Anabolic Steroids and their role in Bodybuilding and Fitness
Anabolic steroids have been at the most popular topic of discussion for decades as current, past, future, and non-users debate, defend, and demonize the use of anabolic steroids as a means to cut fat, build muscle, and gain strength.
So much confusion over this topic due to news media, TV, Movies, and conflicting advice makes this issue even more confusing.
The idea that anabolic steroids will turn you into MR. OLYMPIA within a year or two is complete nonsense. Another myth that desperately needs to be debunked is that anabolic steroids will give you super powers on the “athletic field” or whatever your sport of choice or discipline is.
Steroids simply do give you an edge. They make things a bit better. However if you are thinking that you can do what the best athlete you see on TV is doing if you just took some steroids, you will be sadly mistaken. It won’t and doesn’t work that way.
The same thought process needs to be addressed as people who only have the genetic ability to grow 18inch arms think they will measure 24inch arms after they take steroids for a period of time. Also untrue.
Steroids will help grow you to your own personal genetic ability, no further.
So if your genetic cap is 18inch arms, that’s what you will get with effort applied.
Sorry to burst that bubble but it is true.
If you are genetically tapped, things like Human Growth Hormone are things you may want to employ along with anabolic steroids so that you can push past your genetic cap.
The below text is excerpts taken from William Llewellyn’s, ANABOLICS
We highly recommend you pick up a copy of this book. This book will be invaluable to you as a new or experienced user of anabolic steroids and various other compounds. If you are interested please see our article on where to buy steroids online.
1. Brief History of Anabolic/Androgenic Steroids
2. Synthetic Anabolic Steroids Development
3. Methylated Compounds and Oral Dosing
4. Non-Alkylated Orals
5. Esters and Injectable Anabolic Steroid Compounds
6. Anabolic/Androgenic Dissociation
7. Nandrolone and 19-norandrogens
8. 5-alpha Irreducible Anabolic Steroids
9. 3-alpha Hydroxysteroid Dehydrogenase
10. Anabolics and Potency
11. Synthetic Anabolic Steroids Chemistry
12. Testosterone derivatives
13. Nandrolone derivatives
14. Dihydrotestosterone derivatives
While it had been clear for many centuries that the testicles were crucial for the male body to properly develop, it was not until modern times that an understanding of testosterone began to form. The first solid scientific experiments in this area, which eventually led to the discovery and replication of testosterone (and related androgens), were undertaken in the 1800s. During this century a number of animal experiments were published, most of which involved the removal and/or implantation of testicular material from/in a subject. Although very crude in design by today’s standards, these studies certainly laid the foundation for the modern field of endocrinology (the study of hormones). By the turn of the century, scientists were able to produce the first experimental androgen injections. These were actualized either through the filtering of large quantities of urine (for active hormones), or by extracting testosterone from animal testicles. Again, the methods were rough but the final results proved to be very enlightening.
Chemists finally synthesized the structure of testosterone in the mid-1930’s, sparking a new wave of interest in this hormone. With the medical community paying a tremendous amount of attention to this achievement, the possible therapeutic uses for a readily available synthetic testosterone quickly became an extremely popular focus. Many believed the applications for this type of a medication would be extremely far-reaching, with uses ranging from the maintenance of an androgen deficiency, to that of a good health and well-being treatment for the sickly or elderly. During the infancy of such experimentation, many believed they had crossed paths with a true “fountain of youth.”
Dihydrotestosterone and nandrolone, two other naturally occurring steroids, were also isolated and synthesized in the early years of steroid development. To make things even more interesting, scientists soon realized that the androgenic, estrogenic, and anabolic activity of steroid hormones could be adjusted by altering their molecular structure. The goal of many researchers thereafter became to manufacture a steroid with extremely strong anabolic activity, but will display little or no androgenic/estrogenic properties. This could be very beneficial, because side effects will often become pronounced when steroid hormones are administered in supraphysiological amounts. A “pure” anabolic would theoretically allow the patient to receive only the beneficial effects of androgens (lean muscle mass gain, increased energy and recuperation, etc.), regardless of the dosage. Some early success with the creation of new structures convinced many scientists that they were on the right track. Unfortunately none of this progress led researchers their ultimate goal. By the mid-1950’s, well over one thousand testosterone, nandrolone, and dihydrotestosterone analogues had been produced, but none proved to be purely anabolic compounds.
