Long Shutdown, Tripto+SERM PCT?

Pharma
21

[quote]MassiveGuns wrote:

[quote]Singhbuilder wrote:
Wow Rob still shutdown? How longs it been now?

In regards to your post, it has been speculated that clomid has some properties that nolva does not, however I have used both in all combinations and it doesnt seem to be any difference except depression from clomid.
So go with nolva its fine Rob.

The hCG shots, I personally feel the doses are too low to elicit any sort of stimulatory response on the testes. I had to do shots of 2500iu EOD to see any sign of recovery on my previous cycle. My theory is that using hCG doses at LH-replacement dose is not going to stimulate the atrophied testes. You must bring the testes to life first with high doses and then do a SERM PCT, i actually did an AI. And it actually worked.
I feel when the testicles are atrophied they will not respond to low dose as the leydig cells will be atrophied.

Although what MG states is also create and I have utmost respect from him, I just dont agree with the such low dose hCG.
Regarding the Trip, I feel you dont need it. Ive used it and it didnt work for me, my levels still stayed the same.

SB[/quote]

You’re right, an LH replacement dose will no stimulate the testes enough for recovery if they have severely atrophied. The dosing protocol I advocate of 300IU a day is much higher than that. You wanted instant results, which you will get by bumping the dose up. If you follow 300IU per day for up to the 30 days reccomended you will see your testes come back online, just not as fast. You do run the risk of desensitisation with a higher dose.

How you dilute your HCG also has an effect on how potent it is. The more concentrated the solution, the stronger the effect it seems to have. There are studies that have documented this effect with subcutaneous injections of HGH but not hcg, but from personal experience I am sure it makes a big difference.

And I wouldn’t rule out the trip for rob, he’s been shutdown such a long time it might be exactly what he needs. Along with D aspartic acid.[/quote]

Ya I see what you were saying in your previous post about the AI after the SERM prolonging the time before the HPTA can function on its own, I guess my logic is that I should have recovered by now on my own anyway - but maybe after the SERM stimulation my system will be reconditioned and ready to take over once I come off. My worry was that my HPTA might be very fragile even after the SERM run and the idea KSman seems to have offered in other threads is that the AI can help to continue to shield the HPTA from negative feedback for a while as it gets used to working again. I need to re-read his posts but the suggestion was that it is easier for the HPTA to take over by itself from an AI taper than it is from a SERM taper.

The HCG seems like a sensitive drug to use but probably necessary for me to start on. Based on what you guys and others have said, I’ll probably start with a slightly higher dose for a couple of shots and then drop to the 250 iu EOD and gauge responsiveness. This way I can keep the level as low as possible and only increase as much as necessary to gain the desired effect. Not sure what increments I should move up in if I do have to increase, or where I should cap the dosage at to avoid desensitizing the testes, but I’ll prob edge up by 50 IUs at a time.

  • Regarding the HCG dilution, I think the stuff I’m ordering comes 5000 IUs of powder in a 10 mL bottle, sterile & sealed w/ rubber stopper. No bac water though so I was planning on just injecting 10 mL bac water straight into the vial to yield a concentration of 500 IUs/mL - then I can just shoot 1/2 mL slin pin shots for my 250 IUs. Would it be better to use less bac water for a more concentrated solution? Maybe 5 mLs for a concentration of 1000 IUs/mL?

DAA is something I’ve dabbled with to try to get some temporary relief while I’ve been shutdown. On separate occasions I’ve felt the effects very noticeably at a couple of points after a two or three days on but the feeling disappeared almost the next day. Since I know my estrogen is pretty low and T couldn’t have increased by a crazy amount - this makes me wonder if my set point has been lowered for the point at which estrogen causes inhibition at the hypothalamus and/or pituitary. I don’t know if this is even possible but it could explain why I haven’t recovered yet and why I stop feeling the benefits of supps like DAA very quickly. I’m not sure but I think an extended SERM run might be able to reverse a change like this - but don’t quote me on that one.

I think the DAA could be a good add in for after I come off everything, for a little extra support, but I want to understand it’s mechanism of action a little bit better before I throw it in at that delicate time.

22

[quote]Robert Paulson wrote:

[quote]MassiveGuns wrote:

[quote]Singhbuilder wrote:
Wow Rob still shutdown? How longs it been now?

In regards to your post, it has been speculated that clomid has some properties that nolva does not, however I have used both in all combinations and it doesnt seem to be any difference except depression from clomid.
So go with nolva its fine Rob.

The hCG shots, I personally feel the doses are too low to elicit any sort of stimulatory response on the testes. I had to do shots of 2500iu EOD to see any sign of recovery on my previous cycle. My theory is that using hCG doses at LH-replacement dose is not going to stimulate the atrophied testes. You must bring the testes to life first with high doses and then do a SERM PCT, i actually did an AI. And it actually worked.
I feel when the testicles are atrophied they will not respond to low dose as the leydig cells will be atrophied.

Although what MG states is also create and I have utmost respect from him, I just dont agree with the such low dose hCG.
Regarding the Trip, I feel you dont need it. Ive used it and it didnt work for me, my levels still stayed the same.

SB[/quote]

You’re right, an LH replacement dose will no stimulate the testes enough for recovery if they have severely atrophied. The dosing protocol I advocate of 300IU a day is much higher than that. You wanted instant results, which you will get by bumping the dose up. If you follow 300IU per day for up to the 30 days reccomended you will see your testes come back online, just not as fast. You do run the risk of desensitisation with a higher dose.

How you dilute your HCG also has an effect on how potent it is. The more concentrated the solution, the stronger the effect it seems to have. There are studies that have documented this effect with subcutaneous injections of HGH but not hcg, but from personal experience I am sure it makes a big difference.

And I wouldn’t rule out the trip for rob, he’s been shutdown such a long time it might be exactly what he needs. Along with D aspartic acid.[/quote]

Ya I see what you were saying in your previous post about the AI after the SERM prolonging the time before the HPTA can function on its own, I guess my logic is that I should have recovered by now on my own anyway - but maybe after the SERM stimulation my system will be reconditioned and ready to take over once I come off. My worry was that my HPTA might be very fragile even after the SERM run and the idea KSman seems to have offered in other threads is that the AI can help to continue to shield the HPTA from negative feedback for a while as it gets used to working again. I need to re-read his posts but the suggestion was that it is easier for the HPTA to take over by itself from an AI taper than it is from a SERM taper.

The HCG seems like a sensitive drug to use but probably necessary for me to start on. Based on what you guys and others have said, I’ll probably start with a slightly higher dose for a couple of shots and then drop to the 250 iu EOD and gauge responsiveness. This way I can keep the level as low as possible and only increase as much as necessary to gain the desired effect. Not sure what increments I should move up in if I do have to increase, or where I should cap the dosage at to avoid desensitizing the testes, but I’ll prob edge up by 50 IUs at a time.

  • Regarding the HCG dilution, I think the stuff I’m ordering comes 5000 IUs of powder in a 10 mL bottle, sterile & sealed w/ rubber stopper. No bac water though so I was planning on just injecting 10 mL bac water straight into the vial to yield a concentration of 500 IUs/mL - then I can just shoot 1/2 mL slin pin shots for my 250 IUs. Would it be better to use less bac water for a more concentrated solution? Maybe 5 mLs for a concentration of 1000 IUs/mL?

