Hcg

[Dr JIM]

One additional note. If exogenous AAS blunted/prevented testes response to hCG, then the studies showing its use with TRT for many to preserve fertility would be unusual.

There are studies that show "chronic" exposure to exogenous androgens down regulate or desensitize the LH receptor and this may explain what I have noted, a blunted response to HCG when AAS are run concurrently with HCG.

Also TRT (AIH in particular) patients are the antithesis of those cycling AAS, as the former possess LOW androgen levels and are more susceptible to the effects of HCH and or LH.

So it should be no surprise TRT patients are amenable to HCG
therapy.

Finally I'm unaware of any study that has investigated the effects of HCG in the presence AAS at those levels run by BB.

The effects of E-2 have a considerable impact on Spermatogenesis during HCG infertility therapy and the amount required of either TT or E-2 preserve said function is MUCH lower than serum levels, as you already know.

 

[Michael Scally MD]

There are studies that show "chronic" exposure to exogenous androgens down regulate or desensitize the LH receptor and this may explain what I have noted, a blunted response to HCG when AAS are run concurrently with HCG.

Also TRT (AIH in particular) patients are the antithesis of those cycling AAS, as the former possess LOW androgen levels and are more susceptible to the effects of HCH and or LH.

So it should be no surprise TRT patients are amenable to HCG
therapy.

Finally I'm unaware of any study that has investigated the effects of HCG in the presence AAS at those levels run by BB.

The effects of E-2 have a considerable impact on Spermatogenesis during HCG infertility therapy and the amount required of either TT or E-2 preserve said function is MUCH lower than serum levels, as you already know.

I would be interested in those studies. If you can locate one that will help with finding others.

"There are studies that show "chronic" exposure to exogenous androgens down regulate or desensitize the LH receptor."


It is well known that spermatogenesis can take place with low TT levels. Also, a cite for the following. I am unclear as to what you mean.

"The effects of E-2 have a considerable impact on Spermatogenesis during HCG infertility therapy and the amount required of either TT or E-2 preserve said function is MUCH lower than serum levels, as you already know."

It is a disgrace to the medical community for the lack of studies dealing with AAS use. I find it disheartening.

Thanks.

 

[BirdieNumNum]

It's because they simply do not give a fuck about helping people whom have done it to themselves.

 

[BirdieNumNum]

Also Jim Stop talking shit pal

 

[Dr JIM]

1)I would be interested in those studies. If you can locate one that will help with finding others.

"There are studies that show "chronic" exposure to exogenous androgens down regulate or desensitize the LH receptor."


2)It is well known that spermatogenesis can take place with low TT levels. Also, a cite for the following. I am unclear as to what you mean.

"The effects of E-2 have a considerable impact on Spermatogenesis during HCG infertility therapy and the amount required of either TT or E-2 preserve said function is MUCH lower than serum levels, as you already know."

3)It is a disgrace to the medical community for the lack of studies dealing with AAS use. I find it disheartening.

Thanks.

1) have to get back w u on this as I've no ML access at present

2) a significant proportion of hypogonadal males remain fertile in spite of their low TT levels

- - the effects of HCG in infertility patients are mediated by improvements in intrastitial
testicular TT levels which are many fold lower than serum values

- the imtratesticular to serum concentration disparity seems to be necessary as higher androgen levels (esp in dosages used by BB) are well known to decrease sermatid formation.

- Consequently I've reason to suspect the effects of HCG are attenuated by HIGH ANDROGEN levels and the MOA is likely to be LH receptor down regulation

- Such up/down regulation is in line with existing data on a number of clinical entities such as Metabolic Syndrome, ETOH withdrawal, opiate withdrawal

3) while I agree the medical community could do much more to understand the physiology of PED use, BB themselves must LEARN to become more proactive and conduct their own testing when confronted with
"confusing" or nonexistent data.

And one great example is the number do drop in Clowns like
@Jay Monks who do nothing but talk out their ass and propagate bro science such as HMG, Prolactin and the use of Liver supplements.

Fools like him add NOTHING to Meso and never will

Thanks for your input
@Michael Scally MD

 

[BirdieNumNum]

1) have to get back w u on this as I've no ML access at present

2) a significant proportion of hypogonadal males remain fertile in spite of their low TT levels

- - the effects of HCG in infertility patients are mediated by improvements in intrastitial
testicular TT levels which are many fold lower than serum values

- the imtratesticular to serum concentration disparity seems to be necessary as higher androgen levels (esp in dosages used by BB) are well known to decrease sermatid formation.

- Consequently I've reason to suspect the effects of HCG are attenuated by HIGH ANDROGEN levels and the MOA is likely to be LH receptor down regulation

- Such up/down regulation is in line with existing data on a number of clinical entities such as Metabolic Syndrome, ETOH withdrawal, opiate withdrawal

3) while I agree the medical community could do much more to understand thepropagate bro science such as HMG, Prolactin and the use of Liver supplements w

Jim 1 thing u need to learn is - YOUR NOT ALWAYS RIGHT. Remember this going forward u absolute muppet.

 

[BirdieNumNum]

Ps I never given advice on prolactin to anyone - chatting shit mate.