Question concerning LH and HCQ and supression of natural Test

[Jorlen]

As I have come to see it you should use HCG to jog your balls so they dont atrophy during a cycle. Thats perfectly logical. You dont wanna let your boys starve so long that they die on you.
But here is when I get curious, does the level of starvation (lowering of LH production) your body does to your balls correlate to the dosage of steriods you take?
Cause that would explain why your balls die harder and faster if you inject more juice, but could stay potentially fine during a 12-15 week beginners cycle of merely 300mgs a week.
The other way it could work as far as I know is that as long as you have more testosterone then your body wants you to have it shuts LH down. No matter if its cause you take 300mgs a week or 2000mgs a week.
But then why is it ok to skip HCG during a long beginners cycle?

[Jorlen]

*self bump*

[Skyefire]

OK, first off is there are levels of shut down, however any steriod will shut you down, its just that some are worse then others. Its really a question of how long you have been on in the case of test but other like deca or fina are known to be very supressive and take longer to recover from. HCG will not in itself do anything for the recovery of test production. What it does is prevent (or reverse if your taking it after a cycle) testicular atrophy. This is again more a question of time, its just that fina and deca work faster (being more suppresive they kill your test production almost in the first week) so the atrophy sets in sooner. and sence they are stronger the repression last longer. (This is the simplified version, swales wrote some papers on this if I recall)

[Jorlen]

Got some further insight. Read what you posted here:
SWALES PCT protocol(taken for a post at AM by theprolangtum)

So according to Swales the LH production is not very supressed when serum androgen levels of testosterone fall below a 200mg per week dosing.
Take home points would be that it takes a lot longer for your balls to hypertrophy back to normal size then it takes for LH procuction to return to normal. So HCG should be used to keep balls big and ready for when LH pops back up.
Which I find easy to accept.

Are there any good info on how much suppression given amounts of given steriods induce?
I realise it cant be to exact since people react differently, but a relative comparison between the steriods at different dosages.

[Skyefire]

Originally Posted by Jorlen

Got some further insight. Read what you posted here:
SWALES PCT protocol(taken for a post at AM by theprolangtum)

So according to Swales the LH production is not very supressed when serum androgen levels of testosterone fall below a 200mg per week dosing.
Take home points would be that it takes a lot longer for your balls to hypertrophy back to normal size then it takes for LH procuction to return to normal. So HCG should be used to keep balls big and ready for when LH pops back up.
Which I find easy to accept.

Are there any good info on how much suppression given amounts of given steriods induce?
I realise it cant be to exact since people react differently, but a relative comparison between the steriods at different dosages.

What it says is "dominates" and further he is refering to the LH, not test production. (it is inter related though) Test is still supressed even at nomanal doses. also the artical does not include it but it takes a week or two for the nolvadex to build up, it has a half life of 6 days so it takes almost 2 weeks to get to full dosage if you were not taking it before.

The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM’s at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.

[Jorlen]

Is he saying even if you use nolvadex from the start, to block estrogen, it will still inhibit HP from producing LH even when androgen levels drop?
Or is he saying that Nolva blocks estrogen even in the feedback loop to HP and by that it will responds to falling androgen levels even when estrogen really is abundant and should inhibit LH production?

Then arimidex looks really useful since it will keep estrogen low from the start. Which means all the HP feedback loop is waiting only for the drop in androgen levels. And you dont risk that estrogen dominates your hormone balance during the whole cycle.

Swales has changed my view on HCG. It seems really smart to use it from the start. The research he quoutes indicate that HCG doesnt directly inhibit production of LH. Does anyone however the experience that your own test production is lowered long after a cycle is over, possibly due to receptor desensitation caused by the use of HCG?