DAA is something I’ve dabbled with to try to get some temporary relief while I’ve been shutdown. On separate occasions I’ve felt the effects very noticeably at a couple of points after a two or three days on but the feeling disappeared almost the next day. Since I know my estrogen is pretty low and T couldn’t have increased by a crazy amount - this makes me wonder if my set point has been lowered for the point at which estrogen causes inhibition at the hypothalamus and/or pituitary. I don’t know if this is even possible but it could explain why I haven’t recovered yet and why I stop feeling the benefits of supps like DAA very quickly. I’m not sure but I think an extended SERM run might be able to reverse a change like this - but don’t quote me on that one.

I think the DAA could be a good add in for after I come off everything, for a little extra support, but I want to understand it’s mechanism of action a little bit better before I throw it in at that delicate time.[/quote]

I don’t mean to be rude but I’d like to point a few things out. You are really overanalysing this faffing. I don’t mind giving advice out, I actually like helping people out but why does everyone feel the need to adjust the protocols given to them for dubious reasons at best? You have a protocol ready to go which does everything you want. SERM for LH and recovery and keeping estrogen in check, HCG to get the testes running and you have a time frame and the option of cutting it short before the maximum 30 days assuming you have significant evidence of recovery.

Where is your rationale for switching to 250IU EOD, because you’ll run less risk of desensitisation? if 300iU per day causes no desensitisation, what possible benefit is this giving you? Its just providing less stimulation to the testes, possibly jeopardising your recovery. There are good reasons why that protocol works as it is, and why you are supposed to get bloodwork done at the specified intervals, its a mugs game going on feel for recovery. If you get the bloodwork done at each stage, you can accurately and objectively track your recovery.

Running any AI with a normal endocrine system can tank your libido rapidly since some estrogen is necessary for proper endocrine function. Fucking about for longer than neccessary is exactly what you want to avoid.

Take my advice, you wont be sorry, and I’d dilute your HCG at 1mL per 1000IU.

23

[quote]MassiveGuns wrote:

[quote]Robert Paulson wrote:

[quote]MassiveGuns wrote:

[quote]Singhbuilder wrote:
Wow Rob still shutdown? How longs it been now?

In regards to your post, it has been speculated that clomid has some properties that nolva does not, however I have used both in all combinations and it doesnt seem to be any difference except depression from clomid.
So go with nolva its fine Rob.

The hCG shots, I personally feel the doses are too low to elicit any sort of stimulatory response on the testes. I had to do shots of 2500iu EOD to see any sign of recovery on my previous cycle. My theory is that using hCG doses at LH-replacement dose is not going to stimulate the atrophied testes. You must bring the testes to life first with high doses and then do a SERM PCT, i actually did an AI. And it actually worked.
I feel when the testicles are atrophied they will not respond to low dose as the leydig cells will be atrophied.

Although what MG states is also create and I have utmost respect from him, I just dont agree with the such low dose hCG.
Regarding the Trip, I feel you dont need it. Ive used it and it didnt work for me, my levels still stayed the same.

SB[/quote]

You’re right, an LH replacement dose will no stimulate the testes enough for recovery if they have severely atrophied. The dosing protocol I advocate of 300IU a day is much higher than that. You wanted instant results, which you will get by bumping the dose up. If you follow 300IU per day for up to the 30 days reccomended you will see your testes come back online, just not as fast. You do run the risk of desensitisation with a higher dose.

How you dilute your HCG also has an effect on how potent it is. The more concentrated the solution, the stronger the effect it seems to have. There are studies that have documented this effect with subcutaneous injections of HGH but not hcg, but from personal experience I am sure it makes a big difference.

And I wouldn’t rule out the trip for rob, he’s been shutdown such a long time it might be exactly what he needs. Along with D aspartic acid.[/quote]

Ya I see what you were saying in your previous post about the AI after the SERM prolonging the time before the HPTA can function on its own, I guess my logic is that I should have recovered by now on my own anyway - but maybe after the SERM stimulation my system will be reconditioned and ready to take over once I come off. My worry was that my HPTA might be very fragile even after the SERM run and the idea KSman seems to have offered in other threads is that the AI can help to continue to shield the HPTA from negative feedback for a while as it gets used to working again. I need to re-read his posts but the suggestion was that it is easier for the HPTA to take over by itself from an AI taper than it is from a SERM taper.

The HCG seems like a sensitive drug to use but probably necessary for me to start on. Based on what you guys and others have said, I’ll probably start with a slightly higher dose for a couple of shots and then drop to the 250 iu EOD and gauge responsiveness. This way I can keep the level as low as possible and only increase as much as necessary to gain the desired effect. Not sure what increments I should move up in if I do have to increase, or where I should cap the dosage at to avoid desensitizing the testes, but I’ll prob edge up by 50 IUs at a time.

  • Regarding the HCG dilution, I think the stuff I’m ordering comes 5000 IUs of powder in a 10 mL bottle, sterile & sealed w/ rubber stopper. No bac water though so I was planning on just injecting 10 mL bac water straight into the vial to yield a concentration of 500 IUs/mL - then I can just shoot 1/2 mL slin pin shots for my 250 IUs. Would it be better to use less bac water for a more concentrated solution? Maybe 5 mLs for a concentration of 1000 IUs/mL?

DAA is something I’ve dabbled with to try to get some temporary relief while I’ve been shutdown. On separate occasions I’ve felt the effects very noticeably at a couple of points after a two or three days on but the feeling disappeared almost the next day. Since I know my estrogen is pretty low and T couldn’t have increased by a crazy amount - this makes me wonder if my set point has been lowered for the point at which estrogen causes inhibition at the hypothalamus and/or pituitary. I don’t know if this is even possible but it could explain why I haven’t recovered yet and why I stop feeling the benefits of supps like DAA very quickly. I’m not sure but I think an extended SERM run might be able to reverse a change like this - but don’t quote me on that one.

I think the DAA could be a good add in for after I come off everything, for a little extra support, but I want to understand it’s mechanism of action a little bit better before I throw it in at that delicate time.[/quote]

I don’t mean to be rude but I’d like to point a few things out. You are really overanalysing this faffing. I don’t mind giving advice out, I actually like helping people out but why does everyone feel the need to adjust the protocols given to them for dubious reasons at best? You have a protocol ready to go which does everything you want. SERM for LH and recovery and keeping estrogen in check, HCG to get the testes running and you have a time frame and the option of cutting it short before the maximum 30 days assuming you have significant evidence of recovery.

Where is your rationale for switching to 250IU EOD, because you’ll run less risk of desensitisation? if 300iU per day causes no desensitisation, what possible benefit is this giving you? Its just providing less stimulation to the testes, possibly jeopardising your recovery. There are good reasons why that protocol works as it is, and why you are supposed to get bloodwork done at the specified intervals, its a mugs game going on feel for recovery. If you get the bloodwork done at each stage, you can accurately and objectively track your recovery.

Running any AI with a normal endocrine system can tank your libido rapidly since some estrogen is necessary for proper endocrine function. Fucking about for longer than neccessary is exactly what you want to avoid.

Take my advice, you wont be sorry, and I’d dilute your HCG at 1mL per 1000IU.
[/quote]

MG,

Please don’t think I am under-appreciating your advice, your protocol looks very intelligent and it is most likely the one I will proceed with - maybe with very minor adjustments, maybe none at all. I am not one to arbitrarily change an effective plan someone is kind enough to offer to me, I am simply trying to effectively take the advice I’ve been given by those who have shown to be the most knowledgeable, and utilize it optimally and safely.

Regarding the HCG dose, my rationale for wanting to start from the lower 250 iu EOD is minimizing risk of desensitization, as you suggest. I have read a lot of posts and studies regarding HCG dosing, many found or linked to from the TRT forum - the recurring conclusion being that 250 iu EOD is an effective dose which does not risk LH desensitization. This is the reason I would prefer to start from this lower dose and move up from there, as high as 300 iu ED which I don’t see as being excessive either and I’m sure is probably relatively safe as well. I don’t see anything wrong with starting at a low but proven effective dose for safety’s sake and slowly increasing by only as much as is needed. If the lower dose is effective for me, which I believe it will be, then why take any more? However, if needed I can always up the dose.