The failure to reach this goal was primarily due to an initial flawed understanding of testosterone’s action. Scientists had noticed high levels of DHT in certain tissues, and believed this indicated an unusual receptor affinity for this hormone. This led to the belief that the human body had two different androgen receptors. According to this theory, one receptor site would respond only to testosterone (eliciting the beneficial anabolic effects), while the other is activated specifically by the metabolite, dihydrotestosterone. With this understanding, eliminating the conversion of testosterone to DHT was thought capable of solving the problem of androgenic side effects, as these receptors would have little or none of this hormone available for binding. More recently, however, scientists have come to understand that only one type of androgen receptor exists in the human body. It is also accepted that no anabolic/androgenic steroid can possibly be synthesized that would participate only with receptors in tissues related to anabolism. DHT, which was once thought not to bind to the same receptor as testosterone, is now known to do so at approximately three to four times the affinity of its parent, and the unusual recovery of DHT from androgen responsive tissues is now attributed to the distribution characteristics of the 5a-reductase enzyme.
In order to develop products that would be effective therapeutically, chemists needed to solve a number of problems with using natural steroid hormones for treatment. For example, oral dosing was a problem, as our basic steroids testosterone, nandrolone, and dihydrotestosterone are ineffective when administered this way. The liver would efficiently break down their structure before reaching circulation, so some form of alteration was required in order for a tablet or capsule to be produced. Our natural steroid hormones also have very short half-lives in the body, so when administered by injection, an extremely frequent and uncomfortable dosing schedule is required if a steady blood level is to be achieved. Therefore, extending steroid activity was a major goal for many chemists during the early years of synthetic AAS development. Scientists also focused on the nagging problems of possible excess estrogenic buildup in the blood, particularly with testosterone, which can become very uncomfortable for patients undergoing therapy.
Chemists realized that by replacing the hydrogen atom at the steroid’s 17th alpha position with a carbon atom (a process referred to as alkylation), its structure would be notably resistant to breakdown by the liver. The carbon atom is typically added in the form of a methyl group (CH3), although we see oral steroids with an added ethyl
(C2H5) grouping as well. A steroid with this alteration is commonly descirbed as a C-17 alpha alkylated oral, although the terms of methylated or ethylated oral steroid are also used. The alkyl group cannot be removed metabolically, and therefore inhibits reduction of the steroid to its inactive 17-ketosteroid form by occupying one of the necessary carbon bonds. Before long, pharmaceutical companies had utilized this advance (and others) to manufacture an array of effective oral steroids including methyltestosterone, Dianabol, Winstrol®, Anadrol 50®, Halotestin®, Nilevar, Orabolin, and Anavar. The principle drawback to these compounds is that they place a notable amount of stress on the liver, which in some instances can lead to actual damage to this organ.
Because the alkyl group cannot be removed, it mediates the action of the steroid in the body. Methyltestosterone, for example, is not simply an oral equivalent of testosterone, as the added alkylation changes the activity of this steroid considerably. One major change we see is an increased tendency for the steroid to produce estrogenic side effects, despite the fact that it actually lowers the ability of the hormone to interact with aromatase.45 Apparently with 17-alkylation present on a steroid, aromatization (when possible) produces a more active form of estrogen (typically 17alpha-methyl or 17alpha-ethyl estradiol). These estrogens are more biologically active than estradiol due to their longer half-life and weaker tendency to bind with serum proteins. In some instances, 17alpha-alkylation will also enhance the ability of the initial steroid compound to bind with and activate the estrogen or progesterone receptor.46 An enhancement of estrogenic properties is also obvious when we look at methandrostenolone, which is an alkylated form of boldenone (Equipoise®), and Nilevar, which is an alkylated form of the mild anabolic nandrolone. Dianabol is clearly more estrogenic than Equipoise®, a drug not noted for producing strong side
effects of this nature. The same holds true for the comparison of Nilevar to Deca-Durabolin, a compound that we also know to be extremely mild in this regard.
