My introduction.....

[Sworder]

The concept that even though he is already producing a high LH signal that somehow blasting the testicles with an even higher unnatural signal from Hcg will supposedly result in the testicles being more sensitive to an even lower LH signal later defies logic to me...

Ask Dr Scally about why you blast the testes with hCG. If the logic defies you I cannot be the one to convince you neither, I have seen tons of success following his principles and Power PCT.

 

[Dr JIM]

Yes I must agree FY, Although stimulating the testis w HCG seems beneficial as pre-SERM therapy, especially if atrophy is present, using HCG to evaluate a patients testicular reserve is inherently flawed.

That's bc using HCG in this manner only evaluates TT secretion as a response to exogenous HCG stimuli, rather than under the influence of endogenously produced LH.

A more reliable estimate can be made by upward titration of the SERM dosage, IME.

Regs
Jim

 

[Dr JIM]

Ask Dr Scally about why you blast the testes with hCG. If the logic defies you I cannot be the one to convince you neither, I have seen tons of success following his principles and Power PCT.

Your misapplying the objective of HCG use Sworder.

P PCT primary purpose is to reverse the atrophy that has occurred THRU CYCLING.

The intent being to stimulate Leydig cells to begin producing TT once again, having been exposed to high doses of AAS for many weeks.

And while atrophy may occur with traditional TRT the degree of atrophy is minimal on a comparative basis, thus the need for HCG is also of less importance.

Moreover IDSTER lab results have already proven his testicles can produce effective levels of TT under the influence of ENDOGENOUS LH.

Ergo the use of HCG is relatively redundant at this juncture AND is less than optimal therapy since it's use will cause E-2 levels to rise.

In this case patience is of paramount importance bc effective PCT simply takes time.

 

[MR10X]

Dr Scally uses HCG to see if your capable producing test on your own,if it doesn't no amount of serm will help.His use is mainly for guys that are hypo and not PCT...

 

[idmd]

Dr. S - I'm 6'5" 275lbs. Workout a minimal of 3x per week doing both lifting and HIIT. I'm no beast at the gym and I certainly have some adipose around the midsection but in fairly good shape - especially considering where I started. I think 250lbs is ideal for me and that was my goal but last time I tried I really had to starve myself even to get to 260lbs. I have no issues eating and exercising to maintain 275 - so I compromised.

I want to thank everyone for their input - much appreciated!

 

[idmd]

Yo try not to be such a stranger mate. Do stay in touch and update us on your progress.

Will do Jim. Thanks for your help.

 

[toolman]

IDMD your alive!?!? Welcome back! What is the reason you want to discontinue? If I recall you had other issues going on medically. Have they all been resolved? Did Dr. H try a restart with you when you first went there?

 

[idmd]

toolman,

Nothing more than curiosity and a touch of laziness. I've moved away from the good Dr. H and haven't found a new doc and was running low on test and figured what the hell...why not try and see if I can restart? It was easier to get my hands on clomid and tamox than go through what will be the arduous task of getting hooked up with a new doc. If I have to then I have to - just wanted to see what would happen.

All other medical issues resolved. I've kept the weight off, still eating well, still exercising, feeling good with no issues. Still feel good even during this restart attempt.

How are you doing toolman?

 

[idmd]

Did Dr. H try a restart with you when you first went there?

Dr. H and I did not try a restart initially but we were planning on trying it and then I moved out-of-state.

 

[Sworder]

Your misapplying the objective of HCG use Sworder.

P PCT primary purpose is to reverse the atrophy that has occurred THRU CYCLING.

The intent being to stimulate Leydig cells to begin producing TT once again, having been exposed to high doses of AAS for many weeks.

And while atrophy may occur with traditional TRT the degree of atrophy is minimal on a comparative basis, thus the need for HCG is also of less importance.

Moreover IDSTER lab results have already proven his testicles can produce effective levels of TT under the influence of ENDOGENOUS LH.

Ergo the use of HCG is relatively redundant at this juncture AND is less than optimal therapy since it's use will cause E-2 levels to rise.

In this case patience is of paramount importance bc effective PCT simply takes time.

I strongly disagree.

Idmd is showing high LH so we know his pituitary is working, no problem there. The timing on the PCT seems to be fine, SERMs wouldn't increase LH that much otherwise. His balls need help and need to be woken up, although physical size of the testes are good. That doesn't mean that his leydig cells have atrophied on a cellular level.
Idmd is showing low tT along with his LH being high so obviously the leydig cells are not responding unless there is another problem. This conclusion is strengthened by the fact he was on TRT for 2 years and he didn't use any hCG.

Like MR10X said, no SERM in the world will help if your testes are not accepting the LH/hCG signal.

idmd your leydig cells aren't responding to LH, blast that shit with hCG. There is a reason to why Dr Scally's PCT program uses hCG and a lot of it.