With the AI, I have been shutdown for a very long time, almost a year and a half - I may not recover. This PCT is not immediately or even closely following a steroid cycle, it is more like a restart. The cycle that shut me down was a long time ago and I fucked myself over by losing the PCT I had ready and not having access to anything else. My HPTA has been compromised and is not functioning properly. I don’t know what kind of shape my axis is actually in, but it may need every bit of extra support it can get. I have almost zero libido as is, so adding in the AI to keep my pituitary pumping out some LH after I go off the SERM is no biggie for me if I don’t have a killer sex drive - if it is easier for my HPTA to take over on its own coming off an AI than it is coming off a SERM, then this might be the best option for me. I admit though, I don’t know if this is the case, and if it turns out it’s not then I probably don’t need the AI - these are the things I’m trying to sort out right now.

Whatever I can do to support my system and run the best recovery possible is what I need to do. If I’d only been shutdown for a few extra weeks after finishing a cycle then I wouldn’t be as concerned or as focused on the smaller details, but I don’t think I have any other choice at this point.

I want to stress again, I deeply value your help and the help and knowledge everyone else has shared with me so far. I think I have a good shot at recovery if I am smart about what I’m doing, and these forums have enabled me to learn a lot. Thank you again for all you’ve offered so far.

24

[quote]Robert Paulson wrote:

[quote]MassiveGuns wrote:

[quote]Robert Paulson wrote:

[quote]MassiveGuns wrote:

[quote]Singhbuilder wrote:
Wow Rob still shutdown? How longs it been now?

In regards to your post, it has been speculated that clomid has some properties that nolva does not, however I have used both in all combinations and it doesnt seem to be any difference except depression from clomid.
So go with nolva its fine Rob.

The hCG shots, I personally feel the doses are too low to elicit any sort of stimulatory response on the testes. I had to do shots of 2500iu EOD to see any sign of recovery on my previous cycle. My theory is that using hCG doses at LH-replacement dose is not going to stimulate the atrophied testes. You must bring the testes to life first with high doses and then do a SERM PCT, i actually did an AI. And it actually worked.
I feel when the testicles are atrophied they will not respond to low dose as the leydig cells will be atrophied.

Although what MG states is also create and I have utmost respect from him, I just dont agree with the such low dose hCG.
Regarding the Trip, I feel you dont need it. Ive used it and it didnt work for me, my levels still stayed the same.

SB[/quote]

You’re right, an LH replacement dose will no stimulate the testes enough for recovery if they have severely atrophied. The dosing protocol I advocate of 300IU a day is much higher than that. You wanted instant results, which you will get by bumping the dose up. If you follow 300IU per day for up to the 30 days reccomended you will see your testes come back online, just not as fast. You do run the risk of desensitisation with a higher dose.

How you dilute your HCG also has an effect on how potent it is. The more concentrated the solution, the stronger the effect it seems to have. There are studies that have documented this effect with subcutaneous injections of HGH but not hcg, but from personal experience I am sure it makes a big difference.

And I wouldn’t rule out the trip for rob, he’s been shutdown such a long time it might be exactly what he needs. Along with D aspartic acid.[/quote]

Ya I see what you were saying in your previous post about the AI after the SERM prolonging the time before the HPTA can function on its own, I guess my logic is that I should have recovered by now on my own anyway - but maybe after the SERM stimulation my system will be reconditioned and ready to take over once I come off. My worry was that my HPTA might be very fragile even after the SERM run and the idea KSman seems to have offered in other threads is that the AI can help to continue to shield the HPTA from negative feedback for a while as it gets used to working again. I need to re-read his posts but the suggestion was that it is easier for the HPTA to take over by itself from an AI taper than it is from a SERM taper.

The HCG seems like a sensitive drug to use but probably necessary for me to start on. Based on what you guys and others have said, I’ll probably start with a slightly higher dose for a couple of shots and then drop to the 250 iu EOD and gauge responsiveness. This way I can keep the level as low as possible and only increase as much as necessary to gain the desired effect. Not sure what increments I should move up in if I do have to increase, or where I should cap the dosage at to avoid desensitizing the testes, but I’ll prob edge up by 50 IUs at a time.

  • Regarding the HCG dilution, I think the stuff I’m ordering comes 5000 IUs of powder in a 10 mL bottle, sterile & sealed w/ rubber stopper. No bac water though so I was planning on just injecting 10 mL bac water straight into the vial to yield a concentration of 500 IUs/mL - then I can just shoot 1/2 mL slin pin shots for my 250 IUs. Would it be better to use less bac water for a more concentrated solution? Maybe 5 mLs for a concentration of 1000 IUs/mL?

DAA is something I’ve dabbled with to try to get some temporary relief while I’ve been shutdown. On separate occasions I’ve felt the effects very noticeably at a couple of points after a two or three days on but the feeling disappeared almost the next day. Since I know my estrogen is pretty low and T couldn’t have increased by a crazy amount - this makes me wonder if my set point has been lowered for the point at which estrogen causes inhibition at the hypothalamus and/or pituitary. I don’t know if this is even possible but it could explain why I haven’t recovered yet and why I stop feeling the benefits of supps like DAA very quickly. I’m not sure but I think an extended SERM run might be able to reverse a change like this - but don’t quote me on that one.

I think the DAA could be a good add in for after I come off everything, for a little extra support, but I want to understand it’s mechanism of action a little bit better before I throw it in at that delicate time.[/quote]

I don’t mean to be rude but I’d like to point a few things out. You are really overanalysing this faffing. I don’t mind giving advice out, I actually like helping people out but why does everyone feel the need to adjust the protocols given to them for dubious reasons at best? You have a protocol ready to go which does everything you want. SERM for LH and recovery and keeping estrogen in check, HCG to get the testes running and you have a time frame and the option of cutting it short before the maximum 30 days assuming you have significant evidence of recovery.

Where is your rationale for switching to 250IU EOD, because you’ll run less risk of desensitisation? if 300iU per day causes no desensitisation, what possible benefit is this giving you? Its just providing less stimulation to the testes, possibly jeopardising your recovery. There are good reasons why that protocol works as it is, and why you are supposed to get bloodwork done at the specified intervals, its a mugs game going on feel for recovery. If you get the bloodwork done at each stage, you can accurately and objectively track your recovery.

Running any AI with a normal endocrine system can tank your libido rapidly since some estrogen is necessary for proper endocrine function. Fucking about for longer than neccessary is exactly what you want to avoid.

Take my advice, you wont be sorry, and I’d dilute your HCG at 1mL per 1000IU.
[/quote]

MG,

Please don’t think I am under-appreciating your advice, your protocol looks very intelligent and it is most likely the one I will proceed with - maybe with very minor adjustments, maybe none at all. I am not one to arbitrarily change an effective plan someone is kind enough to offer to me, I am simply trying to effectively take the advice I’ve been given by those who have shown to be the most knowledgeable, and utilize it optimally and safely.

Regarding the HCG dose, my rationale for wanting to start from the lower 250 iu EOD is minimizing risk of desensitization, as you suggest. I have read a lot of posts and studies regarding HCG dosing, many found or linked to from the TRT forum - the recurring conclusion being that 250 iu EOD is an effective dose which does not risk LH desensitization. This is the reason I would prefer to start from this lower dose and move up from there, as high as 300 iu ED which I don’t see as being excessive either and I’m sure is probably relatively safe as well. I don’t see anything wrong with starting at a low but proven effective dose for safety’s sake and slowly increasing by only as much as is needed. If the lower dose is effective for me, which I believe it will be, then why take any more? However, if needed I can always up the dose.

