So, why do we only wait two weeks until after a last injection of say test enanthate if the halflife is ~2 weeks? Wouldn't that mean in two weeks, there is still ~125mg left in the system at the two week mark, so PCT really isn't going to do any good yet, correct? Shouldn't one wait about four weeks then to start with real PCT, and just use HCG and possibly an AI or SERM up until that point? What am I missing here?

~125 mg will depend on what dosage you're using, right?

What else do you need to qualify as "real PCT" beyond HCG + (AI and/or SERM)?

Sorry...should've clarified. But considering I said halflife, then if the last injection was 250mg, 2 weeks later it should be 125mg, correct?

As far as "real PCT", HCG should NOT be used during post cycle therapy. Only during cycle and during the transition to PCT, but not really in it as it can be suppressive in itself. So, let's say our drug of choice for PCT is clomid, since it offers no gyno protection, you use raloxifene during the cycle and during your HCG, then you hit PCT and want to use clomid (because it's far superior, maybe toremifene as well though). So, I'm saying, when should you really start the clomid for it to have a real effect on natural endogenous testosterone production? You could start it at 2 weeks after the last shot, but you would be wasting way too much of it it seems. Thoughts?

You are correct about the t1/2; 125mg would remain in the depot.

So we should be waiting about a month or so after a long ester shot to start "real PCT" as defined above. This can't be any new knowledge, so why is it "brotelligence" saying to wait just two weeks?

are you continuing this PCT as well? Two SERMs and an AI PCT? I may be a little confused here Jeff... Help the slow minded.

No, I worded that wrong. I meant, switch from raloxifene to clomid or to toremifene, not both. But that really depends on the person, they may want to run ralox, clomid, and say aromasin for PCT for the gyno protection with ralox if aromasin isn't enough...especially if they are working on reducing existing gyno. That's not my goal, so I switch to just clomid/AI.

Technically, you can start restoring endogenous testosterone levels while ON cycle so long as androgen levels have began dropping. The TWO WEEK wait is simply based on the assupmtion that ALL exogenous androgens must exit the system before the HPTA can begin to recover, and this is not true.

However, to maximize the effectiveness of your PCT, you should wait until androgens have cleared the system, then start your AndroGenerator/Aromasin.

I suggest HCG be continued until test reaches normal endogenous levels to prevent so-called "testicular atrophy" (I'm cautious with the usage of that term since nightop's comments on it in a previous post). I'm not sure how "125 mg" works out in the whole half-life equation in comparison with normal endogenous levels, which is what this thread will hopefully work out for us, but HCG should probably be used up until that point, beyond which the low androgen levels + SERM should stimulate LH, making HCG unnecessary.



If you're suggesting that supraphysiological levels of androgens aren't suppressive as long as they're dropping, that's an interesting idea that I haven't heard before. I'd love to get a reference (I ask because I notice that you're very good about representing your comments in other threads).

If you're meaning that exogenous test isn't suppressive as long as its below the natural endogenous levels, then I guess the above just repeated you in different words.

There indeed is a THRESHOLD androgen level that will allow for LH secretion, but that number is different for everyone.

Having said that, one can start recovering endogenous testosterone levels prior to ALL androgens exiting the system, depending on what compounds were used and for what duration.

Any references for any of the claims here?

It sounds to me, that one should probably run HCG 3-4 weeks after his last injection (with whatever is needed for gyno control if one is prone to it, and possibly even an oral androgen until the very end of HCG usage), depending on the compound (TE for example), then switch to normal PCT (SERM/AI). I've never read anything to indicate that endogenous testosterone will start to increase while there are still exogenous androgens in the system, which would be the rational for the above statement. So, we need some references.

Not ALL Androgens suppress the HPTA to the same degree.

Some steriods, such as Proviron and Halotestin, will not even significantly(or at all) reduce testosterone:


Horm Metab Res. 1984 Sep;16(9):492-7.Related Articles, Links

Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.

Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.

We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS

http://www.bodybuilding.com/fun/par31.htm

Looks like I wasn't far off in my original assumption...check out the chart. Looks to me HCG should be run until then, cease, and continue with SERM of choice, which should be clomid.

Nice find. I wish the chart showed from week 0, as it's kinda ambiguous whether or not to run HCG that first week after your last injection. If the LH is already coming up in that week (looks like it might be?), then it's probably a bad idea. But if the LH is flat-ish that first week, it might not be a bad idea. Def do not need it after day 7, though, as LH is already coming up. This was with 250 mg -- great find. Again, with 500 mg, the HCG might be continued for a while, as the test levels will likely still be suppressive until they get down to a point that triggers LH production again (you'll notice that this chart starts with test levels just slightly elevated above baseline, where it makes sense for LH to be coming up already).

I'd say it looks like a good plan.

The amount of hormones most average muscle heads will use to get noticable anabolic androgenic effects will be FAR FAR FAR higher than the amount required to inhibit LH.

Your body only produces 50mg of endogenous test weekly. How many people do you know who DON'T run at least ten times that amount each week?

I think Lewellyn was trying to say that even though it's coming up, you would still want to bombard your system in hopes that more increases the LH response...if that makes sense...I don't know, I'm tired...

Another thing I just noticed, look how long it takes to get back to baseline! 17 weeks??? Maybe our PCT plans should be a lot longer than we think...

I wouldn't be surprised if a proper PCT cut that 17 weeks down significantly though.

EDIT: And HCG on cycle would do wonders, I'd bet.

True...those levels are probably without using PCT so I guess that's the idea is to speed that process up...duh

The use of 2500iu to 5000iu of hCG for PCT is somewhat dated. Dependant on the cycle used, its unlikely the HPTA will return to normal quickly and eaisly with that protocol.

250iu to 500iu MAX on an EOD basis would be a better option - thus limiting any desensitisation to the Leydig cells as a result of the hCG spiking LH too high and causing hypertrophic leydig cells...

The jury is still out as to wether hCG should be used all the way throughout the cycle (keeping the testes ticking over...) or just in the final 2 weeks of cycle and all the way through PCT, mainly due to the fact only anecdotal evidance would seem to be available.

Then again, there are better options than hCG out there, but getting hold of them is somewhat of a pain...