My introduction.....

[Northern Nutrition]

Fair enough. Thanks for the correction, Doc.

I was thinking more in terms like 250iu two to three times per week, compared to 1000iu every four days. This doesn't have to be exact, only an example. The question remains the same however.

 

[Michael Scally MD]

Fair enough. Thanks for the correction, Doc.

I was thinking more in terms like 250iu two to three times per week, compared to 1000iu every four days. This doesn't have to be exact, only an example. The question remains the same however.

The question is what is the clinical endpoint. For PCT/ASIH, the studies are not done. TV as well. I doubt we will ever see the studies. What are you shooting for? There are the fertility studies on TRT that use 500 IU EOD, IIRC. IMO, at less than 500 IU can be of little effect unless dosed frequently. At EOD dosing, there will be an accumulative effect. My published treatment is from 10+ years ago. I have modified it since then to a smaller dose less frequently.

 

[Northern Nutrition]

Im a huge advocate of using the least amount of drugs to achieve similar results. In my experience i have never (had to) used more than 500mg of hCG in one dose, nor have i used more than 750iu in one week, to prevent testicular atrophy. Years ago when i used to end each cycle and run a recovery program (PCT), I included hCG on cycle and the transition into PCT was almost seamless. Post cycle bloods returned normal. Im now almost 50 years old and on TRT. And although Ive chosen not to include hCG in my TRT protocol, i know many others that do @ 250iu 2-3 times per week for the additional benefits - brain function, fertility, testicular atrophy..ect.

Im wondering if would agree that an alternative to blasting hCG @ 2000iu E3-4D is including it on cycle using a dose conducive to preventing testicular atrophy, rather than treating after the fact? Kinda like allowing a cold to manifest and then treating it afterwards, when you could have prevented it in the first place.

 

[Dr JIM]

Im wondering if would agree that an alternative to blasting hCG @ 2000iu E3-4D is including it on cycle using a dose conducive to preventing testicular atrophy, rather than treating after the fact?

No amount of HCG will completely PREVENT the natural decline of TT secretion providing the dose of AAS being used is "anabolic". You can't fool Mother Nature you cycle, endogenous TT levels WILL DECLINE!

Actually I'm not convinced HCG has ANY benefit in preserving TT production when used WHILE cycling, especially with more potent or high dose AAS

Finally testicular size correlates poorly with TT secretion bc well over 90% of testicular volume is reserved for spermatogenesis.

 

[MR10X]

I used HCG between my last shot of AAS and start of PCT for 3 weeks at 500iu Q3D.It worked really well for me.

 

[Northern Nutrition]

Thanks for your comment, Jim. Im in agreement with you on what you wrote about the decline of total testosterone and the PD of hCG. However, im still looking for an opinion on blasting after cycle vs on cycle hCG protocol to achieve same/similar results?

 

[Dr JIM]

I used HCG between my last shot of AAS and start of PCT for 3 weeks at 500iu Q3D.It worked really well for me.

It worked compared to what?

I'm not saying it's not useful as PCT adjunctive therapy bc I believe that's when it's MOST beneficial.

But intra-cycle HCG will do little to restore or even maintain endogenous TT secretion once supraphysiologic exogenous AAS levels are achieved.

In other words, the effects of HCG are blunted by the presence of AAS when cycling.

The answer is NO blasting or using high dose HCG DURING A CYCLE will not prevent the decline in endogenous TT production. Will the decline be as remarkable perhaps not, but those nads will lose volume, everything else being equal.

 

[MR10X]

Its the only time i used HCG for PCT.I have never use it during a cycle because i felt it was unnecessary for me because i only do 8 week cycles.The only time i used HCG during a cycle was my very first cycle of HCG and Anavar back in 1980. I used it in my last PCT as DOC Scally calls it to jump start my balls then started Clomid and Nolvadex when i took my last shot of HCG. I felt different when i included the HCG for that PCT,evidently it does more than Clomid and Nolvadex alone.

 

[Sworder]

In other words, the effects of HCG are blunted by the presence of AAS when cycling.

Can you please further your statement with an explanation of how hCG gets "blunted" during the presence of a AAS cycle? Do AAS show competitive inhibition @ the leydig cells or do the leydig cells have a connection/signal back to the Pit/Hyp before producing the testosterone?

Any articles or anything to support this? If not, just a description or further explanation to how you came to this conclusion would suffice.

 

[Northern Nutrition]

Can you please further your statement with an explanation of how hCG gets "blunted" during the presence of a AAS cycle? Do AAS show competitive inhibition @ the leydig cells or do the leydig cells have a connection/signal back to the Pit/Hyp before producing the testosterone?

Any articles or anything to support this? If not, just a description or further explanation to how you came to this conclusion would suffice.

This is what i was driving at. Which is the dominant signal, and how is this feedback measured? We know that hCG ON CYCLE does in fact prevent testicular atrophy, but perhaps not 100% as this is subjective. FTR, i feel hCG is effective both blasting and on cycle. But my position has and always will be prevention, not cure. And if prevention can be achieved as successfully as cure, why not prevent testicular atrophy in the first place rather than treat it afterwards?

 

[Dr JIM]

PREVENT? HCG may DIMINISH atrophy but it does not eliminate it when AAS are used in a traditional anabolic manner.

Moreover is the degree of atrophy being relatively subjective (unless followed by sonography atrophy) can not be used to predict the magnitude of endogenous TT suppression!

There are limited TRT studies that demonstrate the effect of HCG is blunted at higher doses of TT, (if I recall correctly the highest dose was 600mg /wk).

