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Old 07-19-2007, 05:53 PM   #61
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Originally Posted by thesinner
"Technically" zero is an asymptote, so your test levels will only approach zero.

Your natural test levels decrease as the exogeneous levels begin taking its place in various biochemical reactions. Then we factor in a fun word called "reaction rate" and yeah, it's not always instantaneous. Shutdown is dependent on compound, dosage, and time.

You're throwin' out some tough Q's there Travis. I'll try my best to answer them, just remember that I'm not the guy with ALL the answers.


You must spread some Reputation around before giving it to thesinner again.


Thanks bro. I guess endocrinology is pretty interesting to me. You seem to have a very good handle on it! Any suggestions on beginner reading material? I have a degree in economics so basically this stuff is all new.

If nothing else its nice to have these discussions. It's why I love coming to AM!
 
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Old 07-19-2007, 06:06 PM   #62
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Originally Posted by Travis
You must spread some Reputation around before giving it to thesinner again.


Thanks bro. I guess endocrinology is pretty interesting to me. You seem to have a very good handle on it! Any suggestions on beginner reading material? I have a degree in economics so basically this stuff is all new.

If nothing else its nice to have these discussions. It's why I love coming to AM!
Oh, endocrinology interests the crap out of me as well. If it weren't for the fact that I'd have accelerated Pharm. students f*cking up the grading curves, I would have signed up for Biochemistry, but I'd rather have a nice GPA than get another chunk taken out from taking overlapping courses with them.

The concepts expressed in my original post, you could probably read about in any good general chemistry book. Of course, they would be applying it to much simpler chemical reactions. Le Chatelier's principle and chemical equilibria are concepts taught in Freshman Chemistry II, but are used in much more advanced chemistry.
 
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Old 07-19-2007, 09:27 PM   #63
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Originally Posted by thesinner
Oh, endocrinology interests the crap out of me as well. If it weren't for the fact that I'd have accelerated Pharm. students f*cking up the grading curves, I would have signed up for Biochemistry, but I'd rather have a nice GPA than get another chunk taken out from taking overlapping courses with them.

The concepts expressed in my original post, you could probably read about in any good general chemistry book. Of course, they would be applying it to much simpler chemical reactions. Le Chatelier's principle and chemical equilibria are concepts taught in Freshman Chemistry II, but are used in much more advanced chemistry.
Cool. I'll pry check out some basic chemistry books on amazon. Should be able to find something I can understand.

Thanks again for the help. Mad props.
 
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Old 07-20-2007, 05:35 PM   #64
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Originally Posted by thesinner
Let's also start by saying that you don't have to run post cycle therapy.........you also don't have to wipe your ass after taking a dump: it's just a really really good idea to do these things

The first thing we need to understand is what is going on with our bodies when we're taking anabolic steroids:
Exogeneous anabolic hormones (or derivatives of anabolic hormones) are being brought into your system. This causes the body to take a number of responsive actions. The first and foremost (as you already know) is increased muscle mass. Unfortunately, other things are also going on that aren't so great

When an enzyme or hormone is brought exogeneously into the system, chemical balances shift around to attain a certain equilibrium. This is a chemical concept known as Le Chatelier's Principle of Chemical Equilibria. In a nutshell, your body will increase production of estrogen, cortisol, and other hormones in response to heightened testosterone levels, while simultaneously slowering (or completely stopping) natural production of testosterone. Biologist call this negative feedback.......biology sucks doesn't it?

Le Chatelier's Principle for the scientifically impaired:
Let's pretend A and B react to make C (can't get much simpler than that).

A + B --------> C

So we have a mixture containing A, B, and C. According to LeChatlier's principle, if we add more C to the mixture, the amounts of A and B will increase. If we remove some of the C from the mixture, A and B will decrease. And if we were to add A, B, or a combination of the two, C will increase. Still with me here? Good.


