Cortisol Estrogen Suppression Phases Example 1 Chart

DAY

DRUGS

DAY

DRUGS

1.

Cytadren 250mg 2xd

15.

Teslac 250mg

2.

Cytadren 250mg 2xd

16.

Teslac 250mg

3.

Teslac 250mg

17.

Cytadren 250mg 2xd

4.

Teslac 250mg

18.

Cytadren 250mg 2xd

5.

Cytadren 250mg 2xd

19.

Teslac 250mg

6.

Cytadren 250mg 2xd

20.

Teslac 250mg

7.

Teslac 250mg

21.

Cytadren 250mg 2xd

8.

Teslac 250mg

22.

Cytadren 250mg 2xd

9.

Cytadren 250mg 2xd

23.

Teslac 250mg

10.

Cytadren 250mg 2xd

24.

Teslac 250mg

11.

Teslac 250mg

25.

Cytadren 250mg 2xd

12.

Teslac 250mg

26.

Cytadren 250mg 2xd

13.

Cvtadren 250mg 2xd

27.

Teslac 250mg

14.

Cytadren 250mg 2xd

28.

Teslac 250mg

This protocol utilized multiple strategies. Cytadren is a biosynthesis inhibitor. This means that it inhibits endogenous synthesis of androgens, estrogens, glucocorticoids, and mineralcorticoids. So on one side the protocol (as outlined) this allowed for inhibition of estrogens and subsequent water retention inducing steroids, and on the other side allowed for the suppression of catabolic hormone production.

Unfortunately Cytadren also inhibits the production/synthesis of natural androgens (uh, like testosterone). Cytadren does this by preventing the enzymic conversion of cholesterol into the first step in all steroid biosynthesis...pregnenolone. This of course did not have any negative effect upon AAS activity (except inhibition of aromatization) nor prevented any conversion factors relating to prohormones or prosteroids.

So when this protocol was utilized as a layer beginning the 1 5th day of a Max Androgen Phase overall results improved significantly and post-cycle lean mass retention became something to brag about. Frank followed this protocol and added site-injection work using Protest fairly often.

As said prior, estrogen was a major enemy of post-cycle lean mass retention. This was only partly due to estrogen attempting dominance over declining AAS/androgenic levels. This also meant that water retention and female pattern fat accumulation as well attempting to over-ride muscle anabolism in the absence of control measures. Which of course sucked.

Cytadren inhibits estrogen production at its first biosynthesis step and prevents aromatization of most AAS. Teslac also inhibits estrogen, but is actually a relative of testosterone that has a low androgenic effect. Remember; it didn't take much to induce anabolism if catabolism was reduced. Teslac was one of the most effective anti-estrogens I had employed (rivaled only by Arimidex and Aromasin (exemestane). This cycle was further enhanced for Frank at a later date by stacking 50-100 mg of Proviron daily. This went well with the second reason I liked Teslac.

Teslac has a profound direct influence upon the hypothalamus. This influence causes dramatic HPTA function up-regulation, which eventually leads to increased endogenous testosterone and sperm production as a positive rebound factor.

"Look mom, post-protocol big nuts"

Though this combination almost completely suppressed estrogens and catabolic hormones, there were a few side effects. Teslac had few side effects of course, though beasts had to avoid excessive calcium intake during use.

However, Cytadren did pose a few concerns. Strangely enough, long-term use has been noted to actually lead to increased stimulation of the release of catabolic hormones from the adrenal gland. The two day on - two day off protocol outlined (utilized for under 30 days) has of yet not done so. Joint soreness was common when high dosages were utilized for long periods, however.

The good new was that Cytadren can mangle cortisol receptor-sites long after discontinuance. Additionally, Teslac use has been reported to lead to permanent estrogen suppression (oh darn!). I doubt it needs to be said again, but Cytadren dosages were divided through out the day. (250-500mg each)

My problem concerning Cytadren was that it negated the body's ability to inhibit an inflammatory response. This meant a possibility of hemorrhaging from some types of injuries since it also inhibits blood clotting. (Avoiding knife fights is always a good idea) It could have also decrease our body's ability to fight infections.

However, this was unlikely and not noted at reasonable dosages and when utilized in a 2 on - 2 off administration schedule.

