T Nation

Author Rea Cortisol/Estrogen Phases

Looking for any input on Cortisol/Supression drugs. This is an excerpt for BTPB…I always felt cortisol could/should be dealt with post cycle…he claims you can keep the majority of gains by running short cycles and “layering in” C/E phase. Any comments would be appreciated.


Pretty much anyone who has ever used a supplement or drug for increased muscle mass has realized that post use much of the gains are lost. Naturally, in the case of AAS and other anabolics this greatly depends upon correct accounting for the actual Action/Reaction Factors relating to the chemistries employed and how each affects the body in positive or negative ways. This includes during and post use.
As you known the body maintains a state of balance called homeostasis. We both gain and lose protein-based tissue daily at a rate of bodyweight x 1.818 expressed in grams. This homeostasis is a balance between anabolism (tissue building/protein synthesis) and catabolism (tissue wasting/protein breakdown).
Several hormones and hormone-like-substances trigger catabolism. Glucagon does so by setting into motion a series of metabolic events that results in the release of fatty acids, amino acids, and glucose/glycogen from body tissue to restore blood circulatory glucose levels. However the group we are most concerned with are called corticosteroids.
This is a group of steroids that originated at the adrenal cortex. The most commonly discussed hormone of this group is cortisol. When a cortisol molecule merges with a muscle cell cortisol receptor-site, it triggers the release of amino acids from the cell. That probably does not sound like a big deal until one realizes that these amino acids come from the breaking down of the muscle cell proteins. This of course means all of that hard earned lean mass tissue begins to waste away.
Cortisol levels are elevated as a result of stress. Unfortunately, the body views stress stimuli such as increases in muscle tissue mass, training, sickness, and the spouse in a bad mood as reason to increase circulatory cortisol levels. Cortisol production can also inhibit endogenous GH and testosterone production.
The use of Androgens (AAS) of exogenous origin in excess of natural endogenous production triggers anabolism or tissue building /protein synthesis in excess of normal. This is a means of altering the balance or ratio between anabolism/catabolism in favor of anabolism.
During Max Androgen Phases (or any AAS protocol), like all other beasts, Frank’s body attempted to re-establish the balance between anabolism/catabolism (homeostasis) in a variety of ways. First, after a few weeks, his body began to step-up cortisol production to trigger catabolism equal to AAS induced anabolism.
Second, through aromatization, his body attempted to create excessive estrogen levels that would induce a negative feed-back loop resulting in HPTA

suppression. The excessive unnatural estrogen levels would have also triggered female pattern fat deposits, gyno, and water retention, (which are counter-productive for the most part) Excess fat accumulation is also a major aromatase enzyme production site. (Yikes!)
Brief hard-hitting Max Androgen Phases did not increase cortisol production as much as the old longer AAS cycles. But, there was still an elevation to deal with… and if post AAS cycle cortisol levels are a little below normal…
Now, Cortisol /Estrogen Suppression Phases were a means of creating a state of “protein sparing”. When we altered the anabolic/catabolic ratio by decreasing protein wasting, we realized a net gain in lean tissue mass. Let me explain.
If we gain and lose daily equal amounts of protein based tissue at a rate of bodyweight x 1 .818 expressed in grams then we have the ability to increase protein based tissue mass either by addition (Anabolism) or by accumulation (Protein sparing/anti-catabolic/saving). This is like a checking account.
If we have a daily deposit of $100 and withdrawal $100 daily, then our account is in a state of homeostasis or “no change balance”. But if we increase our daily deposits without also increasing or daily withdrawals we increase by addition (Anabolism). Now, how about if we left our daily deposits at $100 but decreased our daily withdrawals? Yes, you are right. Our account would experience an increased balance daily due to accumulation.
In theory this would mean that a (Small) 200 Ib bodybuilder could experience a net gain in lean mass tissue daily of 363.6 grams (200 Ib x 1 .818 = 363.6 grams) if the catabolism side of the anabolic/catabolic ratio were reduced 100%. That would result in a net gain of about 24 lbs of lean tissue in a month. Of course this is not only impossible, it would also be very unhealthy.
But… we did decrease the catabolic side of the ratio enough to not only put an end to cortisol induced post AAS cycle lean mass tissue loss, but in many beasts cases we actually augmented gains while “off-cycle”.
My experience was that estrogen is an evil hormone during AAS protocol exit periods or when an athlete was attempting to maintain a reasonably lean musculature and significant muscle mass during off-periods. Most readers realize that estrogen seriously inhibits HPTA function and therefore inhibits natural/endogenous androgen synthesis in the male body (female don’t have testes).
So it should be obvious to the non-cross dressing reader that elevated estrogen levels and suppressed androgen levels post-cycle resulted in far more than “shrunken nuts syndrome” and female pattern fat deposits.

"Normal or above endogenous androgen production and post-cycle lean mass tissue retention/addition (Yes, I said “addition”) was dependent upon the suppression and subsequent system clearing of estrogen.
Cortisol/Estrogen Suppression Phases had helped to create the amazing monsters of the new era. Many of these monsters would not have been able to retain anywhere near the freak-status viewed today if not for the ability to arrest run-away catabolism and fat accumulation either naturally occurring or resulting from Action/Reaction Factors of chemical muscle enhancement.

The cycle calls for:
Day 1
180 mg of Trilostane/50-150mg of Proviron
Day 2
Nolvadex 30 MG and Proviron 50-150 MG

You run this for 22 days,one EOD.

Trilostane inhibits 3-beta hydroxysteroid dehydrogenase delta 5-4 isomerase and was never utilized longer than 28 days (2 on/2 off) or with any related prohormone substance dependent upon 3-BHSD since it also inhibited their conversion. But the stuff did do a great job on inhibiting cortisol. Obviously, Trilostane was taken in 60 mg divided daily dosages.
Due to Trilostane’s 3-beta inhibiting properties an “androgenic”-estrogen inhibitor such as Proviron or 4-OH Testosterone was utilized to elevate androgen levels daily, while 10 mg AM, 20 mg PM of Nolvadex suppressed estrogen activity with a 2 day on-2 day off protocol. When this protocol was utilized following a Max Androgen or AAS site injection phase, Frank began administration on the first day of the last active week of that phase.
By now, you are aware that this refers to the period when the AAS plasma level was ramping down. And that all Cortisol/Estrogen Suppression protocols have been successfully layered over any AAS cycle. But what about post-cycle feed-back loops? Simple: We began by the last week of activity.

You know what I think.

I can’t comment on that protocol but Retain and PS seems to do just fine for cortisol control and combining that with proviron makes gains very keepable. IMO ALR cycle outlines are very useful for someone looking to progress from cycle to cycle.

Wideguy- What do you dose your ps at? 800mg/day?

600 to 1 gram. I start out high and taper down, imo combining it with lean extreme or retain dose more then enough in terms of cortisol control.



Thanks. Where do you get those products (Retain/PS) from?

I managed to get my hands on some Trilostane, Metraypone and Remeron and have a plan for a series of max androgen phases and C/E Phases. We’ll see how it all works out. I am a little concerned since inhibiing cortisol too much has sides w/ joints and other nasty things.