Do the assay yourself mate. Cycle anything BUT TT and blast HCG during that interval, then check a TT level at 36 hrs and agin in 2 weeks or so, you should note what I'm referring to, the responsiveness to HCG is attenuated significantly. (Don't run Deca however bc of it's cross reactivity with some TT ELISA assays

I suspect another consideration is the cost even if blasting HCG was proven effective at at dose of say 2500IU twice a week the cost for a 12 week cycle would be prohibitive approximating $500 bucks.

These are some the reasons I believe the latter part of a cycle is where HCG has it's place, as a means of expediting gonadal recovery.

Regs
JIM

 

[Northern Nutrition]

PREVENT? HCG may DIMINISH atrophy but it does not eliminate it when AAS are used in a traditional anabolic manner. Youre right Jim, i should have been more specific.

Moreover is the degree of atrophy being relatively subjective (unless followed by sonography atrophy) can not be used to predict the magnitude of endogenous TT suppression! I agree , its subjective.

There are limited TRT studies that demonstrate the effect of HCG is blunted at higher doses of TT, (if I recall correctly the highest dose was 600mg /wk). I also agree with this as well. The results of hCG diminishes relative to the amount of exogenous testosterone introduced.

Do the assay yourself mate. Cycle anything BUT TT and blast HCG during that interval, then check a TT level at 36 hrs and agin in 2 weeks or so, you should note what I'm referring to, the responsiveness to HCG is attenuated significantly. (Don't run Deca however bc of it's cross reactivity with some TT ELISA assays

I suspect another consideration is the cost even if blasting HCG was proven effective at at dose of say 2500IU twice a week the cost for a 12 week cycle would be prohibitive approximating $500 bucks. This is the part im referring to. For an average 12 week cycle a single 5000IU of lyophilized hCG can be used effectively to significantly reduce testicular atrophy in the average healthy AAS user. This has been demonstrated by many AAS users and TRT patients. And the cost is nowhere near $500.

These are some the reasons I believe the latter part of a cycle is where HCG has it's place, as a means of expediting gonadal recovery. Again, expediting gonadal "recovery" ?? Why "recover" from something that is easily prevented? Why allow a cold to manifest when you can prevent it from occurring in the first place?

Regs
JIM

Just some of my thoughts, and of course my million dollar question that doesn't appear to have an answer - except my opinion that prevention is a very valid option.

Thanks for taking the time to comment, Jim.

 

[Dr JIM]

Just some of my thoughts, and of course my million dollar question that doesn't appear to have an answer - except my opinion that prevention is a very valid option.

Thanks for taking the time to comment, Jim.

There is one sure fire way to prevent TT atrophy, don't cycle

 

[Northern Nutrition]

^^ LOL

 

[Sworder]

(Don't run Deca however bc of it's cross reactivity with some TT ELISA assays

Ok, so the word "blunted" maybe was the wrong term?

I am seemingly questioning everything you say Jim, but on this one too what cross re-activity can tT reading have while running deca?

 

[idmd]

So labs are back...this is just about 4 weeks after stopping all meds (SERMS) and no other meds other than my usual 100mcg Synthroid. - numbers in brackets are from 1 month ago.

tT - 377 (422)
LH - 4.0 (7.5)
E2 - 24 (25)

Subjectively, I feel a little run down and not quite there physically but that could ALL be in my head...

As always thoughts and comments welcome. Would anyone call this a "restart"? Since I never officially had a diagnosis prior to starting TRT would you call me normal, primary, secondary or mixed? Where to go from here?

 

[Bridger]

So labs are back...this is just about 4 weeks after stopping all meds (SERMS) and no other meds other than my usual 100mcg Synthroid. - numbers in brackets are from 1 month ago.

tT - 377 (422)
LH - 4.0 (7.5)
E2 - 24 (25)

Subjectively, I feel a little run down and not quite there physically but that could ALL be in my head...

As always thoughts and comments welcome. Would anyone call this a "restart"? Since I never officially had a diagnosis prior to starting TRT would you call me normal, primary, secondary or mixed? Where to go from here?

As someone who has been off trt for a year following a restart, the more important question is how do you feel being off? And are you living healthy, like good sleep, nutrition, exercise, stress, etc?

I did my labwork about 6-7 weeks after i finished my restart and my results were okay. not what i got used to seeing while one TRT but not bad. I felt pretty shitty for a while. kinda depressed, low energy, not motivated to workout, lower sex drive. But i think alot of that was in my head too. I was very concerned about mood swings (im bipolar) and sexual abilities among other things. I had to remind myself that labwork and how you feel are not necessarily correlated.

I think you may need to give it more time before you decide. Treat it well in the meantime.

 

[idmd]

I feel ok. I've been working a lot so maybe a little run down but I can't blame that on my numbers. Sex drive is good and erections have been great.

Any other comments about numbers appreciated.

 

[LW64]

I agree with Bridger. I'm not sure 4 weeks is long enough after SERMs.

If you feel ok then let it ride for a while longer and get labs again in another month or so.

 

[idmd]

Thanks LW64.....
Dr. Jim said three weeks should be enough time to washout the SERMs so I went an additional week. I fully understand even in the absence of SERMs after 2 years on TRT I may still be in the process of recovering. I honestly wasn't expecting these results. LH dropped by half but tT only dropped by 10%. In some ways I think that's encouraging. On the other hand, I don't THINK (the all too subjective part) I feel as good as when I was on TRT. I don't feel bad...just not as good.

My unanswered questions are:
1. Can we get a definitive diagnosis from these results? I see a primary trend here with LH at 50% the normal range and tT near the bottom of the range (350-1200). It has always been assumed I was secondary since I'm a big guy yet my E2 has never deviated more than 4-5 points in either direction with the exception of being on AIs where I had it around 10 for a while. It has never been elevated even with a tT of 1000 on TRT.
2. Does anyone think if I continue with these numbers and I don't feel as good the best option is TRT? What about SERMs for another month to really see what my current tT maximum output is now?