What's going on when we come off a cycle:
Ok, so while we're on the cycle, are natural test production is going down to compensate for the exogeneous test intake, and our production of other steroid hormones (i.e. Estrogen, Cortisol, etc.) is going up to compensate for the heightened test levels. When we come off a cycle, we cease intake of exogeneous testosterone. In other words, we have very low test levels, and very high cortisol and estrogen levels: it's the EXACT OPPOSITE of what we had while starting our cycle.

REMEMBER Le Chatelier's Principle because this is where it gets really important. When we have an excess of one hormone, the others will start shifting around, to attain a certain equilibrium. Ok, I'm gonna say it (and bold it) again because it's just that important. When we have an excess of one hormone, the others will start shifting around, to attain a certain equilibrium. It is a very common misconception that we want to eradicate estrogen . High estrogen levels play an integral part in Post Cycle therapy. That's right, you want to welcome high estrogen with open freaking arms, but there's a trick to it. And that trick is the almighty SERM (Selective Estrogen Receptor Modulator).

SERM's: the foundation of post cycle therapy:
Selective Estrogen Receptor Modulators are (and damn well should be) the foundation for any proper post-cycle therapy plan. A post cycle therapy plan without them, isn't a post cycle therapy plan: it's a bunch of crap you decided to take after doing a cycle. The purpose of a SERM is to block the negative effects estrogen, while your hormone levels go back to equilibrium.

SERM's are prescription drugs, and are NOT SOLD IN SUPPLEMENT STORES. In fact, there are only 3 ways ( can think of) in which you can obtain a SERM:

1) Through a Doctor's Prescription.
2) Through the Black Market (a.k.a. illegally)
3) As a research chemicals intended for use in lab rats.


The Different SERM's:

Tamoxifen (Nolvadex):
Reputation: Most popular SERM for post cycle therapy
Pros: Cheap. Effective for gyno prevention.
Cons: Heptatoxicity. Studies have shown it to lower IGF levels (I don't feel like citing, but it's about 20% decrease...IMO no biggie).
Popular Dosage (for a 4-week cycle): 40/40/20/20
Note: Tamoxifen Citrate is less potent, and should be dosed at an extra 30%.

Clomiphene Citrate (clomid):
Reputation: Second most popular. Usually taken the first week or so to speed up Testosterone recovery with Tamoxifen being taken the whole therapy.
Pros: Better than Tamoxifen for HTPA regernation. Less heptatoxicity. Does not lower IGF.
Cons: Less effective against gyno. Can cause emotional issues. May Cause blurred vision. Hot Flashes.
Popular Dosage (for a 4-week cycle): 100-200mg/100mg/50mg/50mg

Toremifene:
Reputation: Very popular on this board
Pros: Much less toxic.
Con's: $$$$$expensive$$$$$
Popular Dosages (for a 4-week cycle): 120-240mg/120mg/60mg/30mg

Raloxifene:
Reputation: Very effective against gyno
Pros: Strong protection against gyno. Less toxic than Tamoxifen.
Con's: Cost Restricting. Can cause abnormal blood clotting in the eyes, lunges, and legs. May also cause hot flashes trouble breathing, and blurred vision.
Popular Dosages: (for a 4-week cycle): 120-240mg/120mg/60mg/30mg


Moving down the PCT Hierarchy: Cortisol Control
Excess cortisol can be damaging to your newly found muscle mass. Because of this, it is a good idea to use something to block or lower the excessive cortisol levels. Always start high, and taper your way down. Here's what we have to work with:

B-Androstenetriol (b-triol): This is one of the better cortisol suppressors. It has a terrible oral bioavailability, and should be taken transdermally. Dosages range from 25-50mg every 12 hours.

Methyl B-Androstenetriol (mb-triol): This is an enhanced version of b-triol designed for oral use. Because it is not an androgenic steroid, there is minimal heptatoxicity associated with it's alkylation. Found in the following products: Retain (by Anabolic Xtreme), Restore (by ALRI), Thyrogen-X (by ALRI)

7-Hydroxy-DHEA: Another potent cortisol suppressor with great oral bioavailability. Found in the following products: Lean Xtreme (by Designer Supplements), Reduce XT (by SNS)

7-oxo-DHEA (7-keto-DHEA): Still a decent contender, this has a terrible oral availability and an even worse half life (2 hours). This is best taken transdermally, where such effects can by bypassed.