HPTA restarts are really simple and you should start with your testicles and not the Hypo/Pit. Again, no amount of SERM in the world will help unless you make sure your testes can use the LH. HCG is used to bring testes back to working order, restimulate them and prime them for the future incoming LH signal. GET LABS WHILE ON HCG to see how much test the testes are producing at that point. If your testes are only producing 200ng/dl obviously hCG needs to be continued OR your testes are not responsive in which the case the diagnosis of being primary occurs.
If during hCG your testes are up in the 600ng/dl range, you know they are capable of that production, in my opinion, at that level you can start the SERM treatment.
Figure out the problem:
HPT
Hypothalamus/Pit: Is LH/FSH being produced? If yes, they are good to go.
Testes: Is testosterone being produced?

 

[Sworder]

Didn't have time to finish my post, but idmd's blood work is stating the problem lies with his testes.
As you said, his testes has worked before. They are currently not working with the LH signal being sent.

They need a jump start, the leydig cells have been hibernating for over 2 years. Blast them with hCG or do something to the balls! Smack em! Kick em! Just kidding, but you can sit and wait for your testes to acclimate to the LH and hope they will respond. You may be waiting for a while though! Tick tock

 

[idmd]

A lot of receptor-mediated processes are determined by both the amplitude as well as the duration of the signal. The question is, Sworder, does high dose hCG really do anything more than lower dose but longer duration LH (driven by SERMs)? Additionally, hCG has a suppressive effect that needs to be considered. I don't know the answer conclusively but my guess is SERMS as a way of increasing LH over a longer period of time are comparable to shorter duration hCG therapy and without the suppression. Any one who has actual data please feel to correct me - just thinking out loud.

 

[Sworder]

A lot of receptor-mediated processes are determined by both the amplitude as well as the duration of the signal.

Where do you find the duration of LH/hCG @ receptor site? This data is not to be found from my experience if you are talking about receptor activity on hCG vs LH. And again, you need more LH/hCG to stimulate the receptors so they can wake up out of the 2 year hibernation!

The question is, Sworder, does high dose hCG really do anything more than lower dose but longer duration LH (driven by SERMs)?

YES!!!! This is why Scally uses higher doses (2.5k iu), when your cells are atrophied you need a stronger signal to get them up and running again.

Additionally, hCG has a suppressive effect that needs to be considered.

No it doesn't need to be considered because you aren't using the SERMs at the same time..

I don't know the answer conclusively but my guess is SERMS as a way of increasing LH over a longer period of time are comparable to shorter duration hCG therapy and without the suppression. Any one who has actual data please feel to correct me - just thinking out loud.

HCG and SERMs act on completely different systems of the HPTA. SERMS-> Hypo/PIT
HCG-> Testes

Your problem is your testes/leydig cells in testes from what your bloodwork is showing.

Suppression is irrelevant to the HPTA(more accurately Hypo/Pit) when you need to awaken your Testes.

And again, no SERM(which helps Hypo/Pit) in the world will help you if your testes aren't responsive which seems to be the case here IMO!

Seems like you have 2 choices:
1. Redo the PCT and do it Power PCT style like Scally recommends. Get bloods while on the hCG to see the total T before starting SERMs.
2. Wait for testes to start being responsive to LH. It may take a long time FYI

 

[foreveryoung]

...3. blast the testes with way supra equivalent doses of hcg and further desensitize them to future normal endogenous LH stimulation

 

[Sworder]

...3. blast the testes with way supra equivalent doses of hcg and further desensitize them to future normal endogenous LH stimulation

That's option 1. and no the doses of hCG are not equivalent to LH. The hCG you can use will be much stronger than the current LH.
That's why you use hCG because you can STIMULATE the leydigs, it doesn't Desensitize them... Why would Dr Scally come up with these doses and durations if it would? The guy is a genius...

You cannot desensitize leydigs with endogenous LH...

 

[Michael Scally MD]

Finally, there is an excellent study on down-regulation modeling. This paper has some good modeling graphs. I use 1,000-2,000 IU E3D now.

"The model we developed allows us to simulate arbitrary dosing schemes. The example we provide shows an informal way to obtain a maximum response while using the minimum amount of drug. The simulated testosterone levels show that to reach a target testosterone concentration of 25 nmol/liter [~720 ng/dL], a dose of 1000 IU of rhCG every other 4 days would be sufficient. A higher 2500 or 5000 IU dose would produce a slightly higher response, but the highest dose will produce a lesser response according to the model. Clearly, the predicted pattern of decreased response at high doses and the pronounced rebound effect at treatment cessation is intriguing. The extrapolation to a clinical setting certainly deserves confirmation."

