|Place of Origin:||China|
|Certification:||ISO 9001, USP,GMP|
|Model Number:||Anabolic Steroids|
|Minimum Order Quantity:||10g|
|Packaging Details:||Disguised package ; Foil bag|
|Delivery Time:||3-5 work days|
|Payment Terms:||Western Union, MoneyGram, T/T, bitcoin|
|Supply Ability:||Mass in stock|
|Subject:||How Some Anabolic Steroid Use And Abuse||Delivery Date:||3-5 Work Days|
|Policy:||Re-Shipping Policy||Delivery Express:||DHL, TNT, FEDEX, HKEMS, EMS, Etc|
|Payment Terms:||Western Union, MoneyGram, T/T, Bitcoin||Grade:||Pharmaceutical Grade|
anabolic steroid hormones,
fat loss injections steroids
An Detailed Article About How Some Anabolic Steroid Use and Abuse
Steroids are a general class of agents that all have the steroid ring in common. The steroid ring is comprised of three 6-carbon rings and one 5-carbon ring joined, of which cholesterol is the most basic form and, indeed, the precursor. Although the term steroid includes all agents derived from this ringed structure, this discussion includes only testosterone and the anabolic-androgenic steroids (AASs).
Testosterone is the principle hormone in humans that produces male secondary sex characteristics (androgenic) and is an important hormone in maintaining adequate nitrogen balance, thus aiding in tissue healing and the maintenance of muscle mass (anabolic). Testosterone has a dual action and can be described in terms of its androgenic and anabolic capacities.
AASs are drugs derived from the modification of the testosterone molecule in order to augment or limit certain characteristics of testosterone. In general, testosterone has been altered to produce drugs that are more or less anabolic, are more or less androgenic, have differing affinity for the testosterone receptor, have different metabolic breakdown pathways, or are efficacious for oral use; they can also have any combination of these changes.
Well over a thousand different compounds have been synthesized and studied since the 1950s in the hope of producing compounds that have an anabolic orandrogenic effect superior to that of testosterone. Biochemists quickly noted that additions or subtractions to the testosterone molecule at specific locations would have a somewhat predictable effect on the inherent qualities of said compound. Specifically, qualities including (but not limited to) anabolic/androgenic ratio, metabolism, receptor affinity, and oral efficacy were noted.
In general, the goal of altering an AAS is to increase its anabolic characteristics and to decrease its androgenic features, thus multiplying the compound's desirable, anabolic, nitrogen-sparing effects and minimizing its generally undesirable, androgenic, virilizing effects. To date, however, complete dissociation of the anabolic effects of an AAS from its androgenic characteristics has not been possible.
Clinically, AASs have been used to treat a host of conditions, including the following:
Almost since their inception, testosterone and anabolic-androgenic analogues have been used and abused by individuals seeking to augment their anabolic and androgenic potential. By doing so, these persons aim to boost their physical performance in athletic endeavors or improve their physique. Stories of Eastern-bloc athletes receiving testosterone and AASs as part of their training regimens as early as the 1950s abound. The Eastern-bloc weightlifters and track athletes subsequently ruled the athletic stage for decades.
The degree to which AASs affect performance enhancement in healthy athletes is widely debated, as are the precise mechanisms of action. Anecdotal evidence, including increases in strength and lean body mass (LBM), has been reported, but steroid effect is difficult to study in a true placebo-controlled, double-blind fashion. Most athletes would notice testicular atrophy if receiving AASs, which would interfere with a study's double-blind structure. Dosing, nutrition, and training parameters would need to be monitored extensively to completely satisfy the most critical review.
Certainly, the use of AASs has become a worldwide phenomenon, slowly trickling down to collegiate, high school, and even junior high levels. The early assertion from the medical community that "anabolic steroids have not been shown to enhance athletic ability," still in print in the 2002 Physicians Desk Reference, contributed to this phenomenon. Technically, the statement is correct; however, people misusing and abusing these drugs quickly realized that the performance-enhancing effects were real and subsequently dismissed the rest of the medical community's contraindications, dosing recommendations, and warnings.
Biopharmacology of Testosterone
Testosterone, the primary male sex hormone, is manufactured in the testes under the influence of luteinizing hormone (LH) in amounts of 2.5-11 mg/d. Testosterone is produced under a negative feedback loop between the hypothalamus, the anterior pituitary, and the testes. Testosterone, dihydrotestosterone, and estrogen all act at the hypothalamus to exert negative feedback inhibition upon gonadotropin-releasing hormone (GnRH). Since GnRH stimulates follicle-stimulating hormone (FSH) and LH release in the pituitary, this negative feedback can be seen to inhibit subsequent testosterone production and effect spermatogenesis.
Testosterone activity is mediated via an androgen receptor that is present in various tissues throughout the human body. Testosterone binds to an intracellular receptor found in the cytosol of cells, forming a receptor complex that migrates into the nucleus, where it binds to specific deoxyribonucleic acid (DNA) segments. This, in turn, activates specific messenger ribonucleic acid (mRNA) to increase transcription, leading to an increased rate of protein synthesis; in the case of muscle cells, this means increased production of the proteins actin and myosin. After this process is complete, the receptor complex dissociates and is recycled along with the hormone, to repeat this process multiple times prior to metabolism.