C17 alpha alkylation also typically lowers the affinity in which the steroid binds to the androgen receptor, as is noted with the weak relative binding affinity of such popular agents as Dianabol and Winstrol (stanozolol). However, since this alteration also greatly prolongs the half-life of a steroid, as well as increases the tendency for it to exist in an unbound state, it creates a more potent anabolic/androgenic agent in both cases. This explains why Dianabol and stanozolol are notably effective in relatively lower weekly doses (often 140 mg weekly will produce notable growth) compared to injectables such as testosterone and nandrolone, which often need to reach doses of 300-400 mg weekly for a similar level of effect.
In an attempt to solve the mentioned problems with liver toxicity we see with c17-alpha alkylated compounds, a number of other orals with different chemical alterations (such as Primobolan®, Proviron®, AndriolË, and Anabolicum Vister) were created. Primobolan® and Proviron® are alkylated at the one position (methyl), a trait which also slows ketosteroid reduction. Andriol® uses a 17beta carboxylic acid ester (used with injectable compounds, discussed below), however, here the oil-dissolved steroid is sealed in a capsule and is intended for oral administration. This is supposed to promote steroid absorption through intestinal lymphatic ducts, bypassing the first pass through the liver. In addition to 1 methylation, Primobolan® also utilizes a 17 beta ester (acetate) to further protect against reduction to inactive form (here there is no lymphatic system absorption). Anabolicum Vister uses 17beta enol ether linkage to protect the steroid, which is very similar to esterification as the ether breaks off to release a steroid base (boldenone in this case). While all of these types of compounds do not place the same stress on the liver, they are also much less resistant to breakdown than 17 alkylated orals, and are ultimately less active milligram for milligram.
You may notice that many injectable steroids will list long chemical names like testosterone cypionate and testosterone enanthate, instead of just testosterone. In these cases, the cypionate and enanthate are esters (carboxylic acids) that have been attached to the 17-beta hydroxyl group of the testosterone molecule, which increase the active life span of the steroid preparation. Such alterations will reduce the steroid’s level of water solubility, and increase its oil solubility. Once an esterified compound has been injected, it will form a deposit in the muscle tissue (depot) from which it will slowly enter circulation. Generally the larger the ester chain, the more oil soluble the steroid compound will be, and the longer it will take for the full dosage to be released. Once free in circulation, enzymes will quickly remove the ester chain and the parent hormone will be free to exert its activity (while the ester is present the steroid is inert).
There are a wide number of esters, which can provide varying release times, used in medicine today. To compare, an ester like decanoate can extend the release of active parent drug into the blood stream for three to four weeks, while it may only be extended for a few days with an acetate or propionate ester. The use of an ester allows for a much less frequent injection schedule than if using a water-based (straight) testosterone, which is much more comfortable for the patient. We must remember when calculating dosages, that the ester is figured into the steroid’s measured weight. 100 mg of testosterone enanthate, therefore, contains much less base hormone than 100 mg of a straight testosterone suspension (in this case it equals 72mg of testosterone). In some instances, an ester may account for roughly 40% or more of the total steroid weight, but the typical measure is somewhere around 15% to 35%. Below are the free base equivalents for several popular steroid compounds.
