Taking Anabolic Steroids !
There are currently 1 users browsing this thread. Anabolic steroids, bodybuilding discussion forums. Results 1 to 1 of 1. 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" Anabolic Androgenic Steroids 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. 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 C 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. 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 T 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. 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.
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 Anabolic Androgenic Steroids 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 Anabolic Androgenic Steroids AAS and the receptor are in a state of flux binding and un-binding , just like with the Carrier proteins.
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. However, this mechanism by itself does not explain the differences between steroids i.
Other actions involve primarily the central nervous system, and involve actions such as motor activation muscle coordination and mood i.
Another effect occurs in the liver, where some steroids cause the release of certain Growth Factors. 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. Elevated levels of these enzymes are seen in patients with liver damage from other causes, so the conclusion is that Anabolic Androgenic Steroids 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 Anabolic Androgenic Steroids AAS are used, and now it is questioned whether Anabolic Androgenic Steroids AAS are really damaging to the liver the 17 alpha-alkylated Anabolic Androgenic Steroids 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. 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. 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.
This then stimulates the pituitary gland. 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. 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 Anabolic Androgenic Steroids 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: This can be done, for example, by using oral Anabolic Androgenic Steroids AAS only in the morning, with the last dose being approximately at noontime.
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. Again, gains will be compromised compared to a more substantial cycle. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses.
The pituitary is not inhibited at all: After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH.
This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse.
Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few I can recall two were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.
This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise not an exclusive list of aromatizable AAS, but the main ones to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition.
Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug.
Some individuals suffer some lethargy feeling of tiredness and laziness, or sleepiness from Cytadren, but that is uncommon at this dose. This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg. The timing of the dosage does not matter, since the drug has a long half-life.