With the AI, I have been shutdown for a very long time, almost a year and a half - I may not recover. This PCT is not immediately or even closely following a steroid cycle, it is more like a restart. The cycle that shut me down was a long time ago and I fucked myself over by losing the PCT I had ready and not having access to anything else. My HPTA has been compromised and is not functioning properly. I don’t know what kind of shape my axis is actually in, but it may need every bit of extra support it can get. I have almost zero libido as is, so adding in the AI to keep my pituitary pumping out some LH after I go off the SERM is no biggie for me if I don’t have a killer sex drive - if it is easier for my HPTA to take over on its own coming off an AI than it is coming off a SERM, then this might be the best option for me. I admit though, I don’t know if this is the case, and if it turns out it’s not then I probably don’t need the AI - these are the things I’m trying to sort out right now.

Whatever I can do to support my system and run the best recovery possible is what I need to do. If I’d only been shutdown for a few extra weeks after finishing a cycle then I wouldn’t be as concerned or as focused on the smaller details, but I don’t think I have any other choice at this point.

I want to stress again, I deeply value your help and the help and knowledge everyone else has shared with me so far. I think I have a good shot at recovery if I am smart about what I’m doing, and these forums have enabled me to learn a lot. Thank you again for all you’ve offered so far.[/quote]

I hope I didn’t come across as too harsh. Tapering off AI’s can be a pain in the ass, dosing them correctly is hard to do, you need to know.

If you think your HPTA is fragile, what good will it do you if you get an estrogen rebound from your AI taper and shut yourself down again. Less is more. If you want to run the AI instead of the SERM then I guess you could do that, but then I’ve never done that for PCT. I would definately try the tripto if I were in your situation. I hope you’ve got a plan now, and let us now how you get on.

25

You need hCG OR SERM [to increase LH]. Stay on that until testes have recovered size and firmness. At that point you can do labs for LH+FSH, TT, FT and E2. If LH+FSH is weak, then a restart is in doubt. If T levels are weak, then a restart will be weak [testes may not be recovered/ready].

So not use a SERM with hCG, only one or the other at one time. Suggest SERM+AI to recover testes, then switch to SERM+AI to get the top end of the HPTA into the game. Then one tapers off of the SERM and remains on, AI indefinitely after that, typical anastrozole 0.5mg/week in divided doses.

High levels of LH and/or hCG lead to high levels of E2 production inside the testes. Anastrozole cannot control that, only T–>E2 aromatization in peripheral tissues. We see this where doctors keep increasing anastrozole dose, based on a flawed understanding of the drug and physiology. If anastrozole is not working for you, this can provide the explanation.

If you use too much SERM or hCG you risk LH receptor desensitization; which is a disaster for someone attempting HPTA restart. Do use an anastrozole with either one. SERMs increase E2 levels; if you find that confusing, you may be confused about what a SERM really does.

26

[quote]KSman wrote:
You need hCG OR SERM [to increase LH]. Stay on that until testes have recovered size and firmness. At that point you can do labs for LH+FSH, TT, FT and E2. If LH+FSH is weak, then a restart is in doubt. If T levels are weak, then a restart will be weak [testes may not be recovered/ready].

So not use a SERM with hCG, only one or the other at one time. Suggest SERM+AI to recover testes, then switch to SERM+AI to get the top end of the HPTA into the game. Then one tapers off of the SERM and remains on, AI indefinitely after that, typical anastrozole 0.5mg/week in divided doses.

High levels of LH and/or hCG lead to high levels of E2 production inside the testes. Anastrozole cannot control that, only T–>E2 aromatization in peripheral tissues. We see this where doctors keep increasing anastrozole dose, based on a flawed understanding of the drug and physiology. If anastrozole is not working for you, this can provide the explanation.

If you use too much SERM or hCG you risk LH receptor desensitization; which is a disaster for someone attempting HPTA restart. Do use an anastrozole with either one. SERMs increase E2 levels; if you find that confusing, you may be confused about what a SERM really does.[/quote]

Are you the poster he mentioned saying that its easier to taper off an AI than a SERM? Could you explain why this is the case? Also, why cant you use HCG and a SERM concurrently? How can using a SERM desensitize your LH receptors? If you’ve got something solid to back this up then I’ll take it on board. Are you also aware of why using arimidex and tamoxifen concurrently is also a bad idea?

27

[quote]MassiveGuns wrote:

[quote]KSman wrote:
You need hCG OR SERM [to increase LH]. Stay on that until testes have recovered size and firmness. At that point you can do labs for LH+FSH, TT, FT and E2. If LH+FSH is weak, then a restart is in doubt. If T levels are weak, then a restart will be weak [testes may not be recovered/ready].

So not use a SERM with hCG, only one or the other at one time. Suggest SERM+AI to recover testes, then switch to SERM+AI to get the top end of the HPTA into the game. Then one tapers off of the SERM and remains on, AI indefinitely after that, typical anastrozole 0.5mg/week in divided doses.

High levels of LH and/or hCG lead to high levels of E2 production inside the testes. Anastrozole cannot control that, only T–>E2 aromatization in peripheral tissues. We see this where doctors keep increasing anastrozole dose, based on a flawed understanding of the drug and physiology. If anastrozole is not working for you, this can provide the explanation.

If you use too much SERM or hCG you risk LH receptor desensitization; which is a disaster for someone attempting HPTA restart. Do use an anastrozole with either one. SERMs increase E2 levels; if you find that confusing, you may be confused about what a SERM really does.[/quote]

Are you the poster he mentioned saying that its easier to taper off an AI than a SERM? Could you explain why this is the case? Also, why cant you use HCG and a SERM concurrently? How can using a SERM desensitize your LH receptors? If you’ve got something solid to back this up then I’ll take it on board. Are you also aware of why using arimidex and tamoxifen concurrently is also a bad idea?
[/quote]

If KSman has a chance to reply he will probably do a better job than me of explaining, but my understanding is:
Re tapering off SERM vs AI - not necessarily that it is easier to manage dosing but simply that it is easier for the system to function on its own tapering off the AI as compared to SERM. The way I see it the SERM should be more effective at stimulating the top end of the axis to produce LH because it blocks the feedback receptors more or less completely, regardless of actual estrogen levels (basically), whereas the AI is not blocking the feedback receptors but simply reducing estrogen levels - so here the hypothalamus and pituitary still see some E. However, the SERM will both increase E levels from what is aromatized, as well as act as E in some tissues - even as you taper off the SERM you are still increasing E levels in your body over what they would be normally. AI can control this by preventing aromatization as you taper off the SERM and because it is not completely blocking the feedback receptors from seeing any E at all, but rather just maintaining lower levels - it can be more smoothly tapered with lesser rebound or sudden appearance of E from the receptors perspective - instead you can gradually allow your body to aromatize more T to E by lowering AI dose and let your receptors see a gradual increase.

I may not have the full picture here but logically this makes sense. It basically comes down to the different mode of action each drug uses with estrogen - because the AI prevents aromatization and therefore actually keeps real E levels down, vs the SERM which just hides E from the hypothal and pituitary, causing the HPTA to create more E. Both can increase T through a similar mechanism - top of axis sees less or no E, but one produces more E and the other doesn’t. This is why it should be easier to taper off AI with less negative feedback to the hypothal and pituitary.