It is also important to stress the fact that esters do not alter the activity of the parent steroid in any way. They work only to slow its release. It is quite common to hear people speak about the properties of different esters, almost as if they can magically alter a steroid’s effectiveness. This is really nonsense. Enanthate is not more powerful than cypionate (perhaps a few extra milligrams of testosterone released per injection, but nothing to note), nor is Sustanon some type of incredible testosterone blend. Personally, I have always considered Sustanon a very poor buy in the face of cheaper 250 mg enanthate ampules. Your muscle cells see only testosterone; ultimately there is no difference. Reports of varying levels of muscle gain, androgenic side effects, water retention, etc. are only issues of timing. Faster releasing testosterone esters will produce estrogen buildup faster simply because there is more testosterone free in the blood from the start of the cycle. The same is true when we state that Durabolin® is a milder nandrolone for women compared to Deca. It is simply easier to control the blood level with a faster acting drug. Were virilization symptoms to become apparent, hormone levels will drop much faster once we stop administration. This should not be confused with the notion that the nandrolone in Durabolin® acts differently in the body than that released from a shot of Deca-Durabolin®.
It is also worth noting that while the ester is typically hydrolyzed in general circulation, some will be hydrolyzed at the injection site where the steroid depot first contacts blood. This will cause a slightly higher concentration of both free steroid and ester in the muscle where the drug had been administered. On the plus side, this may equate to slightly better growth in this muscle, as more hormone is made available to nearby cells. Many bodybuilders have come to swear by the use of injection sites such as the deltoids, biceps, and triceps, truly believing better growth can be achieved if the steroid is injected directly into these muscles. The negative to this is that the ester itself may be irritating to the tissues at the site of injection once it is broken free. In some instances it can be so caustic that the muscle itself will become swollen and sore due to the presence of the ester, and the user may even suffer a lowgrade fever as the body fights off the irritant (the onset of such symptoms typically occurs 24-72 hours after injection). This effect is more common with small chain esters such as propionate and acetate, and can actually make a popular steroid such as Sustanon (which contains testosterone propionate) off-limits for some users who experience too much discomfort to justify using the drug. Longer chain esters such as decanoate and cypionate are typically much less irritating at the site of injection, and therefore are preferred by sensitive individuals.
Although never complete, scientists had some success in their quest to separate the androgenic and anabolic properties of testosterone. A number of synthetic anabolic steroids had been developed as a result, with many being notably weaker and stronger than our base androgen. In order to first assess the anabolic and androgenic potential of each newly developed steroid, scientists had generally used rats as a model. To judge androgenic potency the typical procedure involved the post-administration measure (% growth) of the seminal vesicles and ventral prostate. These two tissues will often respond unequally to a given steroid, however, so an average of the two figures is used. Anabolic activity was most commonly determined by measuring the growth of the levator ani, a sex organ (not skeletal) muscle. This tissue may not be the most ideal one to use though, as it contains more androgen receptor than most skeletal muscles (the AR is still less abundant here than in target tissues such as the ventral prostate).47 48 In integrating both measures, the anabolic index is used, which relates the ratio of anabolic to androgenic response for a given steroid. An anabolic index greater than one indicates a higher tendency for anabolic effect, and therefore classifies the drug as an anabolic steroid. A measure lower than one in turn assesses the steroid as androgenic. There is some variance between experimental results and the actual real world experiences with humans, but (with a few exceptions) designations based on the anabolic index are generally accepted. Below are discussed a few factors that greatly affect anabolic/androgenic dissociation.
The section of this book dealing with DHT conversion is important, because it helps us understand the anabolic steroid nandrolone and many of its derivatives. Nandrolone is identical to testosterone except it lacks a carbon atom in the 19th position, hence its other given name 19-nortestosterone. Nandrolone is very interesting because it offers the greatest ratio of anabolic to androgenic effect of the three natural steroids (see: Synthetic AAS Chemistry).This is because it is metabolized into a less potent structure (dihydronandrolone) in androgen target tissues with high concentrations of the 5-alpha reductase enzyme, which is the exact opposite of what happens with testosterone. Apparently the removal of the c4-5 double bond, which normally increases the androgen receptor binding capability of testosterone, causes an unusual lowering of this ability with nandrolone.Instead of becoming three to four times more potent, it becomes several times weaker. This is a very desirable trait if you want to target anabolic effects over androgenic. This characteristic also carries over to most synthetic steroids derived from nandrolone, making this an attractive base steroid to use in the synthesis of new, primarily anabolic, steroids.
