AI is just to head of any sides from The E and to dead at least some of the circulating cortisol...and E rebound is a non issue due to the Nolva. Respectfully, that part makes sense to me,
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Stretch
Subscriber
Well, I've been reading this post trying to learn something and at least 50% of what's being talked about is over my head.
But if I understand newb's question properly then I think I can answer it.
Take 6000ng/dl and cut it in half = 3000, that's 7 days and ONE half life....
Now you have 3000ng/dl after 7 days
take 3000ng/dl and cut it in half = 1500, that's 14 total days and 2 half lifes
Your at least as smart as I am newb. cut it two more times and your at 375ng/dl after 4 half lives OR 1 month.
newbie23
New Member
lololol- i know i just wanted to be 100% sure i figured that was the way to do it. and i like how BBC explains every aspect-and some parts that i may forget
i guess my last question would be are the current half lifes on the net accurate-cause i have heard others say they are not.
i guess my last question would be are the current half lifes on the net accurate-cause i have heard others say they are not.
Correctamundo! It was not the use of 4 half-lifes, as much as the resulting T level, 375ng/dL. If the AAS cycle is different, the ending T level (or AAS) will change and also the amount of time for HPTA function!