As stated prior, Cytadren does not inhibit 3b-hydroxysteroid dehydrogenase enzymes. This means that the prohormones 4-diols and 19 nor -diols and prosteroid 3-hydroxy androstanes converted to active androgens, but in truth they where already quite active as is.

As we have discussed prior, Action/Reaction Factors had to be anticipated and accounted for if the intent was maximum results with minimum negative side effects. Negative side-effects should have never been something mindlessly endured. They have also derail progress for the unknowing; significantly reducing positive results.

Cytadren (Aminoglutethimide) was utilized as a biosynthesis inhibitor by many competitive athletes as a means of inhibiting cholesterol conversion to pregnenolone, the first step in sex hormone biosynthesis. This means less or no (dosage dependant) production of glucocorticoids, mineralocorticoids, estrogens, and androgens occurred endogenously.

Sports use was intended to suppress the formation of cortisol and estrogen, thus decreasing the catabolic side of the anabolic/catabolic ratio and estrogenic activity. When layered into a Max Androgen Phase beginning day #1 5 there was still enough androgenic activity from AAS to counter-act the suppression of endogenous androgen production for about 21-28 days total, or about 7-14 days after the termination of a 30 day Max Androgen Phase.

However, when Cytadren was utilized in the absence of AAS, some form of exogenous androgen had to be utilized. Low dosages of Low-HPTA suppressing steroids such as Primobolan Depot or Anavar were Frank's options. Proviron was another option for androgenic support I had included in other beasts protocols.

Prohormones such as 4-Androstene 3,17,diol (4-AD) or prosteroids like 1-Test, 4-OH Testosterone or 4-OH Nandrolone (like those contained in some products by Hardcore Muscle Gear or Bio-Design Labs) were also useful. Remember, when the catabolic side of the ratio was reduced, even normal androgen levels were greatly effective.

However, we had negative feed-back loops to consider if Frank was to utilize the potential growth inducing properties of biosynthesis inhibitors. Prolonged high dosages of cortisol suppressing drugs such as Cytadren can induce a negative feedback loop. My experience has been that when biosynthesis of cortisol production is nearly totally suppressed for more than 3 weeks, the body reacts by producing more ACTH (Adenocortico tropic hormone) which is released from the pituitary gland. This in turn stimulates cortisol production/release by the adrenal glands. So Cytadren's action would be over ridden by the pituitary/adrenal glands as a reaction.

When Cytadren is prescribed for Cushings Syndrome patients, the dosage is 500-2500 mg daily. This strongly supported my belief that as little as 125 mg 2xd would have been moderately effective for bodybuilding purposes for a brief period. To counter act the possible negative feed-back loop, Cushings patients are given low dosages of hydrocortisone so some circulatory level of glucocorticoid steroids exists.

Again, this supported my belief that some form of cortisol had to exist in lower values and levels to fully utilize the benefits of Cytadren. And Cushings Syndrome victims produce far more cortisol than even the hardest training bodybuilder.

I have noted that once a negative feed-back loop begins, it slowly ramps up cortisol plasma levels until it reaches homeostasis or balance between anabolism /catabolism. In this situation, once Cytadren was discontinued, the existing elevated pituitary/adrenal produced cortisol levels were joined by normal endogenous cortisol production through biosynthesis. This obviously resulted in several steps back in the progress of the individuals whom erred in this manner.

The solution was simple: Utilizing a 2 day on - 2 day off protocol that allowed a ramping dosage of Cytadren for no more than 6 weeks (30 day maximum use was even more effective) did not allow the body's adaptive response to induce a concernable negative feed-back loop. This allowed for a very low level of circulatory glucocorticoid steroids to exist which in turn prevented triggering of adrenal hyper-function.

Another option utilized for very advanced athletes was a 30 day protocol with 2 day rotations of Cytadren and Metyrapone. Metyrapone inhibits 11-beta-hydroxylation in the adrenal cortex. (A light should go on above the reader's head now)

DAY

DRUGS

DAY

DRUGS

1.

Trilostane 180mg/Proviron 50mg-150mg

12.

Nolvadex 30mg/Proviron 50mg-150mg

2.

Nolvadex 30mg/Proviron 50mg-150mg

13.

Trilostane 180mg/Proviron 50mg-150mg

3.

Trilostane 180mg/Proviron 50mg-150mg

14.