When we look at the other mild anabolic steroids Primobolan®, Winstrol®, and Anavar, none of which are derived from nandrolone, we see another interesting commonality. These steroids are DHT derivatives that are unaffected by 5alpha-reductase, and therefore become neither weaker nor stronger in androgen responsive target tissues with high concentrations of this enzyme. In essence, they have a very balanced effect between muscle and androgen tissues, making them outwardly less androgenic than testosterone. This is why these steroids are technically classified as anabolics, and are undeniably less troublesome than many other steroids in terms of promoting androgenic side effects. However, if we wanted to look for the absolute least androgenic steroid, the title would still go to nandrolone (or perhaps one of its derivatives). Female bodybuilders should likewise take note that despite the recommendations of others, steroids like Anavar, Winstrol and Primo are not the least risky steroids to use. This is of great importance, as male sex hormones can produce many undesirable and permanent side effects when incorrectly taken by females (See: Side Effects, Virilization).
The 3-alpha hydroxysteroid dehydrogenase enzyme is also important, because it can work to reduce the anabolic potency of certain steroids considerably. As follows, not all potent binders of the androgen receptor are, as a rule, great muscle-building drugs, and this enzyme is an important factor. Dihydrotestosterone is a clear example. Just as the body converts testosterone to DHT as a way to potentiate its action in certain tissues (skin, scalp, prostate, etc.), it also has ways of countering the strong activity of DHT, in other tissues where it is unneeded. This is accomplished by the rapid reduction of DHT to its inactive active metabolites, namely androstanediol, before it reaches the androgen receptor. This activity occurs via interaction with the 3-alpha hydroxysteroid dehydrogenase enzyme. This enzyme is present in high concentrations in certain tissues, including skeletal muscle, and DHT is much more open to alteration by it than other steroids that possess a c4-5 double-bond (like testosterone).49 This causes dihydrotestosterone to be an extremely poor anabolic, despite the fact that it actually exhibits a much higher affinity for the cellular androgen receptor than most other steroids. Were it able to reach the cellular androgen receptor without first being metabolized by 3a-HSD, it certainly would be a formidable muscle-building steroid. Unfortunately this is not the case, explaining why injectable dihydrotestosterone preparations (no longer commercially produced) were never favorite drugs among athletes looking to build mass. This trait is also shared by the currently popular oral androgen Proviron®, which is, in essence, just an oral form of DHT (1-methyl dihydrotestosterone to be specific) and known to be an extremely poor tissue builder.
One must remember that being classified as an anabolic just means that the steroid is more inclined to produce muscle growth than androgenic side effects. Since both effects are mediated through the same receptor, and growth is not produced by androgen receptor activation in muscle tissue alone (other CNS tissues, for example, are integral to this process as well), we find that a reduction in the androgenic activity of a compound will often coincide with a similar lowering of its muscle-building effectiveness. If we are just looking at overall muscle growth, androgenic steroids (usually potent due to their displaying a high affinity to bind with the androgen receptor in all tissues) are typically much more productive muscle-builders than anabolics, which usually bind with lower affinity in many tissues. In fact, with all of the analogues produced throughout the years, the base androgen testosterone is still considered to be one of the most effective bulking agents. The user must simply endure more side effects when acquiring his or her new muscle with this type of drug. Individuals wishing to avoid the stronger steroids will, therefore, make a trade-off, accepting less overall muscle gain in order to run a more comfortable cycle.
Another way of evaluating the potential ratio of anabolic to androgenic activity is the practice of comparing the relative binding affinity (RBA) of various steroids for the androgen receptor in rat skeletal muscle versus prostate. When we look at the detailed study published in 1984, we see some recognizable (and expected) trends. Aside from dihydrotestosterone and Proviron® (mesterolone), which undergo rapid enzymatic reduction in muscle tissue to inactive metabolites, the remaining anabolic/androgenic steroids seem to bind with near equal affinity to receptors in both tissues. They seem to be relatively “balanced” in effect. This study also discusses the unique activity of testosterone and nandrolone compounds, which are good substrates for the 5a-reductase enzyme found in androgen target tissues (such as the prostate), and seem to provide the most notable variance between anabolic and androgenic effect in humans due to this local metabolism. When it comes to real-world use in humans, anabolic steroids do not always behave in 100% uniformity with their anabolic and androgenic profiles as determined by animal models, so all such figures need to be taken with a small grain of salt.