I know you are fully aware of how these compounds work MG, I dont mean to sound like I’m now explaining to you, I’m just trying to outline how the difference between the two seems logically conclusive with an AI taper being an easier transition.

-Re the concurrent SERM + HCG, I think the idea is that SERM increases LH, plus HCG acts as LH - testes see both as LH - may be overload for leydig cells just as too much HCG can be overload and cause desensitization. This is all just my basic understanding and I could be wrong about any part of it but it all seems to make sense. If anyone knows differently please interject.

28

[quote]Robert Paulson wrote:

[quote]MassiveGuns wrote:

[quote]KSman wrote:
You need hCG OR SERM [to increase LH]. Stay on that until testes have recovered size and firmness. At that point you can do labs for LH+FSH, TT, FT and E2. If LH+FSH is weak, then a restart is in doubt. If T levels are weak, then a restart will be weak [testes may not be recovered/ready].

So not use a SERM with hCG, only one or the other at one time. Suggest SERM+AI to recover testes, then switch to SERM+AI to get the top end of the HPTA into the game. Then one tapers off of the SERM and remains on, AI indefinitely after that, typical anastrozole 0.5mg/week in divided doses.

High levels of LH and/or hCG lead to high levels of E2 production inside the testes. Anastrozole cannot control that, only T–>E2 aromatization in peripheral tissues. We see this where doctors keep increasing anastrozole dose, based on a flawed understanding of the drug and physiology. If anastrozole is not working for you, this can provide the explanation.

If you use too much SERM or hCG you risk LH receptor desensitization; which is a disaster for someone attempting HPTA restart. Do use an anastrozole with either one. SERMs increase E2 levels; if you find that confusing, you may be confused about what a SERM really does.[/quote]

Are you the poster he mentioned saying that its easier to taper off an AI than a SERM? Could you explain why this is the case? Also, why cant you use HCG and a SERM concurrently? How can using a SERM desensitize your LH receptors? If you’ve got something solid to back this up then I’ll take it on board. Are you also aware of why using arimidex and tamoxifen concurrently is also a bad idea?
[/quote]

If KSman has a chance to reply he will probably do a better job than me of explaining, but my understanding is:
Re tapering off SERM vs AI - not necessarily that it is easier to manage dosing but simply that it is easier for the system to function on its own tapering off the AI as compared to SERM. The way I see it the SERM should be more effective at stimulating the top end of the axis to produce LH because it blocks the feedback receptors more or less completely, regardless of actual estrogen levels (basically), whereas the AI is not blocking the feedback receptors but simply reducing estrogen levels - so here the hypothalamus and pituitary still see some E. However, the SERM will both increase E levels from what is aromatized, as well as act as E in some tissues - even as you taper off the SERM you are still increasing E levels in your body over what they would be normally. AI can control this by preventing aromatization as you taper off the SERM and because it is not completely blocking the feedback receptors from seeing any E at all, but rather just maintaining lower levels - it can be more smoothly tapered with lesser rebound or sudden appearance of E from the receptors perspective - instead you can gradually allow your body to aromatize more T to E by lowering AI dose and let your receptors see a gradual increase.

I may not have the full picture here but logically this makes sense. It basically comes down to the different mode of action each drug uses with estrogen - because the AI prevents aromatization and therefore actually keeps real E levels down, vs the SERM which just hides E from the hypothal and pituitary, causing the HPTA to create more E. Both can increase T through a similar mechanism - top of axis sees less or no E, but one produces more E and the other doesn’t. This is why it should be easier to taper off AI with less negative feedback to the hypothal and pituitary.

I know you are fully aware of how these compounds work MG, I dont mean to sound like I’m now explaining to you, I’m just trying to outline how the difference between the two seems logically conclusive with an AI taper being an easier transition.

-Re the concurrent SERM + HCG, I think the idea is that SERM increases LH, plus HCG acts as LH - testes see both as LH - may be overload for leydig cells just as too much HCG can be overload and cause desensitization. This is all just my basic understanding and I could be wrong about any part of it but it all seems to make sense. If anyone knows differently please interject.
[/quote]

Right now I see no logic to it being easier to come off an AI than a SERM. If you taper off a serm, estrogen levels will reduce as the dose decreases if they are elevated. Also, nolvadex with block estrogen at the HTPA at even a 5mg daily dose. There may be another mechanism whereby lowering estrogen as opposed to blocking it aids recovery, I’ll hold off judgement of that until I see some evidence. And the idea that SERMS raise LH so much that adding HCG with desensitize the leydig cells? That sounds like science fiction to me and I’d like to see some hard evidence in order to accept that. SERMS help with LH production, they don’t jack it to the levels possible with HCG use.

29

[quote]MassiveGuns wrote:

[quote]Robert Paulson wrote:

[quote]MassiveGuns wrote:

[quote]KSman wrote:
You need hCG OR SERM [to increase LH]. Stay on that until testes have recovered size and firmness. At that point you can do labs for LH+FSH, TT, FT and E2. If LH+FSH is weak, then a restart is in doubt. If T levels are weak, then a restart will be weak [testes may not be recovered/ready].

So not use a SERM with hCG, only one or the other at one time. Suggest SERM+AI to recover testes, then switch to SERM+AI to get the top end of the HPTA into the game. Then one tapers off of the SERM and remains on, AI indefinitely after that, typical anastrozole 0.5mg/week in divided doses.

High levels of LH and/or hCG lead to high levels of E2 production inside the testes. Anastrozole cannot control that, only T–>E2 aromatization in peripheral tissues. We see this where doctors keep increasing anastrozole dose, based on a flawed understanding of the drug and physiology. If anastrozole is not working for you, this can provide the explanation.

If you use too much SERM or hCG you risk LH receptor desensitization; which is a disaster for someone attempting HPTA restart. Do use an anastrozole with either one. SERMs increase E2 levels; if you find that confusing, you may be confused about what a SERM really does.[/quote]

Are you the poster he mentioned saying that its easier to taper off an AI than a SERM? Could you explain why this is the case? Also, why cant you use HCG and a SERM concurrently? How can using a SERM desensitize your LH receptors? If you’ve got something solid to back this up then I’ll take it on board. Are you also aware of why using arimidex and tamoxifen concurrently is also a bad idea?
[/quote]

If KSman has a chance to reply he will probably do a better job than me of explaining, but my understanding is:
Re tapering off SERM vs AI - not necessarily that it is easier to manage dosing but simply that it is easier for the system to function on its own tapering off the AI as compared to SERM. The way I see it the SERM should be more effective at stimulating the top end of the axis to produce LH because it blocks the feedback receptors more or less completely, regardless of actual estrogen levels (basically), whereas the AI is not blocking the feedback receptors but simply reducing estrogen levels - so here the hypothalamus and pituitary still see some E. However, the SERM will both increase E levels from what is aromatized, as well as act as E in some tissues - even as you taper off the SERM you are still increasing E levels in your body over what they would be normally. AI can control this by preventing aromatization as you taper off the SERM and because it is not completely blocking the feedback receptors from seeing any E at all, but rather just maintaining lower levels - it can be more smoothly tapered with lesser rebound or sudden appearance of E from the receptors perspective - instead you can gradually allow your body to aromatize more T to E by lowering AI dose and let your receptors see a gradual increase.

I may not have the full picture here but logically this makes sense. It basically comes down to the different mode of action each drug uses with estrogen - because the AI prevents aromatization and therefore actually keeps real E levels down, vs the SERM which just hides E from the hypothal and pituitary, causing the HPTA to create more E. Both can increase T through a similar mechanism - top of axis sees less or no E, but one produces more E and the other doesn’t. This is why it should be easier to taper off AI with less negative feedback to the hypothal and pituitary.

