Short Cycle Information


Some info for the inquiring mind, this is an excerpt…if you have a short attention span don’t waste your time…

The goal of any growth inducing protocol was to gain as much lean mass as possible. To do this with a plan meant to gain, not merely maintain or regain losses from prior cycles.

The body has Action/Reaction periods and factors. Basically the body begins to adapt significantly to most attempts at altering homeostasis after 2-3 weeks. This sucked since the best results from a cycle usually came during days #10-30. But we also profited from this information and used it to Frank’s advantage by utilizing brief phases and cycles of 21-30 days, (this is the point where cycles provided serious results) then got out before side effects out weighed benefits.
“To be successful it is necessary to create maximum growth thresholds and stop before the body is able to achieve its own counter measure thresholds.”
Let me explain. My experience has been that a cycle of 8 weeks providing a continuous plasma level weekly of 400-800 mg testosterone begins to fail to provide results about week #6 in most cases. This is because the level of endogenous catabolic hormones becomes elevated as a reaction to the exogenous testosterone administration and cellular signaling proteins begin to become overwhelmed, which is due to the action of increase androgens. So anabolism and catabolism are again about equal. Remember to create a growth environment one or both sides of the anabolic/catabolic ratio must be altered in favor of either more tissue building or less tissue wasting.

At the 6 weeks point an athlete’s body produces and maintains somewhat higher cortisol levels than normal. An increase in the administered dosage would again overwhelm the cortisol and increase signaling protein activity, but eventually it will catch up… .again. Worse yet, when the athlete goes off cycle, the elevated levels of catabolic hormones overwhelm the declining anabolic chemistry (and activity) and most of the cycle gains are lost.
“Yes, Frank. I realize that you lost a great deal of lean tissue mass after AAS discontinuance in the past. But what if an athlete, yes you Frank, utilized a brief protocol that allowed maximum growth and got out before endogenous catabolic and anabolic chemistry altered significantly? Yes, you are right. The athlete would retain much more of the protocol gains post cycle, and “Look honey, I don’t have raisins” could be declared to your significant other.”
“Now, what if we created following or layered protocols that either reduced the catabolic side of the ratio or used other metabolic possibilities to again increase anabolism? Yes, again you are right. The beast would be in a near continuous growth phase instead of fighting to regain.”
“Now, what if we inhibited the negative feed-back loops responsible for post-cycle loss of lean mass tissue? I will explain this too, my lad. All in good time. The days of the genetically gifted only are over. The hard-core average genetic athlete is and will have their days of domination. Mediocrity sucks, Frank.”

Now that we have discussed theoretical half- and active- lives of drugs and plasma levels/plasma thresholds, let’s look at “most effective periods”. I realize this may seem like a great deal of information to deal with. But to construct any protocol that would provide maximum results all action/reaction factors had to be considered. Frank was not a steroid gun-slinger, but he did become a beast.
We know the half- and active- lives of injectable AAS are determined by the chain length of their ester. We have discussed the method by which the enzyme esterase acts upon an injection site dosage to induce migration of the freed AAS into the vascular system. We have also seen how different stacks and athletes have realized alterations in active- and half- lives. Now we need to understand drug “Most Effective Periods” or ranges.
Any drug introduced into the body by any method will have a range or period of time that it is “most effective.” This is the part of a drug’s active- life that provides the greatest results. It would appear a drug would have the same effect during its complete active-life. Sadly, it is not that simple.

After an injection of a drug is given, it takes a period of time for the enzyme esterase to act upon the drugs ester and subsequent release into the vascular system. The longer the AAS (or any drug) ester chain, the longer its active-life. This also means the longer it will take before migration.
Once the drug has migrated into the vascular system it may, depending on its structure, take a period or time to become effective. Believe it or not, this is not as difficult to predict as it would seem. I will give a few charts and graphs to help in a minute, but generally speaking a drugs most effective period is about equal to its half-life.
No, not the first half of its active-life, but usually the center portion of its active-life. As example, if a drug has an active-life of 16 days, it will have a “most effective period” of about 8 days. (Huh?)