RBA of various anabolic/androgenic steroids as competitors for human SHBG binding of DHT, and for receptor binding of methyltrienolone in cytosol from rabbit, rat skeletal muscle and prostate. Source: Endocrinology 114(6):2100-06 1984 June, “Relative Binding Affinity of Anabolic-Androgenic Steroids…”, Saartok T; Dahlberg E; Gustafsson JA. 2_A10_Section_I_II-edits3.qxd 11/11/10 10:53 PM Page 19
All anabolic/androgenic steroids are preparations containing one of the above three natural steroid hormones, or chemically altered derivatives thereof. In creating new synthetic compounds, one of the three natural hormones is selected as a starting point, typically due to the possession of particular traits that may be beneficial for the new compound. For instance, of the three natural steroids above, dihydrotestosterone is the only steroid devoid of the possibility of aromatization and 5-alpha reduction. It was likewise a very popular choice in the creation of synthetics that lack estrogenic activity and/or exhibit a more balanced androgenic to anabolic activity ratio. Nandrolone was typically used when even lower androgenic action is desired, due to its weakening upon interaction with the 5-alpha reductase enzyme. Nandrolone also aromatizes much more slowly than testosterone. Testosterone is our most powerful muscle-building hormone, and also exhibits strong androgenic activity due to its conversion to a more potent steroid (dihydrotestosterone) via 5-alpha reductase.
Boldenone is testosterone with an added double-bond between carbon atoms one and two. However, this bond changes the activity of the steroid considerably. First, it dramatically slows aromatization, such that boldenone converts to estradiol at about half the rate of testosterone. Secondly, this bond causes the steroid to be a very poor substrate for the 5-alpha reductase enzyme. The more active 5-alpha reduced metabolite 5alpha-dihydroboldenone is produced only in very small amounts in humans. The hormone instead tends to convert via 5-beta reductase to 5beta-dihydroboldenone (a virtually inactive androgen). This makes it lean towards being an anabolic instead of an androgen, although both traits are still notably apparent with this steroid. The c1-2 double bond also slows the hepatic breakdown of the structure, increasing its resistance to 17-ketosteroid deactivation and its functional half-life and oral bioavailability.
This is the most basic derivative of testosterone, differing only by the added 17- alpha methylation that makes the steroid orally active. Conversion to 17-alpha methylestradiol makes this steroid extremely estrogenic, despite the fact that this alteration actually reduces interaction with the aromatase enzyme.
In many regards, methandrostenolone is very similar to boldenone, as it too exhibits reduced estrogenic and androgenic activity due to the c1-2 double-bond. However, this steroid does have a reputation of being somewhat estrogenic, owing to the fact that it converts to a highly active form of estrogen (17alphamethylestradiol See: Methylated Compounds and Oral Dosing). Methandrostenolone is also much more active milligram for milligram, as the 17-alpha methyl group also gives it a longer half-life and allows it to exist in a more free state than its cousin boldenone.
Fluoxymesterone is a c-17alpha alkylated oral derivative of testosterone. The 11-beta group functions to inhibit aromatization, so there is no estrogen conversion at all with this steroid. It also works to lower the affinity of this steroid toward restrictive serum binding proteins, increasing its relative activity. Introduction of fluorine at the 9-position also potentiates the action of this steroid.
Norethandrolone is simply nandrolone with an added 17-alpha ethyl group. This alteration is rarely used with anabolic/androgenic steroids, and is much more commonly found with synthetic estrogens and progestins. Although 17-ethylation inhibits 17-ketosteroid reduction just as well as 17-methylation, and therefore allows this steroid to exhibit a similarly high level of oral activity, this group also tends to increase progesterone receptor binding. Norethandrolone is clearly a “troublesome” hormone in terms of water retention, fat gain, and gynecomastia, which may in part be due to its heightened binding to this receptor.