These anabolic actions of testosterone are thought to be primarily due to testosterone acting upon the androgen receptor in anabolic-responsive tissues. Androgenic effects are likely mediated via the same androgen receptor in androgen-responsive tissues under the influence of dihydrotestosterone (DHT), which is produced by the interaction of 5-alpha reductase (5AR) with testosterone and the subsequent reduction of the C4-5 double bond. Additionally, DHT cannot undergo further reduction, nor is it a substrate for aromatase; thus, it is not converted to estrogenic metabolites. DHT has been shown to bind avidly to receptors in tissues, such as skin, scalp, and prostate, and to exert 3-4 times the androgenic effect of testosterone. Thus, the primary hormone mediating the androgenic effects of testosterone is actually the 5-alpha reduced DHT.
Other mechanisms of direct and indirect anabolic effects include anti-glucocorticoid activity mediated by displacement of glucocorticoids from their receptor, increases in the creatine phosphokinase activity in skeletal muscle, and increases in circulating insulinlike growth factor (IGF)–1, as well as up-regulation of IGF-1 receptors. These mechanisms may play a much larger role in the anabolic/anticatabolic actions of anabolic-androgenic steroids (AASs) than once thought. At physiologic testosterone levels, nearly all androgen receptors are engaged. Therefore, supraphysiologic doses of testosterone or AASs would have no increased anabolic effect in healthy athletes unless other mechanisms of action existed.
Biochemistry and Pharmacology
Because there are many agents in production and literally hundreds more that have been synthesized, this discussion focuses on the basics involving the steroid ring substitutions and how these substitutions affect the properties of the drug. Detailed analysis is limited to those agents that are available or have been approved for use in the United States.
Anabolic-androgenic steroid (AAS) development was centered on the need for agents that exhibited different characteristics than did testosterone. In general, the goal was to develop agents that were more anabolic and less androgenic than testosterone, that were capable of being administered orally, and that had less effect upon the hypothalamic-pituitary-gonadal axis. Most AASs are derived from 3 compounds: testosterone, dihydrotestosterone, and 19-nortestosterone. The third compound is structurally identical to testosterone except for the deletion of the 19th carbon (hence its name). These parent compounds offer different properties with regard to action and metabolism that are generally constant throughout the entire family of compounds.
One of the first changes made to the testosterone molecule was the addition of a methyl group or an ethyl group to the 17-carbon position. This addition was noted to inhibit the hepatic degradation of the molecule, greatly extending the molecule's half-life and making it active when administered orally. Prior to this, testosterone, dihydrotestosterone, and 19-nortestosterone all required parenteral administration due to hepatic metabolism of 17-ketosteroids; this metabolism occurred on the first pass, when the drugs were administered orally.
However, adding a methyl group or an ethyl group did not produce a drug with the exact properties of the parent compound. The alteration of hepatic metabolism was noted to cause strain on the liver, and indeed all oral compounds with this C-17 addition were found to cause dose-related hepatotoxicity. This small change was also found to lower these agents' interaction with aromatase. Therefore, even small changes to these parent compounds cause multiple alterations in the inherent nature of AASs.
Testosterone Esters and Derivatives
Testosterone esters have increasingly been used in replacement therapy, but abuse of these compounds has risen as well. A feature that all testosterone esters have in common is a testosterone molecule with a carboxylic acid group (ester linkage) attached to the 17-beta hydroxyl group. These esters differ in structural shape and size; they function only to determine the rate at which the testosterone is released from tissue. Generally, the shorter the ester chain, the shorter the drug's half-life and quicker the drug enters the circulation. Longer/larger esters usually have a longer half-life and are released into the circulation more slowly. Once in the circulation, the ester is cleaved, leaving free testosterone.
Common testosterone preparations include the following:
See the list below:
Methyltestosterone is a very basic anabolic-androgenic steroid (AAS), with the only addition being a methyl group at C-17. This eliminates first-pass degradation in the liver, making oral dosing possible. It also causes dose-related hepatotoxicity.
Methyltestosterone is metabolized by aromatase to the potent estrogen 17-alpha methyl estradiol and is also reduced by 5AR to 17-alpha methyl dihydrotestosterone.
This compound exhibits very strong androgenic and estrogenic side effects and is generally a poor choice for most, if not all, uses.
Methandrostenolone has an added cis- 1 to cis- 2 double bond that reduces estrogenic and androgenic properties. However, it does undergo aromatization to the rather potent estrogen 17-alpha methyl estradiol, but curiously, it does not show the in-vivo propensity for reduction by 5AR to alpha dihydromethandrostenolone to any large degree.
