Made trip to see Dr. Crisler

[jamotech]

The second peak in endogenous T is larger than the first hourly initial spike. Which is about 48hours after admin.

Then you have the refractory peroid of having to use MORE to get the same effect, so why not use smaller doses. I guess it comes down to effiiciency/cost. Who's to say the levels of estrogen will not also build over time, they will.

I'm not suggesting people use 1000ius every 4 days, but one can use an amount and take into account, spikes in T/E and the refractory peroid to limit sides.

If the goal is small spikes, then ED or EOD might actually be correct. Think about it. We get the hourly spike from injection 1. and admin another HCG dose, does that then decrease the second 48hr spike in T/E the first injection did? It might.

Very interesting, All my initial research was based on half life times of the drugs. Now im starting understand that there is more to it than just half life times. Leydig cell refraction and the two spikes with hcg is very interesting, had not run across it yet. Makes more sense now why some will recommend a longer frequency. Considering the two spikes, what frequency would be best?
I take HCG every 60 hours, maybe the 12 hour difference prevents interfering with the 48 hr spike.

[steroid.com 1]

Very interesting, All my initial research was based on half life times of the drugs. Now im starting understand that there is more to it than just half life times. Leydig cell refraction and the two spikes with hcg is very interesting, had not run across it yet. Makes more sense now why some will recommend a longer frequency. Considering the two spikes, what frequency would be best? I take HCG every 60 hours, maybe the 12 hour difference prevents interfering with the 48 hr spike.

Exactly!

Experts in the field follow a typical two and one day before Test injection with relatively higher doses, ie, 350 to 500 iu each.

That's a lot of hCG back to back.

But the ones prescribing this hCG protocol (Crisler, et al) are all pretty much doing the same thing.

So it begs the question; Why, given above?

Now we see Crisler going in to an ED basis for some strategic reason.

We can find out why; but when it comes to the "guys in the know" who are on the leading edge of this new speciality I tend to follow thier reasoning to a point.

Two and one day before injection didn't work for me; I could feel swings.

Moving to EOD at lower doses and huge night and day difference. I tend to lean towards lower doses more frequently for that reason.

Talk all you want about refractory periods, I know what worked for me and my BW is damn Skippy to prove it.

This is an art...and not a science.

[Swifto]

Ive never heard of the SubQ test is aromatized at a lower rate, i would actually think the oppsite due to thats where alot of adipose tissue is and that is a large source of aromatization. Very interesting.

Can someone link some info that backs up that claim?

I am also a fan of more frequent injections, according to the book i have on testosterone, the hydrolysis of the ester chain is very quick but the release of the testosterone injection depot is the main limiting factor. (Testosterone:action, deficiency, substuition. AMAZING book btw, Nieschlag really knows his stuff)
"the rate of hydrolysis again dependson the structure of the acid chain but this process is much faster than release from the injection depot"

I agree with swifto on the ED/EOD HCG usage, there are 2 LH spikes with the 2nd being just as large or larger than the first. by going ED/EOD with it, you * theoretically* would have a lower 2nd spike b/c the next admin of Hcg wouldnt allow it.
perhaps, by going ED/EOD with the HCG, the LH receptors on the testes to increase (assuming that they didnt properly develop b/c its primary), but this is a double edged sword b/c after long duration those receptors start to not be activated but following the diminished androgen production the natural feedback kicks in and more androgen is produced. *that would support the E3D use of HCG in normal males.

To the OP:
have you always had these issues? did you ever do a cycle? where increased androgens would lead to premature 'aging' of the leydig cells? Did you try gettin the injections closer together than 2 weeks, like E10days? Did you have your thyroid checked? did you get blood work values done of the common/useful things (Test, free test, SHBG, LH, FSH, TSH). Do you have testicular atrophy? how was your 'puberty'.. Normal, late, early?

I'm pretty sure a study does not exist due to lack of data. I think Dr. Crisler has come to this conclusion by studying his patients firsthand and/or other Endo's in his circles.

I don't see how leydig cell LH receptors would "increase" becuase he's primary given HCG stimulus. Leydig cell refraction is due to loss of LH receptor and possibly estrogen, although there is little evidence pointing the finger at estrogen.