Now that we have a few fundamentals let’s begin putting to rest all of the “what and huh?” moments I have created. But first, let’s look at the below graphs …

Graphs omitted

Look at graph A. (next page) This is a drug “most effective period” for an ester with an active- life of 14-16 days. The drug begins activity on day #1 but does not begin its true effect potential until about day #4. This drug would remain in its “most effective period” from about day #4 until or through about day #1 2, which is 8 days. Deca Durabolin, Testosterone Cypionate and Primobolan Depot are examples of the graph. (The drug remains “active” until day #16)
Now look at graph B. (next page) This is a drug with an active- life of about 3 days or 72 hours. The most effective period would be from about hour 18 to hour 54. Remember; the drug is still active before and after the most effective period. That is why it is called an active-life. Durabolin and Testosterone Propionate are examples of this graph. Bet you already knew graph C would be for an ester such as testosterone enanthate. Pretty simple, huh?

PTOR and Homeostasis
The body normally maintains weight and size of all cellular structures through homeostasis (assuming that our discussion focus is our protein synthesis rate/PTOR). The body maintains homeostasis or balance by both building and destroying an equal amount of protein based tissue daily. In fact, most research states that the body both gains and loses protein bases tissue at a rate of bodyweight multiplied by 1 .818 expressed in grams daily. So a 200 LB bodybuilder gains and loses 363.3 grams of protein bases tissue daily; 200 LBS x 1.818 = 363.3 grams. So a 200 LB bodybuilder has a PTOR of 363.3 grams.
Homeostasis is controlled by hormones and hormone-like substances. Some are anabolic and create a state of protein synthesis and growth, while others are catabolic and create a state of protein destruction or waste. When chemical/hormone levels are balanced, or equal in Action/Reaction, there is a state of balance and no change we call homeostasis. If you do not get this yet, do not worry. It is explained and referred to multiple times throughout this book. This is due to the fact that without understanding of this fact, maximum progress is dwarfed. Understanding all details of Frank’s story is paramount.
To increase protein based tissue mass (Like uh, muscle) we must alter the ratio of "protein synthesis/protein wasting in favour of net total protein mass increase. This means triggering either anabolism (protein synthesis) in excess of catabolism (protein wasting) or decreasing protein wasting. Any substance that decreases the catabolic side of this ratio is considered anti-catabolic or protein sparing.
If we could increase the anabolic side of this ratio 100% without altering the catabolic side, our 200 LB bodybuilder would realize a daily net increase in protein based tissue of 363.3 grams. If we decreased the catabolic side of the ratio 100% the result would be the same. Many chemical muscle enhancement substances possess both anabolic and anti-catabolic qualities in carious ratios.
The goal of Frank’s Max Androgen Phases was to stimulate protein synthesis on multiple levels through multiple metabolic pathways. By stimulating the muscle cell androgen receptor-sites, we triggered cellular protein synthesis signals. By inhibiting cortisol receptor-sites, we decreased catabolism.
Also, by inducing a very high androgenic environment we allowed the musculature to significantly increase weight (strength) and work-load capacity. This was quite synergistic: We were able to train muscle more intensely. By increasing protein synthesis and decreasing protein wasting we were able to quickly repair the damage induced. With adequate macronutrient intake, we allowed for super over compensation or adaptation. The result was more muscle mass to carry greater work?loads. This was an adaptive process due to Action/Reaction Factors.
Unfortunately, the body realized we had altered homeostasis and the PTOR all to quickly. The body began to react to our anabolic/androgenic steroid (AAS) induced alteration after two to three weeks and began its own catabolic counter measures as a means of re-establishing homeostasis. To do this the body stepped-up production of cortisol a bit and estrogen as well. Since estrogen triggers a negative feed-back loop that induces H PTA (Hypothalamus/Pituitary/Testes/Axis) inhibition, the result was little or no endogenous testosterone synthesis.
Cortisol is a catabolic hormone that triggers cortisol receptor-sites. This results in protein wasting. If an AAS protocol ran too long, circulatory cortisol levels became elevated to a point where they equaled circulatory androgen activity even from exogenous sources. The result was homeostasis again. When the AAS protocol was discontinued and circulatory androgen levels decreased, the elevated cortisol levels overwhelmed the anabolic/catabolic ratio in favor of protein wasting. The result was

the loss of most, if not all, lean mass tissue gains induced by the AAS protocol. Which sucked! We had to exit before this could happen.
*l have (and will again) explained the effects of elevated estrogen levels post-cycle or after AAS discontinuance.
To further aggravate this post-cycle catabolic situation from long AAS protocols, the HPTA was suppressed and natural or endogenous androgen production was on girl-status. This allowed still existing elevated cortisol and estrogen levels to remain unchecked. (Which should cause testes challenged readers to say “yikes” in a high pitched voice) But this was all so unnecessary and no male needs “raisin syndrome”.
But on the plus side, shaving would be much easier as would singing those old girl-band song of the past. Again, we had to exit the AAS protocol before this can occur.
First things first: The Max Androgen Phases constructed for Frank were intended as a means of altering the anabolic/catabolic ratio in favor of net protein mass increase on a very significant level. (I do like that word “significant”) To do this Frank needed a plan that took into account Action/Reaction Factors so that he could keep much more AAS induced muscle mass gains post-cycle to build further upon as we progressed.
"Okay, we know the body adapts by reaction to AAS beginning after 2-3 weeks. We know that some AAS aromatize to estrogen which needs to be checked and eliminated before we allow you to exit your AAS protocol, Frank. But we also know estrogen levels can actually enhance AAS results by several pathways including increased GH/IGF-1 production and increased muscle glycogen synthesis. We also know any androgenic induced muscle mass gains not solidified into high quality lean muscle tissue by a high anabolic environment will be lost quickly post-cycle. There is only one more main factor to consider. “Support networks”. Think, Frank. Think!

*Just remember the term “support networks” for now. It will be explained later…a lot.
The Right Time Frames
We saw the greatest results from any chemically induced alteration in homeostasis and the PTOR rate when we had a plan. First, we got in, grew hard, and got out before Frank’s body could mount adequate counter measures. This meant a

time frame of 21-30 days. So no Max Androgen Phase (or any other protocol) could have had a high activity level beyond 30 days.
We had to create a quick and elevated androgenic environment to quickly increase mass and strength. No time was wasted that would have allowed the body to catch up with its anti-muscle counter measures. We called this the “androgenic dominance period”. We also had to allow a high anabolic moderate - low androgenic elevated environment to solidify Frank’s mass gains into quality muscle. We called this the “anabolic dominance period”.
Most athletes have realized the greatest results and post-cycle lean mass retention when these two periods were about equal with an equal androgenic - to - anabolic transition period in between. Additionally, we had to create a long “most effective period” without significant inducing HPTA inhibition. Easy !
Estrogen Control, NOT Elimination
Estrogen control was paramount for health and long-term result potential. But estrogen can increase IGF-1 production too, which was good. Estrogen also increases androgen receptor-site sensitivity. So we wanted estrogen to run rampid for the first two weeks of Frank’s Max Androgen Phases without allowing it to cause gyno and female pattern fat deposits. Simple: We used an estrogen antagonist to block receptor-sites but allowed plasma estrogen levels to remain high.
Using Clomid as an example, it has been my experience that a novice AAS user required (if any) only 50 mg/d (50 mg per day). And an intermediate AAS user required 20-30 mg/d. An advanced AAS user commonly required 30-50 mg/d. A very advanced AAS user sometimes required 40-60 mg/d, and in most cases, some additional help from an aromatase inhibitor.
The key was to watch for signs of gyno and female pattern fat deposits, while keeping a close eye on blood pressure. This was always of the utmost concern during the building of the perfect beast. High blood pressure can introduce a variety of long term and life threatening negative side effects.
*Nolvadex decreases GH/IGF-1 synthesis and is therefore a poor choice as an estrogen antagonist.
Things we have learned from experience…
Estrogen levels were kept near normal or below before we exited the AAS protocols. So we added an estrogen esterase inhibitor at about day #15 of a Max Androgen Phase to clear the system of excess estrogen before we exited. I have not noted many novice AAS/Max Androgen Phase users whom needed this precaution. But this was in relevance to dosages administered.

Some intermediate AAS users opted for Arimidex 0.5-1.0 mg/d, or Proviron 50- 100 mg/d. Most advanced AAS users successfully utilized Arimidex 1.0-2.0 mg/d or Aromasin 50mg/d. This was, of course, unnecessary when a Cortisol/Estrogen Suppression Phase was layered in at the half-way point or beginning day #15 of a Max Androgen Phase.
“Patience, Grasshopper!”

I have and will repeat this fact again and again: Any effective plasma threshold exceeded before it failed to provide results was a growth period lost. This was true of any chemical muscle enhancer. This is in fact why so many athletes reached only 50- 70 % of their potential. Receptor-site insensitivity (not AAS receptor sites) and the body learning new tricks to force homeostasis was the number one reason why we had often seen 220 LB 6 foot off-season bodybuilders using crazy dosages with poor results.
Of course there are ways to beat this too that I created for Frank, but we will discuss that later. First let’s look at what the basic threshold for results were when long term potential and permanent gains were to be realized.
Since this section is about Frank’s AAS protocols, let’s focus upon them for now. Growth thresholds were established by plasma level in this discussion. Although there were several thresholds for each level of experience and drug, there were predictable ranges of dosages expressed in daily plasma levels we used as a basis.
First let me say again that it has been my experience that no athlete should have ever utilize AAS or other muscle chemistry until they have trained hard-core for at least 2-3 years as a natural.
If this was Frank, and he was a natural or somewhere in between, I would have utilized the following rough guide-lines. Natural training is a growth threshold also. I have trained some 250 LB, 8% body fat naturals, too.

Never waste a growth threshold. You need to do the physical work required first and foremost, you weenie.

Awsome post, is sent you a PM

Rea is a brilliant guy when it comes to AAS…

I have been getting some PM’s about Short Cycles, here is 1 set of cycle examples, doseages adjustments based on bodyweight are listed below…the examples are for a lifter over 260 +lbs

DAY Cycle 2A

  1.  Sustanon-250 250mg
  2.  Sustanon-250 250mg
  3.  Sustanon-250 250mg
  4.  Sustanon-250 250mg
  5.  Sustanon-250 250mg
  6.  Sustanon-250 250mg
  7.  Sustanon-250 250mg
  8.  Sustanon-250 250mg
  9.  Sustanon-250 250mg
  10. Sustanon-250 250mg
  11. Dura/Deca 250mg (A)
  12. Dura/Deca 250mg
  13. Dura/Deca 250mg
  14. Dura/Deca 250mg
  15. Dura/Deca 250mg
  16. Dura/Deca 250mg
  17. Dura/Deca 250mg
  18. Dura/Deca 250mg
  19. Dura/Deca 250mg
  20. Dura/Deca 250mg

DAY Cycle 2B
1 Test Mix 250mg (B)
2 Test Mix 250mg
3 Test Mix 250mg
4 Test Mix 250mg
5 Test Mix 250mg
6 Test Mix 250mg
7 Test Mix 250mg
8 Test Mix 250mg
9 Test Mix 250mg
10 Test Mix 250mg
11 D/E/D Mix 250mg (c)
12 D/E/D Mix 250mg
13 D/E/D Mix 250mg
14 D/E/D Mix 250mg
15 D/E/D Mix 250mg
16 D/E/D Mix 250mg
17 D/E/D Mix 250mg
18 D/E/D Mix 250mg
19 D/E/D Mix 250mg
20 D/E/D Mix 250mg

DAY Cycle 2C.
1 M/P Mix 250mg (D)
2 M/P Mix 250mg
3 M/P Mix 250mg
4 M/P Mix 250mg
5 M/P Mix 250mg
6 M/P Mix 250mg
7 M/P Mix 250mg
8 M/P Mix 250mg
9 M/P Mix 250mg
10 M/P Mix 250mg
11 D/P Mix 250mg (E1)
12 D/P Mix 250mg
13 D/P Mix 250mg
14 D/P Mix 250mg
15 D/P Mix 250mg
16 D/P Mix 250mg (E2)
17 D/P Mix 250mg
18 D/P Mix 250mg
19 D/P Mix 250mg
20 D/P Mix 250mg
21 D/P Mix 250mg (E3)
22 D/P Mix 250mg
23 D/P Mix 250mg
24 D/P Mix 250mg
25 D/P Mix 250mg
26 Dur.250mg (Optional)
27 Dur.250mg (Optional)
28 Dur.250mg (Optional)

Here is the key:
(A) Durabolin 50 mg + Deca Durabolin 200 mg
(B) Testosterone Propionate 50mg + Testosterone Enanthate 100mg + Testosterone Cypionate 100mg
(C) Durabolin 50mg + Equipoise 50mg + Deca Durabolin 150mg
(D) Masteron 50mg + Test Propionate 200mg
(E1) Durabolin 100mg + Test Propionate 150mg
(E2) Durabolin 150mg + Test Propionate 100mg (E3) Durabolin 200mg + Test Propionate 50mg

(Actual Dosage of Androgen Minus Ester Weight)

As I said, these are the rough guide-lines I utilized and they assumed bodyweights of the following with below 12% bodyfat:

Novices: 185-218 LBS
1.0-2.0 mg/lb weekly
31.25-62.5 mg/daily plasma level
218 mg-437.5 mg total weekly

Intermediates: 21 8 240 LBS
2.0-3.5 mg/lb weekly
62.5-1 25 mg/daily plasma level
437.5 mg-875 mg total weekly

Advanced: 240-265 LBS
3.5-6.75 mg/lb weekly
125-250 mg/d plasma level
875 mg-1 750 mg total weekly

Very Advanced: 265 and up.
6.75 -insanity mg/lb weekly
250 mg/d plasma level
Above 1750 mg total weekly

Of course bone structure and height played a role in potential weight/mass possibilities as did genetics. However, I have met few “average” individuals who could not have realized at least 265 LBS-plus with an off-season body fat level below 12%. Those who have failed usually did so by not planning for long-term potential adequately.
“By learning Phase Cycling and Action/Reaction Factors this, like most obstacles, can be over come.”

Here are the Cortisol Estrogen Suppression Phases…these would start on day 15 of the short cycle and run as listed…

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.

Cortisol/Estrogen Suppression Phases
Example #1 - Chart

  1. Cytadren 250mg 2xd
  2. Cytadren 250mg 2xd
  3. Teslac 250mg
  4. Teslac 250mg
  5. Cytadren 250mg 2xd
  6. Cytadren 250mg 2xd
  7. Teslac 250mg
  8. Teslac 250mg
  9. Cytadren 250mg 2xd
  10. Cytadren 250mg 2xd
  11. Teslac 250mg
  12. Teslac 250mg
  13. Cytadren 250mg 2xd
  14. Cytadren 250mg 2xd
  15. Teslac 250mg
  16. Teslac 250mg
  17. Cytadren 250mg 2xd
  18. Cytadren 250mg 2xd
  19. Teslac 250mg
  20. Teslac 250mg
  21. Cytadren 250mg 2xd
  22. Cytadren 250mg 2xd
  23. Teslac 250mg
  24. Teslac 250mg
  25. Cytadren 250mg 2xd
  26. Cytadren 250mg 2xd
  27. Teslac 250mg
  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.

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 2 1-28 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 feed?back 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)


  1. Trilostane 180mg/Proviron 50mg- 150mg
  2. Nolvadex 30mg/Proviron 50mg- 150mg
  3. Trilostane 180mg/Proviron 50mg- 150mg
  4. Nolvadex 30mg/Proviron 50mg- 150mg
  5. Trilostane 1 80mg/Proviron 50mg- 150mg
  6. Nolvadex 30mg/Proviron 50mg- 150mg
  7. Trilostane 180mg/Proviron 50mg- 150mg
  8. Nolvadex 30mg/Proviron 50mg- 150mg
  9. Trilostane 1 80mg/Proviron 50mg- 150mg
  10. Nolvadex 30mg/Proviron 50mg- 150mg
  11. Trilostane 1 80mg/Proviron 50mg- 150mg
  12. Nolvadex 30mg/Proviron 50mg- 150mg
  13. Trilostane 180mg/Proviron 50mg- 150mg
  14. Nolvadex 30mg/Proviron 50mg- 150mg
  15. Trilostane 1 80mg/Proviron 50mg- 150mg
  16. Nolvadex 30mg/Proviron 50mg- 150mg
  17. Trilostane 180mg/Proviron 50mg- 150mg
  18. Nolvadex 30mg/Proviron 50mg- 150mg
  19. Trilostane 180mg/Proviron 50mg?150mg
  20. Nolvadex 30mg/Proviron 50mg- 150mg
  21. Trilostane 180mg/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.