Cissus: Unlike the above, the components of Cissus do not suppress Cortisol, but rather block cortisol receptors (better than Nandrolone or Dianabol according to some studies). Dosages vary significantly (pending extracts). SuperCissus by USPLabs is a high quality Cissus product.

Branched Chain Amino Acids: These should be a staple to begin with, but are a great anti-catabolic that mitigates the muscle-wasting effects of cortisol.

At the bottom of the PCT hierarchy there's AI's, Test Booster's, and other 'natural' anabolics
Way too many different things going on in here to go into too much detail. Just a word of caution (and this is my personal opinion), but if you're post cycle plan starts to look like a constitutional ammendment: you're over-doing it. And the worst part is if something goes wrong, you won't have a damn clue what caused it.

Honorable mentions of this part of the hierarchy:
Jungle Warfare (by ALRI)
MassFX (by Anabolic Xtreme)
Hyperdrol (by Anabolic Xtreme)
Ecdysterone/Turkesterone
Creatine Monohydrate

Can you tell I was bored after work today?

thesinner

Disclaimer: This post is for entertainment purposes only. I don't use or condone the usage of illegally obtained chemicals.

Author's Note: I cannot and will not give out any information on obtaining any of the drugs mentioned in this article. If you send me a private message asking for sources, I will reply with the following link everytime: Google

i appreciate what youre doing here, great stuff! But i'm planningt a PCT with only stuff that i could find at my supplement store. What would you suggest i buy when i walk into a Vitamin Store?
 
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Old 07-20-2007, 05:43 PM   #65
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Originally Posted by wtfamiiidoing
i appreciate what youre doing here, great stuff! But i'm planningt a post cycle therapy with only stuff that i could find at my supplement store. What would you suggest i buy when i walk into a Vitamin Store?
I would suggest buying nothing, and selling off your whatever steroids you were about to cycle........but that's just me (and about 95% of the other steroid users on this board).
 
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Old 07-20-2007, 06:49 PM   #66
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Originally Posted by thesinner
I would suggest buying nothing, and selling off your whatever steroids you were about to cycle........but that's just me (and about 95% of the other steroid users on this board).
thats great advice! But i think ill try my luck...Last time i gained 15 lbs and was able to maintain. Call me old school..
 
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Old 07-20-2007, 07:02 PM   #67
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thats great advice! But i think ill try my luck...Last time i gained 15 lbs and was able to maintain. Call me old school..
Best of luck to you, but I'm speaking from experience when I say you'll soon wise up to these concepts if you continue 'risking it'. BTW, taking 'PCT Supplements' isn't old school in the least since, SERM's have been around and utilized much longer than most of these supplements people are taking for PCT.
 
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Old 07-20-2007, 08:32 PM   #68
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Originally Posted by thesinner
Best of luck to you, but I'm speaking from experience when I say you'll soon wise up to these concepts if you continue 'risking it'. BTW, taking 'post cycle therapy Supplements' isn't old school in the least since, SERM's have been around and utilized much longer than most of these supplements people are taking for PCT.
Do you know anything close to SERM, that i can get at a store?
 
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Old 07-20-2007, 08:51 PM   #69
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Do you know anything close to SERM, that i can get at a store?
You're trying to cut corners on the protocol I described. How can I help you when you refuse to adhere to the very basis of mt protocol? That's like asking me how to get in shape without working out or eating right......I'm sorry, but I don't have an answer for you.

Quote:
SERM's: the foundation of post cycle therapy:
Selective Estrogen Receptor Modulators are (and damn well should be) the foundation for any proper post-cycle therapy plan. A post cycle therapy plan without them, isn't a post cycle therapy plan: it's a bunch of crap you decided to take after doing a cycle. The purpose of a SERM is to block the negative effects estrogen, while your hormone levels go back to equilibrium.

SERM's are prescription drugs, and are NOT SOLD IN SUPPLEMENT STORES. In fact, there are only 3 ways ( can think of) in which you can obtain a SERM:

1) Through a Doctor's Prescription.
2) Through the Black Market (a.k.a. illegally)
3) As a research chemicals intended for use in lab rats.
I think I've made it pretty clear how to legally obtain the materials which you require, and to avoid doing so is nothing more than cutting corners on this protocol.
 
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Old 07-20-2007, 10:27 PM   #70
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Originally Posted by thesinner
You're trying to cut corners on the protocol I described. How can I help you when you refuse to adhere to the very basis of mt protocol? That's like asking me how to get in shape without working out or eating right......I'm sorry, but I don't have an answer for you.



I think I've made it pretty clear how to legally obtain the materials which you require, and to avoid doing so is nothing more than cutting corners on this protocol.
youre gay
 
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Old 07-20-2007, 10:30 PM   #71
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youre gay
yes.
 
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Old 07-22-2007, 11:13 AM   #72
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Endo stuff

This is older, but I thought it was pretty good in terms of an explanation of some of the endocrinology when using AAS:

Originally Posted by dude2003 @ steroidology.com


TYPES OF STEROIDS
Anabolic/Androgenic Steroids can be roughly classified into two types, oral and injectable. When you eat food or consume anything orally, the great majority of the ingested substances pass through the liver prior to entering the bloodstream. For this reason, "injectable" AAS cannot be taken orally because the liver will deactivate the steroids in this "first pass". Deactivation in the liver usually involves the addition of one or more hydroxyl (OH) groups to increase the solubility of the molecule in water, making excretion in the urine more easily accomplished.

Oral Steroids
Oral steroids involve modification of the parent steroid to make it harder for the liver to degrade the steroid molecules. This modification is almost always the addition of an alkyl (methyl) group at the 17 position of the steroid ring. The liver can still degrade the steroid, but not as effectively as the un-modified steroid. Therefore, oral steroids make several cycles through the bloodstream before being excreted. Most oral steroids are, to various degrees, excreted from the body unchanged.

Injectable Steroids
The injectable AAS are very effectively degraded in just a single pass through the liver. If this is so, then how can the injectables be effective? The answer is called a "depot" (or reservoir), which allows a regular release of steroid into the bloodstream. As steroid is removed from the bloodstream by the liver, more steroid is being released into the bloodstream from the depot. There are several ways to provide such a reservoir of the steroid.

Suspension
The first way is to use pure testosterone (a crystalline solid) suspended in water. Testosterone has a low solubility in water, and the crystals slowly dissolve in the watery environment of the tissue in which it is injected. The dissolved testosterone is carried throughout the body by the bloodstream. For Testosterone suspension, the "depot" is the actual physical site where the injection is made. The crystals do not migrate to other parts of the body, and the presence of the crystalline testosterone can cause some pain at the injection site. The testosterone dissolves at a (relatively) constant rate, and lasts for a few days in the body. Winstrol suspension is similar.

Esters
The other way to provide a depot of steroid is to use a water-insoluble form of the steroid that can be converted in the body to the parent steroid, which has some solubility in water (bloodstream). Most commonly, the parent molecule is esterified with an organic acid, and the resulting ester is soluble in oil, but only very slightly soluble in water. Commonly used organic acid groups are acetate (C2), propionate (C3), enanthate (C7), decanoate (C10), and undecylenate (C11). The longer the carbon chain of the acid, the more oil-soluble the ester, and the longer it takes for the ester to turn into the parent steroid (de-esterification). A type of enzyme that is found throughout the body facilitates the de-esterification reaction to form the parent steroid from the ester. The enzyme actually catalyzes the reaction in both directions, so it can also attach an organic acid back onto the parent steroid. So, for example, testosterone enanthate can actually be turned into testosterone palmitate. There is some good evidence that steroid esters are, to some extent, stored in fat cells.
It is commonly believed that esters form a depot of oil/ester that stays at the injection site. This is not true. While the depot concept holds true for esters (because they slowly release the parent steroid over time), the esters actually disperse throughout the body after injection, prior to (and during) the de-esterification reaction to form the parent steroid. They do not stay at the injection site. For example, the ester testosterone enanthate has been found in tissues throughout the body, including hair samples of subjects who have injected T200. If a bio-contaminant is introduced at the time of injection (non-sterile conditions), the body will attempt to encapsulate the contaminated material, and an abscess will form. In this case it appears as if the ester has remained at the injection site. But under normal sterile conditions, the oily solution will disperse. Injecting too much at one site or injecting too frequently at one site will not cause an abscess.