Gries JM, Munafo A, Porchet HC, Verotta D. Down-regulation models and modeling of testosterone production induced by recombinant human choriogonadotropin. J Pharmacol Exp Ther 1999;289(1):371-7. http://jpet.aspetjournals.org/content/289/1/371.full

Chorionic gonadotropin (CG) is a glycoprotein hormone, whose action is mediated by the luteinizing hormone/CG receptor. Testosterone concentrations from six pituitary-desensitized, healthy male volunteers were obtained after four different administrations of recombinant-human CG (rhCG). We present a modeling study to provide a possible explanation for the observations that increased exposure to rhCG induces higher and then lower testosterone concentrations and that marked rebound effects are observed at the end of repeated administration of rhCG. We used semimechanistic models (in which flexible functions represent unknown parts of the models) to identify the relationship of rhCG concentrations to the testosterone levels. Based on the results obtained with the semimechanistic models, different mechanistic down-regulation models were devised and tested. The final model uses a one-compartment model to describe the endogenous production rate of testosterone; rhCG affects the production rate with a mechanism consistent with a two-site binding site, with effect proportional to one-site bound concentration. The modeling results indicate that when rhCG concentration increases, the testosterone production rate increases to 45 times the baseline value. However, at an rhCG concentration of more than about 30 IU/liter, the production rate decreases. Simulations showed that both dose and dosing interval profoundly influence testosterone response to rhCG.

 

[idmd]

Sworder...I'm talking in broad biological terms. As I stated I don't know the specifics of LH receptors on leydig cells. I don't see why you're splitting hairs between SERMS and hCG? They act differently but have the exact same end result - a ligand binding to LH receptors in my testes. My leydig cells don't care if the it's hCG that's been injected or LH from my pituitary. The only difference is the amplitude of the signal - ex. huge supra physiological doses of hCG can be given but my pituitary has a limit.

My real questions is if the duration of SERM therapy is extended is that just as efficacious as using a shorter duration course of hCG? Is there data to support the testes NEED large supra physiological doses of hCG to restart or is it just faster at getting the restart going? If I remember from my reading long ago many just used hCG as a short duration challenge to see if the testes would respond at all and if so then they would move to SERM therapy. As I said I don't have access to hCG but I do SERMS.

 

[Sworder]

My real questions is if the duration of SERM therapy is extended is that just as efficacious as using a shorter duration course of hCG?

No! HCG is better and I don't even know if just waiting will work.. I don't think so...

Is there data to support the testes NEED large supra physiological doses of hCG to restart or is it just faster at getting the restart going?

Yes, that's why your balls ain't producing tT, you are a prime example of why to use hCG BEFORE SERM.

Yes, there is. Read Scally's book and personally I have seen huge success rate with Scally's Power PCT. You can google it!

Honestly, doesn't it make sense though?
Control for Testes first by using hCG and labs showing they CAN produce e.g. 600ng/dl. - Because if your testes can't produce T your LH/FSH aint gonna do shit. Just like your bloodwork shows.

Then go for the LH/FSH with SERMs(Hypo/Pit) and have them squeeze out LH for your ready to pump testosterone testes?

As I said I don't have access to hCG but I do SERMS.

Ouch! Get it IMO! Or you can always go with option 2 and just wait and hope tT increases.

 

[Sworder]

I don't see why you're splitting hairs between SERMS and hCG? They act differently but have the exact same end result - a ligand binding to LH receptors in my testes.

HELL FUCKING NO!

Read Scally's Power PCT before responding please. Don't mean to be rude, it's for your own benefit.

 

[Sworder]

Finally, there is an excellent study on down-regulation modeling. This paper has some good modeling graphs. I use 1,000-2,000 IU E3D now.

"The model we developed allows us to simulate arbitrary dosing schemes. The example we provide shows an informal way to obtain a maximum response while using the minimum amount of drug. The simulated testosterone levels show that to reach a target testosterone concentration of 25 nmol/liter [~720 ng/dL], a dose of 1000 IU of rhCG every other 4 days would be sufficient. A higher 2500 or 5000 IU dose would produce a slightly higher response, but the highest dose will produce a lesser response according to the model. Clearly, the predicted pattern of decreased response at high doses and the pronounced rebound effect at treatment cessation is intriguing. The extrapolation to a clinical setting certainly deserves confirmation."

Gries JM, Munafo A, Porchet HC, Verotta D. Down-regulation models and modeling of testosterone production induced by recombinant human choriogonadotropin. J Pharmacol Exp Ther 1999;289(1):371-7. http://jpet.aspetjournals.org/content/289/1/371.full

Chorionic gonadotropin (CG) is a glycoprotein hormone, whose action is mediated by the luteinizing hormone/CG receptor. Testosterone concentrations from six pituitary-desensitized, healthy male volunteers were obtained after four different administrations of recombinant-human CG (rhCG). We present a modeling study to provide a possible explanation for the observations that increased exposure to rhCG induces higher and then lower testosterone concentrations and that marked rebound effects are observed at the end of repeated administration of rhCG. We used semimechanistic models (in which flexible functions represent unknown parts of the models) to identify the relationship of rhCG concentrations to the testosterone levels. Based on the results obtained with the semimechanistic models, different mechanistic down-regulation models were devised and tested. The final model uses a one-compartment model to describe the endogenous production rate of testosterone; rhCG affects the production rate with a mechanism consistent with a two-site binding site, with effect proportional to one-site bound concentration. The modeling results indicate that when rhCG concentration increases, the testosterone production rate increases to 45 times the baseline value. However, at an rhCG concentration of more than about 30 IU/liter, the production rate decreases. Simulations showed that both dose and dosing interval profoundly influence testosterone response to rhCG.

Thanks for taking the time to post this!