HCG Replacing Natural Levels of Testosterone

Pharma
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[quote]mephistopheles wrote:
Brook
Since the study shows that gonadotropin is maximally supressed in a couple of days. I think it is wise to start HCG as soon as you start any long cycle. Instead of starting HCG @ week3, the nads would be out of action by then, and possibly atrophied already.

e.g

test 1-8
hcg 1-10
serm 11-14
HCG usage is continued in week 9 and 10, while exo test level drop down to non supressive levels. Then SERM pct would commence. HCG would be stop when SERM is used, to allow FSH, LH etc to return to normal. So that true endo test production can resume.

For longer cycles (20+ weeks), some people have noticed gradually diminishing effect from HCG, and suggested to take 4 weeks break from HCG during mid cycle, to allow resensitisation. Since HCG is a foreign drug, the body will build up resistance regardless of dosage?! I think it is a reasonable assumption.

Also if HCG stasis/taper method is used for longer cycles, would LH, FSH restoration be affected in anyway? Since your testis got used to produce testosterone via artificially induced stimulation.

I guess the best way to find out is to do a cycle, with some blood tests to monitor the progress.
e.g 8 weeks Deca only + HCG + SERM pct
or 12 weeks Deca only + HCG stasis taper + SERM[/quote]

I agree, the best way to find out would be to try it - i cant though as i dont recover. B+C kid here.

As for the cycle examples, as i mentioned above, Deca would NEED caber to control the prolactin, as the libido supression from that often clouds the suppression of the HPTA - so when recovery is completed, a raised prolactin level will still reduce libido massively.
Tren would not as it doesnt seem to have this effect, and benefits from the estrogen from test rather than the DHT - being androgenic enough to support the libido in the presence of estrogen. Therefore i would choose tren only cycles or one of the non-aromatizing ‘cutting’ type drugs…

I know that HCG use during the cycle will aid recovery… and it is interesting that time may be needed off as desensitisation (as you pointed out IFBB) occurs at any dose - this would totally throw a spanner in the works.

And as for the restoration of LH/FSH (the hypo-pituitary hormones) - this would be no more effected by the test from the testes than by exo test as in the stasis taper.
The stasis is supposed to be non-suppressive with serm use, and a break between AAS and stasis, as there is no longer negative feedback. This is a mechanism of testosterone as an aromatisable and androgenic hormone, and would be the same of the test secreted by the testes.

I think the main worry is de-sensitisation.

I doubt the stasis would ever be tried by anyone with HCG, and i am unable at this time - but it is just a theory that interests me.

Thanks for all your discussions!

:slight_smile:

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[quote] Brook wrote:
W.H.B. wrote:
http://jcem.endojournals.org/cgi/content/full/90/5/2595

It’s a good read, good luck!

It is a very interesting read - and according to that study:

250iu HGC EOD is as effective as 500iu EOD in raising serum T levels above the normal range in suppressed*, healthy men supplemented with enough T to give a mid to high/normal range of Testosterone.[/quote]

It’s worth pointing out an oddity of scientific manners of communication.

Most biological measurements have a relatively large random error associated with them. In other words, not every subject given the same treatment will exhibit the exact same response.

This then raises the question, when the numbers of subjects in the test and control groups is small, what about the possibility that one group might have, by chance, been loaded up to a not-unlikely-degree with high-responders and the other with low-responders?

So scientists don’t want to say that a difference occurred as a result of treatment unless the difference is large enough, relative to the random error and number of subjects, that there is less than some small chance (often 5% is chosen) that chance alone might have given the outcome.

But the flip side of this is, there’s a tendency – which I think wrongheaded – to go to the other extreme and despite observing an increase in terms of what you measure, announcing that there WAS no increase on account that statistically, the increase might have been produced by chance alone.

In the case of this particular study, in fact the measurements of free T levels were higher at the higher doses, and substantially so, but the random error was sufficiently great that it was not possible to conclude that chance might have yielded that outcome.

This was reported as there being no increase.

A better way of putting it is that observed values were higher, but the probability of this being caused by chance alone is such-and-such percent (and supplying the calculation.) For example, say 10%.

The reader could then conclude as he wishes with regard to this matter of probability, rather than thinking it was a demonstrated fact that there was no increase. That was not demonstrated. In fact the reverse was indicated, but not proven to at-all high confidence.

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On whether a stasis would ever be tried with HCG: sure, I’ve tried it, along with low-dose Masteron. The key component is having another factor that decreases inhibition – I used letrozole – thus aiming for a net approximately-zero or at least low degree of inhibition.

On whether HCG dosing at this sort of level solves the problem of solely-non-aromatizing cycles such as trenbolone only: Yes.

But of course, for example trenbolone with Dianabol, or substantial amounts of injected testosterone will give more results. (Obviously, and as I’m sure was not in doubt. But just stated to be complete.)

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Thanks Bill - I am glad you got back in time to respond to this thread, i hoped your input might be something like it was.

:smiley: