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07-19-2007, 05:53 PM
| #61 | |
| Banned  | Quote:
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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07-19-2007, 06:06 PM
| #62 | |
| Recovering AXoholic Board Sponsor  | Quote:
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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07-19-2007, 09:27 PM
| #63 | |
| Banned | Quote:
Thanks again for the help. Mad props. | |
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07-20-2007, 05:35 PM
| #64 | |
| Registered User | Quote:
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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07-20-2007, 05:43 PM
| #65 | |
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07-20-2007, 06:49 PM
| #66 | |
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07-20-2007, 07:02 PM
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07-20-2007, 08:32 PM
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07-20-2007, 08:51 PM
| #69 | ||
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07-20-2007, 10:27 PM
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07-20-2007, 10:30 PM
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07-22-2007, 11:13 AM
| #72 |
| Banned | 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 |
. 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). 
thesinner