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Eric090585
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HCG Protocol...Your Thoughts?

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Since I've been hanging out here a bit lately, I've been getting quite a few emails from guys wanting individualized advice on their cycles. In the first place, I cannot design cycles, nor do I prescribe steroids (just ancillary medications). That would be a violation of my Oath as a physician, and DEA law to boot. Also, obviously I cannot afford to give away free Consultations. So, I'll post my PCT Protocols here, for anyone who may choose to use them.

Also, I'm just running to catch a plane for Las Vegas, attending the American Academy of Anti-Aging Medicine International Conference. I guess they are supposed to publish an article I wrote on how to administer TRT for men. Wish me luck!

Here it is:

I advise my AAS patients to use small amounts of HCG (250IU to 500IU) two days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.

Any more than 500IU of HCG per day causes too much aromatase activity. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).

If 250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn’t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.

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.

I want my patients to stop taking HCG within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a “bridge”. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can’t “fool” the body—it is smarter than you are.

I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).

All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other protocols.

www.AllThingsMale.com

ANY ADVICE I MAY GIVE IN NO WAY SUBSTITUTES FOR A PROPER EVALUATION BY YOUR PHYSICIAN; NOR DOES IT CONSTITUTE DR/PT RELATIONSHIP, OR LIABILITY, IN ANY WAY .

www.AllThingsMale.com

STOLEN FROM: http://www.steroidology.com/forum/anabolic-steroids-bodybuilding-article...

TheRoyalPalm's picture

I have personally been using 500i.u's a week through my whole cycle (5 weeks in) at 250i.u. tues/fri. My girl has told me that my balls are huge and seem dense, and I cum like crazy now.

I plan on stopping use the week before last shot and starting Nolva 2 weeks after last shot.

This is my first with HCG but couldnt imagine going without it.

On-A-Hype-Ting's picture

Btw that below was copyed of another forum

On-A-Hype-Ting's picture

What do you think of this?

1) Spermatocytogenesis and maturation of sperm occurs in the testes linked with cells called (IIRC) Sertoli cells. 
2) Sertoli cells are in close proximity to Leydig cells
3) For proper spermatogenesis to occur, you need localised (emphasis) high concentrations of testosterone at the Sertoli cells where the sperm cells are generated and matured.
4) Leydig cells (remember close proximity to Sertoli cells) produce testosterone in your testicles, after stimulated to do so by hormones such as FSH/LH (hypothalamus and pituatory etc).
5) An excess of exogenously administered testosterone (ie. injecting yourself with steroids) will shut down the HPTA axis thus shutting down testosterone production in Leydig cells (and over prolonged periods of steroid use Leydig cells shrink and massively reduce in size due to underuse)
6) Shut down testosterone production from Leydig cells, you shut off the localised high testosterone concentrations at the Sertoli cells inhibiting spermatocytogenesis.

Thus once you understand all the above, how do you go about preventing this? Well the answer is quite straightforward - never allow that localised high testosterone concentration to fully be switched off. But you are on large doses of exogenous hormones that shut down your HPTA, so you need to somehow get the Leydig cells stimulated by FSH/LH despite this. This is where HCG comes in and it does that job.

Hence the moral of the story is, IMHO, the best approach to AAS use is to administer low levels of HCG once a week from the word GO, ie. 500IU once a week throughout the whole cycle/time on. This way you always keep your Leydig cells stimulated to produce SOME testosterone, locally to the Sertoli cells and keep spermatocytogenesis still occurring.

At least thats my take on the matter and this is why I always personally recommend using HCG at say 500IU per week every week from week 1 of AAS use...although many may disagree with me on that approach, I think it is the most sensible IMHO.

That high concentration of sperm that is in the testicles is called Intra-Testicular Testosterone (ITT).
As above on cycle FSH, LH and ITT pretty much drop to low amounts. This lack of stimulation to the Leydig cells (LH), the Sertoli cells (FSH) and ITT (lack of endogenous testosterone production) is most likely the reason for steroids and sterility issues.

A typical PCT can get you close, but pretty much does nothing for FSH and those lazy Sertoli cells, after all without sperm pregnancy wont happen.
I can think of 3 different drugs that address the atrophied Sertoli cells that will stimulate them to produce sperm.
HMG (Human Menopausal Gonadotropins)
rFSH (recombinant follicle stimulating hormone)
Clomid fertility drug used on both women and men, in women is promotes ovulation, in men it is used in fertility and to diagnose if one is primary (nuts), or secondary (pituitary) hypogonadism.
Clomid @ 100mg a day for 5 to 7 days doubles LH output, and increases FSH by 20% to 50%.

So, to produce results, one would need to stimulate all of the cells and glands to get back to work and do their jobs.
HCG is an LH analog; it will stimulate the Leydig cells to produce testosterone even in the presence of exogenous testosterone.
rFHS and HMG will stimulate the Sertoli cells to produce sperm (HMG will also stimulate the Leydig cells too).
Clomid and nolva will promote the body to elevate both LH and FSH when HCG and HMG are discontinued. This pretty much will spark the pituitary to send these signals to the respective cells to help them jump start things.

But, what about desentization issues with the HCG?
Leydig cell desensitization due to HCG usage is blocked and/or minimized by Nolvadex. This occurs by suppressing HCG's ability to inhibit the conversion of 17 alpha hydroxyprogesterone to testosterone.
I have never seen any other SERM that can make this claim other than nolva.

I think Proviron might be helpful for libido, and even to make the man feel even a bit better.

hellraizor22's picture

good post bro! veryy helpful