Transport of Steroids in the Bloodstream
Once the steroid has been released from the depot (or the oral steroid has been absorbed from the intestine), it is transported throughout the body in the bloodstream. Carrier proteins (Albumin and Sex Hormone binding Globulin) bind about 98% of testosterone under natural conditions. Thus, only 2% of the hormone is free to carry out its actions. When exogenous steroid is present, the level of free steroid is much higher than 2%. Bear in mind that the hormone is not permanently bound to the some of the proteins, but is constantly binding and un-binding from the protein. At any given time, about 2% of the hormone is un-bound in the natural state. So, if the 2% unbound hormone were to magically disappear, then the proteins would release more hormone such that 2% (of the remaining total) would come unbound. The bloodstream is the mechanism by which the hormones reach their target tissues (muscle).

Action of Steroids

Androgen Receptor Activation
Once a free molecule of steroid reaches the muscle cell, it diffuses into the cell. The diffusion can be with or without transport-protein assistance. Once in the cell, the AAS is makes its way to the cell nucleus where it can bind with an androgen receptor (AR), and activate the receptor. Two of these activated receptor complexes join together to form the androgen response element (ARE). The ARE interacts with DNA in the nucleus, and increases the transcription of certain genes (such as muscle protein genes). As long as the ARE is intact, it accelerates gene transcription. Remember, though, that the AAS and the receptor are in a state of flux (binding and un-binding), just like with the Carrier proteins. So the ARE can be deactivated just by losing one of the two AAS that are bound to the AR's. This equilibrium situation explains why 1 gram per week testosterone is more effective than 1/2 gram per week, even though 1/2 gram appears to be more than enough to saturate all the AR's in the body. The higher concentration makes it more likely that the receptors will be occupied by an AAS, and the ARE will be intact for a longer period of time, on average.

Other Actions
Activation of the androgen receptor is a key mechanism in the action of AAS. However, this mechanism by itself does not explain the differences between steroids (i.e., nandrolone activates the AR better than testosterone, but is not as good of a mass-building product). Other actions involve primarily the central nervous system, and involve actions such as motor activation (muscle coordination) and mood (i.e., aggressiveness). The mechanism by which AAS effect these actions is not well understood at this time. Another effect occurs in the liver, where some steroids cause the release of certain Growth Factors. The different actions of the different AAS explains why a stack of two different types of AAS is often better than one by itself.

Elimination of Steroids
The liver is a primary route to deactivation of steroids, the chemical structure is changed here to make the steroid more soluble in water for excretion through the kidneys. A good portion of many steroids also are excreted as-is, without any alteration by the liver, or by formation of the sulphate, which is more water soluble. Many in the medical community have believed that AAS cause liver damage because levels of certain enzymes (AST and ALT) are elevated when steroids are used. Elevated levels of these enzymes are seen in patients with liver damage from other causes, so the conclusion is that AAS must cause liver damage because these enzymes are elevated. Recent work, however, has shown that a true marker of liver damage, GGT, remains unchanged when some AAS are used, and now it is questioned whether AAS are really damaging to the liver (the 17 alpha-alkylated AAS do cause damage in some rare cases, and this damage is reversible upon cessation of steroid use). The same thought processes were used to claim kidney damage, but that is unlikely as well.

The Causes of Inhibition
Elevated hormone levels, in general, will cause inhibition of natural testosterone production. What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim’s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.

Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.

The Hypothalamic/Pituitary/Testicular Axis (HPTA)
To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.
The hypothalamus itself cannot produce any sex hormones ?instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.

The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.

LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.
Inhibition From AAS Cycles
Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:

?Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.

?Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and Deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.

?In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.

Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much les