I know you are fully aware of how these compounds work MG, I dont mean to sound like I’m now explaining to you, I’m just trying to outline how the difference between the two seems logically conclusive with an AI taper being an easier transition.

-Re the concurrent SERM + HCG, I think the idea is that SERM increases LH, plus HCG acts as LH - testes see both as LH - may be overload for leydig cells just as too much HCG can be overload and cause desensitization. This is all just my basic understanding and I could be wrong about any part of it but it all seems to make sense. If anyone knows differently please interject.
[/quote]

Right now I see no logic to it being easier to come off an AI than a SERM. If you taper off a serm, estrogen levels will reduce as the dose decreases if they are elevated. Also, nolvadex with block estrogen at the HTPA at even a 5mg daily dose. There may be another mechanism whereby lowering estrogen as opposed to blocking it aids recovery, I’ll hold off judgement of that until I see some evidence. And the idea that SERMS raise LH so much that adding HCG with desensitize the leydig cells? That sounds like science fiction to me and I’d like to see some hard evidence in order to accept that. SERMS help with LH production, they don’t jack it to the levels possible with HCG use.[/quote]

I definitely see your point of view, and I’ll be the first to admit I haven’t read specific studies on the disparate effects of a nolva vs AI taper on the HPTA. I doubt there are any such studies out there but hopefully there’s some info somewhere that will allow us to read between the lines. All I’m suggesting is that it makes sense to me that the HPTA (especially one that has had trouble recovering) should logically have an easier time resuming natural production when we slowly allow the body to aromatize more estrogen until it is very close to its natural level, rather than blocking the top of the axis from seeing any estrogen for nearly the entire duration of nolva use then suddenly showing the axis E again - as you said, the nolva has been shown to block estrogen very effectively at doses as low as 5 mg. how many of us taper their nolva lower than 5 mgs at the end of PCT? Prob very few if anybody.

As far as I have understood up until now, the SERM taper is more to allow reduction in the levels of estrogen that the SERM has caused to rise, before coming off the SERM. I have never understood its purpose to be gradually allowing the hypothalamus and pituitary to see incrementally more E. This is what the AI taper would do. I think most would agree that a SERM is more effective at stimulating LH production than an AI, although I know some will use an AI in place of SERM for PCT. IMO the SERM spurs LH production better largely because it makes the hypothalamus and pituitary think there is nearly no E in the body so they start working very hard to bring about E production and thus restore homeostasis. The AI lowers real E levels, so if they are lowered enough the AI has the similar effect but it will not be to the same extent.

IMHO this difference between the AI and SERMs respective mechanisms of action which makes the SERM a more effective stimulator of LH production, is the same difference which makes the AI taper a smoother transition for the HPTA to take over natural production from. I would not prefer an AI in place of SERM for PCT, but I would prefer to taper the SERM and add in low dose AI at the end of SERM use, then maintain AI for a short period and taper gradually off that as well. Not AI in place of SERM, AI to transition out of PCT which should consist mainly of effective SERM use.

In regards to the HCG + SERM combo and the desensitization issue - you may well be right, it’s possible that the combination would not represent LH levels high enough to affect the leydiggs in this way. It would help to know what amount of HCG is equivalent to what amount of endogenous LH. It would also help to know what the threshold is at which the desensitization occurs.
However, the way I’m looking at it is in homeostasis the body produces a physiological level of LH that maintains the proper levels of T and E. When these hormone levels decrease significantly, the pituitary kicks in with a greater level of LH production to bring them back up. A SERM causes the pituitary to produce LH at closer to the top of the physiological range because it is working harder than it would normally ever have to to restore E levels. If endogenous LH is near the top of the physiological range and we add in moderate HCG doses which the body also perceives as LH, then this may be a supra physiological level of LH and although I don’t know for sure at what level desensitization occurs, I would be pretty cautious about these types of levels. I’m not saying low dose HCG combined with moderate SERM use WILL cause desensitization - but it’s something to consider.

I’d like to note here, that these aspects may not be as important for everybody - if you’ve had zero problems with recovery in the past and don’t run particularly long or suppressive cycles then these may be negligible concerns. However if you’ve likely done some damage to your axis or have had recovery issues and are landing on a questionable HPTA I think these things definitely are worth bearing in mind. Given my lack of natural recovery over such a long period off, I would enter myself in the latter category.

30

[quote]MassiveGuns wrote:

Right now I see no logic to it being easier to come off an AI than a SERM. [/quote]

I’m afraid you may be creating a strawman argument there. Or else I am missing something. I see nowhere where he states it is easier to come off AI than a SERM. I think he is recommending discontinuing the SERM earlier than the AI because by that point the SERM has done its job of recovering endogenous Test levels. The AI is continued (I suppose) to combat estrogen rebound (which I am undecided if it exists or not).

REgardless, it is established that AI monotherapy is effective at increasting T levels, so staying on it longer is ok IMO.

Perhaps slightly, but by how much? The SERM itself does not increase your estrogen levels, so if they were already high before, then it makes sense to discontinue SEERM and continue AI.

But it does not block it in other tissues. I’m not sure what you’re saying here though, just thought I would throw that out there.

Yes this does occur. AI monotherapy is shown to increase T levels.

Agreed here. I’ve never heard it stated that SERMs will decrease leydig sensitivitiy and I find this hard to believe that it would occur.

31

[quote]VTBalla34 wrote:

[quote]MassiveGuns wrote:

Right now I see no logic to it being easier to come off an AI than a SERM. [/quote]

I’m afraid you may be creating a strawman argument there. Or else I am missing something. I see nowhere where he states it is easier to come off AI than a SERM. I think he is recommending discontinuing the SERM earlier than the AI because by that point the SERM has done its job of recovering endogenous Test levels. The AI is continued (I suppose) to combat estrogen rebound (which I am undecided if it exists or not).

REgardless, it is established that AI monotherapy is effective at increasting T levels, so staying on it longer is ok IMO. [/quote]

No he’s right on my view, I am saying that it should be easier for the HPTA to pick up on its own from an AI taper vs a SERM taper - SERM you are blocking E from the receptors at top of axis, even as low as 5mg this is occurring quite effectively with nolva so for most of the taper you are still almost completely hiding E from the H&P. Then you suddenly show the H&P E levels that they have not seen for a long period of time. With an AI, as you taper you are allowing gradually more aromatization to occur until you reach a level of E close to what your body will produce on its own when you go off - E is controlled and kept low when it needs to be, but when it’s time to come off we can slowly show the H&P slight increases in E levels rather than going from almost 0 to normal or slightly elevated.

The idea that it is easier for the HPTA to land coming off an AI taper as opposed to a SERM taper has been suggested by KSman and it makes sense to me. This explanation as to why is mine though, so he may have other reasons.

This seems to be a misunderstanding of a misunderstanding. I would also be hard pressed to believe that SERMs could raise LH enough to cause desensitization, since their action is only to cause the pituitary to work within it’s own natural limits to recover E levels.

What I AM saying is that we know high enough HCG doses can represent enough LH to cause desensitization. Therefore, if we are using a dose of HCG slightly lower than we would expect to cause desensitization but the body is already producing a level of LH at the top of it’s natural limit - then the combination of the significant amount of exogenous LH from HCG + the boosted endogenous LH might = a level of LH that can cause decreased responsiveness of LH receptors to LH. This idea AND explanation for it have also been suggested by KSman, and again it all makes logical sense to me.

^^keep in mind with HCG use on cycle the HPTA is shutdown and we don’t even have to worry about the combined effect of endo + exo HCG. Like I said earlier, these two ideas - the AI vs SERM taper & the HCG + SERM effect, may be of minor importance for a lot of people. But, I think the implications are important for guys with recovery issues or attempting restarts coming off TRT.

32

[quote]VTBalla34 wrote:

[quote]MassiveGuns wrote:

Right now I see no logic to it being easier to come off an AI than a SERM. [/quote]

I’m afraid you may be creating a strawman argument there. Or else I am missing something. I see nowhere where he states it is easier to come off AI than a SERM. I think he is recommending discontinuing the SERM earlier than the AI because by that point the SERM has done its job of recovering endogenous Test levels. The AI is continued (I suppose) to combat estrogen rebound (which I am undecided if it exists or not).

REgardless, it is established that AI monotherapy is effective at increasting T levels, so staying on it longer is ok IMO.

Perhaps slightly, but by how much? The SERM itself does not increase your estrogen levels, so if they were already high before, then it makes sense to discontinue SEERM and continue AI.

But it does not block it in other tissues. I’m not sure what you’re saying here though, just thought I would throw that out there.

Yes this does occur. AI monotherapy is shown to increase T levels.

Agreed here. I’ve never heard it stated that SERMs will decrease leydig sensitivitiy and I find this hard to believe that it would occur.
[/quote]

To base an argument on minute differences between the levels of estrogen in the body when you are using either an AI or a SERM is a waste of time for all of us. Both approaches reduce the estrogen that the HPTA percieves and subsequently increase T levels. SERMS, nolva in particular also has a beneficial effect on LH production secondary to this that aids in recovery. Thats +1 for the SERM

At a 5mg dose estrogen is still blocked at the HTPA, but to think that its going to be to the same extent as a 20mg dose is silly. The point is that whatever estrogen rise is caused by nolvadex is not percieved by the HTPA. Since the estrogen rise will be less with a 5mg dose, as you taper off it, the HTPA will never see that increased estrogen level.

Since tamoxifen(nolva) is the most commonly used SERM, it makes sense to really understand how it works. Tamoxifen itself is not a SERM, it has virtually no action at the estrogen receptor. Tamoxifen is PRO DRUG. That means it converts to its active form in the body. The active form has a very long half life. This means when you come off it, it will naturally taper for weeks after you stop taking it, and way smoother than you could ever hope to manage with any AI.

The fact that AI monotherapy also raises testosterone levels is not evidence that it is superior to a SERM such as tamoxifen, and certainly no evidence of a mechanism by which it is superior. They both increase testosterone levels.

And Robert, 300IU per day is quite a bit more than your natural LH production. The fact you can run this dose for a month with no leydig desensitisation is published in a paper somewhere.

Seriously robert, everything has been thought through for that recovery protocol. All the bases are covered. If you want to add an AI, then use aromasin and taper off that after. That way you’ll have an easier time adjusting the dose AND you wont fuck your liver with a drug interaction between a SERM and an AI OR fuck the levels of both drugs in your system up unpredictably and jeopardise your chances of recovery.

33

On a different note, I’ve received my HCG, liquid adex, and 30cc bac water. Due to miscommunication with the RC supplier, my HCG is in a much smaller vial than I expected - looks like about a 3mL vial (the Chinese one with the white and blue label, don’t know if I can say the name of manufacturer on here). I was expecting it to come in a 10mL vial so I could recon with 10cc bac water but it looks like I can probably only shoot maybe 2.5 mL into the vial the powder is already in.

This might be alright it’ll just be a much higher concentration - if I recon 5000ius with 2.5 mL bac water, the concentration will be 2000iu/mL. Using a slin pin I can shoot 0.125mL to get my 250iu doses. Just two questions if anybody can weigh in:

1- Is there any problem with reconstituting right there in the bottle the dried HCG came in? It’s got a flip cap and is sealed and everything. I only ask because I’ve only read of guys putting the reconstituted solution in a new bottle - don’t know if keeping it in the original bottle is common practice.

2- Regarding the concentration, is it too high? ie. is there too much margin for error or wasted product due to high concentration? Too difficult to administer such tiny amounts? I’m considering trying to get a hold of some 0.5cc slin pins which might make it easier to shoot the 0.125mL doses, but I’m just not used to shooting anything under 0.5mL so don’t really know how well any of this works when things get smaller and more precise.

34

[quote]MassiveGuns wrote:

[quote]VTBalla34 wrote:

[quote]MassiveGuns wrote:

Right now I see no logic to it being easier to come off an AI than a SERM. [/quote]

I’m afraid you may be creating a strawman argument there. Or else I am missing something. I see nowhere where he states it is easier to come off AI than a SERM. I think he is recommending discontinuing the SERM earlier than the AI because by that point the SERM has done its job of recovering endogenous Test levels. The AI is continued (I suppose) to combat estrogen rebound (which I am undecided if it exists or not).

REgardless, it is established that AI monotherapy is effective at increasting T levels, so staying on it longer is ok IMO.

Perhaps slightly, but by how much? The SERM itself does not increase your estrogen levels, so if they were already high before, then it makes sense to discontinue SEERM and continue AI.

But it does not block it in other tissues. I’m not sure what you’re saying here though, just thought I would throw that out there.

Yes this does occur. AI monotherapy is shown to increase T levels.

Agreed here. I’ve never heard it stated that SERMs will decrease leydig sensitivitiy and I find this hard to believe that it would occur.
[/quote]

To base an argument on minute differences between the levels of estrogen in the body when you are using either an AI or a SERM is a waste of time for all of us. Both approaches reduce the estrogen that the HPTA percieves and subsequently increase T levels. SERMS, nolva in particular also has a beneficial effect on LH production secondary to this that aids in recovery. Thats +1 for the SERM

At a 5mg dose estrogen is still blocked at the HTPA, but to think that its going to be to the same extent as a 20mg dose is silly. The point is that whatever estrogen rise is caused by nolvadex is not percieved by the HTPA. Since the estrogen rise will be less with a 5mg dose, as you taper off it, the HTPA will never see that increased estrogen level.

Since tamoxifen(nolva) is the most commonly used SERM, it makes sense to really understand how it works. Tamoxifen itself is not a SERM, it has virtually no action at the estrogen receptor. Tamoxifen is PRO DRUG. That means it converts to its active form in the body. The active form has a very long half life. This means when you come off it, it will naturally taper for weeks after you stop taking it, and way smoother than you could ever hope to manage with any AI.

The fact that AI monotherapy also raises testosterone levels is not evidence that it is superior to a SERM such as tamoxifen, and certainly no evidence of a mechanism by which it is superior. They both increase testosterone levels.

And Robert, 300IU per day is quite a bit more than your natural LH production. The fact you can run this dose for a month with no leydig desensitisation is published in a paper somewhere.

Seriously robert, everything has been thought through for that recovery protocol. All the bases are covered. If you want to add an AI, then use aromasin and taper off that after. That way you’ll have an easier time adjusting the dose AND you wont fuck your liver with a drug interaction between a SERM and an AI OR fuck the levels of both drugs in your system up unpredictably and jeopardise your chances of recovery.[/quote]

Sorry, missed this when I posted last.

Just want to clarify again I’m not arguing an AI is more effective for recovery, I believe a SERM does a better job at getting the pituitary rolling again. I just think for the reasons previously stated that the AI will be a smoother taper and would be beneficial as an add on when ceasing SERM use for this reason.

Interested to hear of the study you mention, showing 300iu ED dosing safe for up to a month. I am willing to go as high as this dose based on testicular responsiveness during treatment. I still prefer to begin with the 250iu EOD dose and increase on an as needed basis simply because this is the replacement dose that has been advocated repeatedly in the TRT context - both through the studies and anecdotal. Also, I will be on the HCG closer to 6 weeks so it will be a bit longer than a month.