Ethylestrenol is an oral derivative of nandrolone, very similar in structure to keto group, which is vital to androgen receptor binding. As such, ethylestrenol is possibly the weakest steroid milligram for milligram ever sold commercially. Any activity this steroid does exhibit is likely from its conversion to norethandrolone, which does seem to occur with some affinity (apparently the 3 oxygen group is metabolically added to this compound without much trouble). This is probably the most interesting trait of ethylestrenol, which is an undistinguished compound otherwise.
Although a derivative of nandrolone, the two additional double-bonds present on trenbolone make any similarities to its parent hormone extremely difficult to see. First, the 9-10 bond inhibits aromatization. Nandrolone is very slowly aromatized, however, some estrogen is still produced from this steroid. Not so with trenbolone. The 11-12 bond additionally increases androgen receptor binding. This steroid also does not undergo 5-alpha reduction like nandrolone, and as such does not share the same dissociation between anabolic and androgenic effects (trenbolone is much more androgenic in comparison).
Mesterolone is a potent orally active derivative of dihydrotestosterone. Similar to methenolone, it possesses a non-toxic 1-methyl group, which increases its resistance to hepatic breakdown. This alteration does not increase the stability of the 3-keto group however, and as such, this steroid is a poor anabolic like its parent.
Drostanolone is simply dihydrotestosterone with an added 2-methyl group. This addition greatly increases the stability of the 3-keto group, vital to androgen binding. As such, the activity of this steroid in muscle tissue is greatly enhanced (see: Anabolic/Androgenic Dissociation).
Oxymetholone is an orally active derivative of dihydrotestosterone. The 17-methyl group is well understood at this point as we have discussed it with many steroids, however, the 2-hydroxymethylene group is not seen on any other commercial steroid. We do know that this group greatly enhances anabolic potency by increasing the stability of the 3-keto group, and that the configuration of this substituent also appears to allow this steroid to bind and activate the estrogen receptor.
Stanozolol is a potent anabolic steroid, owing to the fact that the 3-2 pyrazol group creates a stable configuration off the A-ring that allows for androgen receptor binding (this steroid is one of the few that does not possess an actual 3-keto group). As such, it is highly active in muscle tissue, unlike dihydrotestosterone.
Methenolone also is a potent anabolic steroid, due to the fact that the c1-2 double bond increases the stability of the 3-keto group. The 1-methyl group works to increase its oral bioavailability, making methenolone (as methenolone acetate) one of the few orally active non-17-alkylated orals. The c 1-2 bond may also help increase hepatic resistance (slightly) to 17-ketosteroid deactivation as well.
Oxandrolone is an orally active derivative of dihydrotestosterone, due to its 17-methylation. It also differs from DHT by the substitution of its 2-carbon molecule with oxygen. This is the only commercial steroid to carry this group, and further, the only to have a modification to the base carbon structure of the Steran nucleus. The 2-oxo group increases resistance of the 3-keto group to metabolism considerably, making oxandrolone a potent anabolic.
Perhaps not obvious at first glance, there is a naming convention in place that was used to create identities for the various anabolic/androgenic steroid hormones. This typically involves forming a root word to convey the structural base of the steroid, and signifying other unique structural characteristics by including appropriate prefixes or suffixes. Below, we will look at the common roots, prefixes, and suffixes used in steroid nomenclature, and identify them, as they are used in the various commercial compound names. As you will see, the adoption of names like nandrolone, methandrostenolone, and ethylestrenol were not as arbitrary as one might imagine. This section is also helpful if you wish to understand the deeper chemical designations for the various substances that one might find in the medical literature, which involve the exclusive use of this terminology (such as is the representation of methandrostenolone as 17b-hydroxy-17a-methylandrosta-1, 4-dien-3-one).
For further reading please pick up a copy of ANABOLICS By William Llewellyn