This steroid was first commercially manufactured in 1960 by Ciba under the brand name Dianabol and quickly became the most used and abused steroid worldwide, remaining so to date. It jokingly came to be known as "the breakfast of champions" in sports circles.
This agent is very anabolic, with a half-life of approximately 4 hours. The methyl group at C-17 makes this AAS an oral preparation and potentially hepatotoxic.
Ciba, as well as generic firms in the United States, discontinued methandrostenolone in the late 1980s, but over 15 countries worldwide still produce it in generic form.
Fluoxymesterone is a potent androgen that is produced under the brand name Halotestin. It is an excellent substrate for 5AR and conversion to dihydrotestosterone (DHT) metabolites. With the addition of a 9-fluoro group, it is a very potent androgen that has little anabolic activity. An added 11-beta hydroxyl group inhibits its aromatization. Again, the C-17 methyl group makes oral administration possible, but with hepatic concerns.
This AAS is not favored in clinical practice due to its poor anabolic effects, yet athletes abuse it for its androgenic nature and lack of peripheral aromatization.
Nandrolone decanoate is simply a 19-nortestosterone molecule in which a 10-carbon decanoate ester has been added to the 17-beta hydroxyl group. This addition extends the half-life of the drug considerably. Nandrolone (19-nortestosterone) is a potent anabolic with a relatively favorable safety profile. Nandrolone is reduced by 5AR in target tissues to the less potent androgen dihydronandrolone. Its affinity for aromatization to estrogen is low, being perhaps 3-4 times less than that of testosterone.
Nandrolone and its several esters (decanoate, phenylpropionate) differ only in their half-lives, due to the difference in ester properties.
Nandrolone is a relatively safe drug with minimal androgenic concerns and ample anabolic action at therapeutic doses. Nandrolone decanoate is an intramuscular (IM) preparation and lacks the hepatotoxic C-17 group; however, this agent is one of the most widely abused AASs, due to its efficacy, safety profile, and worldwide manufacture.
Ethylestrenol is an oral 19-nortestosterone derivative and was marketed in the United States under the brand name Maxibolin, but it has since been discontinued.
This agent differs from nandrolone by the addition of a 17-alpha ethyl group to reduce first-pass metabolism, as well as by the deletion of the 3-keto group. This latter omission seems to reduce androgen receptor binding.
Ethylestrenol is a mild AAS, having very little anabolic or androgenic effect at therapeutic doses.
Trenbolone is a derivative of nandrolone with several additions. The addition of acis- 9 to cis- 10 double bond inhibits aromatization, while a cis- 11 to cis- 12 double bond greatly enhances androgen receptor binding.
This drug is androgenically and anabolically potent. It is comparably more androgenic than nandrolone due to its lack of conversion to a weaker androgen by 5AR, as is seen with nandrolone.
Trenbolone is a European drug with a very high abuse record. In the United States, it is used in veterinary preparations as trenbolone acetate; as such, it has found its way into the hands of persons who wish to exploit its androgenic and anabolic potential.
Oxandrolone, a derivative of DHT, is C-17 methylated, making it an oral preparation.
The second carbon substitution with oxygen is thought to increase the stability of the 3-keto group and greatly increase its anabolic component. This AAS is very anabolic, with little androgenic effect at a therapeutic dose. 5AR does not reduce oxandrolone to a more potent androgen, and as a DHT derivative, it cannot be aromatized.
First marketed by Searle, DHT was discontinued in the mid-1990s. BTG remarketed this AAS as Oxandrin, largely for the drug's use in HIV-related disease.
Due to its mild androgenic properties, oxandrolone is one of the few agents to be routinely abused by female athletes. Athletes, from weightlifters to boxers, use oxandrolone, seeking to increase strength without experiencing additional weight gain.
Stanozolol is an active AAS, due to the stability afforded by the 3,2 pyrazole group on the A-ring, which greatly enhances androgen receptor binding. The C-17 methyl group enhances oral availability.
Stanozolol is highly active in androgen- and anabolic-sensitive tissue. It is a weaker androgen than DHT and exerts comparatively less androgenic effect. It will not aromatize to estrogenic metabolites.
This AAS, marketed in the United States and abroad as Winstrol, comes in oral and injectable forms.
Athletes, many in track and field, have abused it. In 1988, Canadian sprinter Ben Johnson was stripped of his Olympic gold medal after testing positive for stanozolol.
This quite potent AAS is a unique agent. Oxymetholone is C-17 methylated and, thus, is an oral agent. The 3-keto stability added by the 2-hydroxymethylene group greatly enhances the drug's anabolic properties. The action of this agent in androgen-sensitive tissues is much like that of DHT and is quite androgenic.
Oxymetholone is the only AAS to date to be considered a carcinogen.
Like this entire class, oxymetholone does not aromatize. It is thought to activate estrogen receptors via the 2-hydroxymethylene group, and it can exert many estrogenic side effects.
Oxymetholone is marketed in the United States as Anadrol-50 and has been abused the world over by weight lifters and strength athletes for its strong anabolic and pronounced androgenic effects.
Contact Person: Coco