35

[quote]Robert Paulson wrote:
1- Is there any problem with reconstituting right there in the bottle the dried HCG came in? It’s got a flip cap and is sealed and everything. I only ask because I’ve only read of guys putting the reconstituted solution in a new bottle - don’t know if keeping it in the original bottle is common practice.

2- Regarding the concentration, is it too high? ie. is there too much margin for error or wasted product due to high concentration? Too difficult to administer such tiny amounts? I’m considering trying to get a hold of some 0.5cc slin pins which might make it easier to shoot the 0.125mL doses, but I’m just not used to shooting anything under 0.5mL so don’t really know how well any of this works when things get smaller and more precise.[/quote]

you can reconstitute in the vial it came in, don’t worry about that. When you do reconstitute the shit then don’t squirt the bac water directly on the freeze dried stuff. Let it slowly drip down the side of the vial til it’s all in there. Don’t shake it to mix it.

2- you can shoot small, concentrated doses but it’ll be a pain in the arse to draw such a tiny amount. I would put 1 ml of water per 1000iu of hcg to make it a bit easier.

36

I haven’t been in for a week or two but thanks for that RDS, I did end up reconning in the small vial - giving a concentration of 2,000iu/mL. Pretty tiny volumes to pin but I got ahold of some 0.5 mL slin pins so it’s actually pretty easy with the smaller barrels.

Unfortunately, when I mixed in the bac water I did end up dropping some straight onto the dried HCG before managing to run it down the side. I’ve also had a cpl of incidents where I accidentally shot the concentration back into the vial a little too quickly from the pin while drawing it out (trying to get rid of air in the syringe). This caused collections of small bubbles within the vial and is not how one would want to handle HCG. Hopefully through all of this I have not disturbed the compound enough to denature the molecule structure, as I know it is supposed to be delicate stuff.

37

I also meant to make this thread a bit of a log so I should update while I’m here. The final protocol I had decided on and have started into is more or less the following:

Day 1&3 = 500iu HCG
Day 3-40 = 250iu HCG EOD
Day 20-40 = 0.125mg arimidex EOD
Day 44 = 100mcg triptorelin
Day 44-86 (6 wks) = 20mg nolvadex ED
Day 87-100 (2 wks) = 10mg nolvadex ED, 0.125mg arimidex EOD
Day 101-107 (1 wk) = 5mg nolvadex ED. 0.125mg arimidex EOD
Day 108-undetermined = 0.125mg arimidex EOD, taper lower from here by switching to 0.125mg E3D or 0.8mg EOD?

This will and has already been subject to slight modifications during the process but this is pretty much what the treatment will look like. Observations and adjustments discussed below.

DAY 1&2 - By the following night after first 500iu pin of HCG, I actually thought I noticed some slight improvements in testicular volume and hanging, as well as improvements in energy & mood. Some or all of this could’ve been placebo effect but I’m pretty sure the boys responded in at least some way.

DAY 9 - I have now completed 2x500iu pins and 3x250iu pins all on an EOD schedule. There seems to have been some effect, most noticeable transiently - significant improvements in mood, energy, confidence; smaller but notable improvements in testicular volume and hanging, slight improvement in libido but far from having the raging animal lust I used to before all this.

The problem is all these improvements have been fleeting and seem to disappear from one day to the next - I know there’s quite a range in responsiveness to HCG and some have mentioned needing up to several weeks for the beneficial effects to show up. I’m only about 12 days in at a moderate but proven effective dose so I’m not too worried yet.

DAY 12 - About 3 days ago I changed my dosing schedule to 120iu ED and have pinned twice at this dose. Reason being to try to gain a more consistent effect. After reading Hockeysledder’s HCG ED thread, this dosing makes sense to me and it sounds like it was slightly more effective for him.

Only problem with the way I’ve done it is if I start to notice better effects right away it will be hard to tell whether the stuff is just starting to work because of the amount of time I’ve been taking it, or rather due to the change in dosing schedule. I can say that I haven’t really noticed any more of the clear but transient improvements over the last two days that I was noticing before, albeit irregularly.

I suspect my T level is climbing, or at least spiking somewhat - just slowly.

Have had some slight increase in acne on the forehead but nothing crazy, may indicate a degree of increased aromatization due to increases in T, but this is actually good for me to a point because E has been quite low along with T for a while, I think around 10pg/mL if I remember correctly. So a bit more of the stuff should be beneficial for my rusty ass joints and shit libido.

^^As planned I have not yet started adex for this reason and may wait a little longer than 20 days into HCG run to do so, if at all. Still haven’t found online labs I can use from my location and prob couldn’t afford them anyway so much of this is going to have to go off subjective feel and sides.

Anyone has thoughts I’d love to hear em

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Glad to hear that you are seeing some sort of a benefit. Always good to know when a fellow lifter is making progress :slight_smile:

I would add the adex in, when I was shutdown (I am now aswell but from my previous cycle not the latest) it helped greatly with a combo of hCG, nolva and low-dose adex. I was using 0.25mg adex EOD and being an adex over-responder it seemed to do the trick for me. Consider it, go by how you feel. If you feel shitty then you know that you are driving E too low.
Also I am not advocating the adex use in an attempt to control E spiked by the hCG as it has generally been agreed that adex cannot prevent testicular aromatisation.

SB

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[quote]Singhbuilder wrote:
Glad to hear that you are seeing some sort of a benefit. Always good to know when a fellow lifter is making progress :slight_smile:

I would add the adex in, when I was shutdown (I am now aswell but from my previous cycle not the latest) it helped greatly with a combo of hCG, nolva and low-dose adex. I was using 0.25mg adex EOD and being an adex over-responder it seemed to do the trick for me. Consider it, go by how you feel. If you feel shitty then you know that you are driving E too low.
Also I am not advocating the adex use in an attempt to control E spiked by the hCG as it has generally been agreed that adex cannot prevent testicular aromatisation.

SB[/quote]

Thanks Singh, always good to hear from you. I was also thinking it might be time to add the adex in, if nothing else at least to try and minimize suppression of the pituitary. I don’t think I’m over aromatizing, but it might also be possible that the initial, mariginal but positive affects I was seeing were a combined effect from the HCG pins plus the endogenous LH my pituitary was still putting out. May be that the exo doses have shut down the minimal natural production that was still going on.

I’ve been running a few days of 120iu ED rather than the 250 EOD in an attempt to gain more consistent effects - so far no luck. May have to continue tweaking/upping the dosing if no benefits are seen after another five days or so. I’ll prob add in the adex soon, I may also have to order some more HCG if it comes to upping the dosage a bit.

Hopefully my problem is not my stuff is weak or that I butchered the molecular structure of the drug while reconstituting. I doubt it’s completely bunk due to the improvements I have felt at different times since starting.

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DAY 17 - After a couple weeks of the 250 EOD protocol and trying several more days on 120iu ED, there had been little to no actual improvement in testicular volume and testes were still mostly drawn up tight majority of the time.

I’ve now pinned 3 days in a row at 250iu ED and hanging has improved along with a slightly fuller appearance to the boys. Its clear to me that there is some sort of response occurring to the HCG, I think it’s just likely my testes needed a bit more stimulation due to the very long period they’ve been starved of LH. 250 ED seems to be having the right effect.

I’m finishing my bottle a bit quicker than anticipated at this dose. May order some more and run another 2500 ius over an additional 10 days. Since the stuff seems to have just started to take effect I’d like to run it for at least 2-3 wks more to try restoring my nuts as much as possible.