"While these findings have emphasized the probability that
endogenous estrogen is involved in the mechanism of hCGinduced
testicular desensitization, there has been little direct
evidence for the role of the estrogen receptors of the Leydig
cell in the refractory process", as found here.

I don't think you thought that "theory" through really, but nice effort.

Exactly!

Experts in the field follow a typical two and one day before Test injection with relatively higher doses, ie, 350 to 500 iu each.

That's a lot of hCG back to back.

But the ones prescribing this hCG protocol (Crisler, et al) are all pretty much doing the same thing.

So it begs the question; Why, given above?

Now we see Crisler going in to an ED basis for some strategic reason.

We can find out why; but when it comes to the "guys in the know" who are on the leading edge of this new speciality I tend to follow thier reasoning to a point.

Two and one day before injection didn't work for me; I could feel swings.

Moving to EOD at lower doses and huge night and day difference. I tend to lean towards lower doses more frequently for that reason.

Talk all you want about refractory periods, I know what worked for me and my BW is damn Skippy to prove it.

This is an art...and not a science.

Its exactly a science.

I'm pretty sure the refractory peroid does not matter if you're wanting low testicular testosetrone and estorgen spikes. One maybe able to use the refractory process to their advantage.

Sometimes I get too caught up on trying to boost endogenous testosterone as much as possible as I'm usually dealing with hypogondal males post androgen admin.

[Lemonada8]

I'm pretty sure a study does not exist due to lack of data. I think Dr. Crisler has come to this conclusion by studying his patients firsthand and/or other Endo's in his circles.

I don't see how leydig cell LH receptors would "increase" becuase he's primary given HCG stimulus. Leydig cell refraction is due to loss of LH receptor and possibly estrogen, although there is little evidence pointing the finger at estrogen.

I don't think you thought that "theory" through really, but nice effort.
.

The thing is that he has low test DUE TO being hypothyroid. Thyroid hormones increase proliferation of Leydig cells, and plays a key part in puberty. I am going with the thought that he never did fully develop his leydig cells due to being hypothyroid. People who are hypothyroid-ic dont usually respond to HCG like a normal person does. This combined with the fact that the OP began puberty late, has decent LH amounts normally, and good thyroid blood tests (which im still wonderin where the hypothyroidism is coming from, what step is not working right.... ) That with the ED use of HCG simulates puberty where LH increases(from what the body sees) and is greater than FSH (LH>FSH is a sign of reproductive stage, FSH>LH is a sign of prepuberty and senescence) combined with sufficient thyroid repla***ent, he can induce leydig cell proliferation which normally would have occured during puberty.

i never said anything about estrogen, im not sure where the article you posted actually deals with what i am saying here... ?

[Swifto]

The thing is that he has low test DUE TO being hypothyroid. Thyroid hormones increase proliferation of Leydig cells, and plays a key part in puberty. I am going with the thought that he never did fully develop his leydig cells due to being hypothyroid. People who are hypothyroid-ic dont usually respond to HCG like a normal person does. This combined with the fact that the OP began puberty late, has decent LH amounts normally, and good thyroid blood tests (which im still wonderin where the hypothyroidism is coming from, what step is not working right.... ) That with the ED use of HCG simulates puberty where LH increases(from what the body sees) and is greater than FSH (LH>FSH is a sign of reproductive stage, FSH>LH is a sign of prepuberty and senescence) combined with sufficient thyroid repla***ent, he can induce leydig cell proliferation which normally would have occured during puberty.

i never said anything about estrogen, im not sure where the article you posted actually deals with what i am saying here... ?

I see your line of thinking.

How sure are you that thyroid hormones increase leydig cell proliferation in adults and not neonatal and prepubertal subjects? Thyroid hormones effect steroli cells moreso than they leydig cells by the way, where they are responsible for changes in differentation, proliferation and function. The effects thyroid hormones have on neonatal's and prepubertal subjects is quite different to that of adults, infact, its the opposite.

I was adding estrogen meerly for others also reading our exchanges. A lot of the time people dont have a clue what we're talking about, so I am concious of that fact, as you should be also. Members learn from our posts.

[Ibreakspawns]

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