Nolvadex 30mg/Proviron 50mg-150mg

4.

Nolvadex 30mg/Proviron 50mg-150mg

15.

Trilostane 1 80mg/Proviron 50mg-150mg

5.

Trilostane 1 80mg/Proviron 50mg-150mg

16.

Nolvadex 30mg/Proviron 50mg-150mg

6.

Nolvadex 30mg/Proviron 50mg-150mg

17.

Trilostane 180mg/Proviron 50mg-150mg

7.

Trilostane 180mg/Proviron 50mg-150mg

18.

Nolvadex 30mg/Proviron 50mg-150mg

8.

Nolvadex 30mg/Proviron 50mg-150mg

19.

Trilostane 180mg/Proviron 50mg-150mg

9.

Trilostane 1 80mg/Proviron 50mg-150mg

20.

Nolvadex 30mg/Proviron 50mg-150mg

10.

Nolvadex 30mg/Proviron 50mg-150mg

21.

Trilostane 180mg/Proviron 50mg-150mg

11.

Trilostane 1 80mg/Proviron 50mg-150mg

22.

Nolvadex 30mg/Proviron 50mg-150mg

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.

DAY

DRUGS

DAY

DRUGS

1.

Metyrapone 500 mg

15.

Metyrapone 500 mg

2.

Arimidex 1 mg

16.

Arimidex 1 mg

3.

Metyrapone 500 mg

17.

Metyrapone 500 mg

4.

Arimidex 1 mg

18.

Arimidex 1 mg

5.

Metyrapone 500 mg

19.

Metyrapone 500 mg

6.

Arimidex 1 mg

20.

Arimidex 1 mg

7.

Metyrapone 500 mg

21.

Metyrapone 500 mg

8.

Arimidex 1 mg

22.

Arimidex 1 mg

9.

Metyrapone 500 mg

23.

Metyrapone 500 mg

10.

Arimidex 1 mg

24.

Arimidex 1 mg

11.

Metyrapone 500 mg

25.

Metyrapone 500 mg

12.

Arimidex 1 mg

26.

Arimidex 1 mg

13.

Metyrapone 500 mg

27.

Metyrapone 500 mg

14.

Arimidex 1 mg

28.

Arimidex 1 mg

• Liquidex was a common replacement for Arimidex

• Liquidex was a common replacement for Arimidex

Metyrapone (metopirone) is an inhibitor of 11-beta hydroxylation within the adrenal cortex so it was a notably good Cortisol inhibitor that prevented or limited production. I preferred Cytadren, but Metryapone worked well in a 2 day on - 2 day off protocol.

This short period of use prevented excessive production of ACTH and therefore no secondary negative feed-back loop. To put it differently, no negative reaction to the anabolic/catabolic ratio altering action.

Arimidex is fast acting as an estrogen inhibitor and possesses a long half-life (about 34 hours). So 1-1.5 mg daily worked very well when higher aromatizing AAS were in the layer, or 1 mg was sufficient if lower dosage or low aromatizing AAS were utilized. Obviously 0.5 mg of Arimidex was more than enough during non-AAS periods.

HCG has been successfully layered in utilizing 1000-3000 iu every 4 th day to boost endogenous androgen production. Additional estrogen control and HPTA up-regulation has been realized with the inclusion of Clomid: 100mg/d day 1-5 and 50mg/d day 6-15. (Arimidex has been documented to increase HPTA activity in males in the absence of AAS use)

It should be obvious that creatine use aided in post AAS cycle mass retention, but I thought I would point this out again. When, for some reason, 1 mg of Arimidex failed to create acceptable results for Frank (due to other metabolic factors), up to 2 mg daily had been utilized. Many have simply included the addition of 20 mg of Nolvadex before bed. 1.0 mg of Arimidex stopped most any degree of ramped estrogen production however in the absence of exogenous AAS use.

*Recently there was a black market product called Liquidex that provided 1-2 mg of anastrozol (Arimidex) per ml of liquid. It came in a 20-100 ml vial. It was not an injection product but when used orally it provided excellent results. The lab claims a 10% over dose on each batch and thus far this was true. It was also WAY cheaper than Arimidex tabs.

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Responses

  • cory
    What is a cortisol/estrogen suppression phase?
    2 years ago

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