1-Test - Anabolic/Androgenic?

[Bill Llewellyn]

Why would LH desensitization be less likely to happen when you use it post cycle as opposed to using it intermittently during the cycle?

Because you are using it for a very short period of time post-cycle. It is difficult to guess exactly how much to use so that testicular mass is maintained, yet the testes are not overstimulated, if you are taking it throughout the course of the cycle. If you have the perfect dosing routine for this I am all ears.

 

[Jacob Creutzfeldt]

Bill if LH levels elevate post cycle and you compound that elevated LH with a synthetic LH like HCG aren't you more apt to cause LH resistance using HCG post cycle? If LH levels fall by say the 2nd week of a cycle and you administer HCG following the LH decrease I would think LH resistance is less likely. Also does HCG tend to increase aromatization? If so then could you be more apt to end up increasing estrogen levels thus inhibiting natural LH production?

 

[Bill Llewellyn]

Bill if LH levels elevate post cycle and you compound that elevated LH with a synthetic LH like HCG aren't you more apt to cause LH resistance using HCG post cycle?

I think if done correctly you should shorten the recovery window rather than extend it. The whole problem is that it takes too long to wait for physiological, or slightly above physiological, levels to do the job. We need to kick start them, otherwise why bother with a T recovery program.

If LH levels fall by say the 2nd week of a cycle and you administer HCG following the LH decrease I would think LH resistance is less likely.

I understand your point, but repeat my above. This works well in theory, but I think you run the risk of not really having a clue what is going on down there and desensitizing the LH receptor inadvertently in practice. We don't know enough about this type of use to say it is recommended. But if that is what you find works, by all means, do it.

Also does HCG tend to increase aromatization? If so then could you be more apt to end up increasing estrogen levels thus inhibiting natural LH production?

It increases testicular aromatase specifically, and therefore should not really increase estrogen levels until it is already working to increase testosterone. If used past this point it will suppress the HP axis.

If it works for you either way it is great. The big point I am trying to make here is that HCG is the most important recovery drug because testicular atrophy is the biggest roadblock to recovery, not LH.

 

[Jacob Creutzfeldt]

Elevating LH while the testes are tiny makes as much sense as putting dual quads on a three cylinder engine.

 

[Bill Llewellyn]

Elevating LH while the testes are tiny makes as much sense as putting dual quads on a three cylinder engine.

You are absolutely right JC. What the hell was I thinking.

We certainly wouldn't want our testosterone levels to return to normal or anything, now would we?

- Bill

 

[Big Cat HH]

Re: Re: 1-Test - Anabolic/Androgenic?

The piece of the puzzle you are missing is the fact that estrogen is necessary for the libido sustaining effects of androgens. That is probably why strong androgens that do not aromatize sometimes lower libido. Case in point: trenbolone acetate

Sorry to be the asshole once again Pat, but where does Mesterolone fit in ? Its probably the best libido booster in the world, yet it does not aromatize. Its an anti-aromatase.

 

[Big Cat HH]

Elevating LH while the testes are tiny makes as much sense as putting dual quads on a three cylinder engine.

The whole point of HCG is to increase testicle size once again so that larger amounts of natural testosterone can be produced once LH production resumes, after treatment with HCG AND either clomid or Nolvadex.

 

[Big Cat HH]

QUESTION for PA and BILL

First of all great thread.

I'm still puzzled by one thing though. If long term androgen use causes a depression of gonadotrophins, starting at the base with GnRH, and the androgen used does not form estrogen, so there is no circulating estrogen in the system at the time the androgen use is discontinued, then how on earth is it possible to have rebound estrogen without increasing GnRH and subsequently LH/FSH first ?

 

[Bill Llewellyn]

Re: QUESTION for PA and BILL

I'm still puzzled by one thing though. If long term androgen use causes a depression of gonadotrophins, starting at the base with GnRH, and the androgen used does not form estrogen, so there is no circulating estrogen in the system at the time the androgen use is discontinued, then how on earth is it possible to have rebound estrogen without increasing GnRH and subsequently LH/FSH first ?

There is no rebound. Estrogen is actually lower post-cycle than pre. Since you get a good amount of estrogen from extragonadal sources however, you do get an imbalance (androgens get suppressed more extensively).

- Bill

 

[Bill Llewellyn]

Re: Re: Re: 1-Test - Anabolic/Androgenic?

Its an anti-aromatase.

For some reason without an in-vivo Human study you will never convince Pat of this.