  1. Metyrapone 500 mg
  2. Arimidex 1 mg
  3. Metyrapone 500 mg
  4. Arimidex 1 mg
  5. Metyrapone 500 mg
  6. Arimidex 1 mg
  7. Metyrapone 500 mg
  8. Arimidex 1 mg
  9. Metyrapone 500 mg
  10. Arimidex 1 mg
  11. Metyrapone 500 mg
  12. Arimidex 1 mg
  13. Metyrapone 500 mg
  14. Arimidex 1 mg
  15. Metyrapone 500 mg
  16. Arimidex 1 mg
  17. Metyrapone 500 mg
  18. Arimidex 1 mg
  19. Metyrapone 500 mg
  20. Arimidex 1 mg
  21. Metyrapone 500 mg
  22. Arimidex 1 mg
  23. Metyrapone 500 mg
  24. Arimidex 1 mg
  25. Metyrapone 500 mg
  26. Arimidex 1 mg
  27. Metyrapone 500 mg
  28. Arimidex 1 mg

? 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.

Cortisol/Estrogen Suppression Phases - With HPTA Layer
Example #4 - Chart

  1.  Remeron 7.5mg/Aromasin 25mg
  2.  Remeron 7.5mg/Aromasin 25mq
  3.  Remeron 15mg/Aromasin 25mg
  4.  Remeron 15mg/Aromasin 25mg
  5.  Remeron 15mg/Aromasin 25mg
  6.  Remeron 15mg/Aromasin 25mg
  7.  Remeron 15mg/Aromasin 25mg/HCC 1000iu
  8.  Remeron 15mg/Aromasin 25mg
  9.  Remeron 15mg/Aromasin 25mg/HCG 1000iu
  10. Remeron 1 5mg/Aromasin 25mg
  11. Remeron 1 5mg/Aromasin 25mg/HCG 1 000iu
  12. Remeron 1 5mg/Aromasin 25mg
  13. Remeron 1 5mg/Aromasin 25mg/HCG 1 000iu
  14. Remeron 15mg/Aromasin 25mg
  15. Remeron 15mg/Aromasin 25mg/HCG 1000iu
  16. Remeron 15mg/Aromasin 25mg
  17. Remeron 1 5mg/Aromasin 25mg/HCG 1 000iu
  18. Remeron 15mg/Aromasin 25mg
  19. Remeron 1 5mg/Aromasin 25mg/HCG 1 000iu
  20. Remeron 15mg/Aromasin 25mg
  21. Remeron 15mg/Aromasin 25mg/HCG 1000iu
  22. Remeron 15mg/Aromasin 25mg
  23. Remeron 15mg/Aromasin 25mg/HCG 1000iu
  24. Remeron 15mg/Aromasin 25mg
  25. Remeron 15mg/Aromasin 25mg/HCG 1000iu
  26. Remeron 15mg/Aromasin 25mg
  27. Remeron 15mg/Aromasin 25mg/HCG 1000iu
  28. Remeron 15mg/Aromasin 25mg

Remeron (mirtazapine) tablets are prescribed as an antidepressant. Before thoughts of Frank on Prozac spin in your head realize that this is a section on cortisol and estrogen control.

Mirtazapine (Remeron) lowers cortisol and prolactin in normal subjects (like athletes are ever normal?) This appeared to an effectual alternative to Cytadren for those interested in lowering cortisol levels. It also lowers prolactin resulting in a decrease in fatty tissue and HPTA inhibition.
Additionally there was a mild (low dose) antidepressant effect as well that some welcomed post-cycle. Kind of like low dose Prozac, Cytadren and bromocriptine or cabergoline all in one. It is noteworthy that many have reported improved appetite during Remeron use, but several have also reported sleeping 12 hours the first few days of use even with the stepped initial dosages.

In studies 15mg/d resulted in a significant decrease in cortisol. What is really interesting is the method of inhibition. ATCH is a hormone that tells the adrenal glands to release corticoid steroids. Naturally most are catabolic to protein tissue (like muscle). However the suppression of ATCH leads to less cortisol being produced without inhibition of sex steroid synthesis.

This means a significant increase potential for LH/FSH production and the resulting increase in natural androgen production. Yup, that is right. Remeron inhibits ATCH secretion. Of course the anti-prolactin effect is nice in the bedroom as well.

Endocrinological effects of mirtazapine in healthy volunteers.
Prog Neuropsychopharmacol Biol Psychiatry 2002 Dec;26(7-8):1253-61