Non-Alkylated Orals

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 350/0. 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. Fasterreleasing 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 levejs 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 DecaDurabolin.

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.

Synthetic AAS Development

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 wasamajor 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.

Brief History ofAnabolic/Androgenic Steroids

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 Sa-reductase enzyme.

Dht Hair Loss Treatments

It is good to note that there are a wide variety of alternatives available to treat DHT hair loss. However, it is advised that we analyze how the entire system works.

Since we are now aware that hair loss is due to hormonal imbalance and how the hormone DHT interacts with androgen, we must also be aware that an itchy and inflamed scalp is another by-product of DHT that should be addressed carefully. Some DHT-caused hair loss incidences may be fought through taking any of the following treatments:

• DHT Inhibitors. This treatment is used to reduce or inhibit the production of DHT and to attack the root cause of hair loss. They are oftentimes called DHT blockers.
• Super Oxide Dismutase Treatment. More specifically known as Immune System Treatment, this helps attack inflamed scalp. As discussed, inflammation of the scalp is caused by too much DHT. If the hair follicle is being attacked by foreign objects, hair loss begins. When the body accepts that hair follicles are foreign objects, then it starts to produce super oxide.
• Growth Stimulators. These promote hair growth but do not actually address the cause of hair loss. These stimulators can only successfully change your appearance in the cosmetic sense. If these stimulators are used in conjunction with other treatments for treating the root cause of hair loss, this may also be an excellent addition to any hair loss regimen.
• Anti-Androgens. This treatment is used to actually reduce or inhibit the level of DHT. The anti-androgen treatment are several steps down the chemical reaction, that leads to hair loss and stop the DHT that binds to the androgen receptors and stops the hair follicle from possible damage.
• Anti-Inflammatory products. When the scalp becomes inflamed, flaky and itchy, it means that the immune system starts to attack the hair follicles. This anti-inflammatory drugs or medicine can help reduce the symptoms of this condition. Treating the symptoms that occur on the scalp can successfully help reduce hair loss.

Natural treatments for DHT hair loss
While the above-mentioned options are readily available elsewhere, you may start preventing DHT outbreak right in your own homes. Self-help is good but this does not mean you have to do medication on your own.

• Coffee. Caffeine basically taken from coffee is a good natural DHT inhibitor. A shampoo which contains such components could address hair follicle growth. Some sprays which contain caffeine are known to suppress hair loss due to aging.
• Scalp massage. We are all aware of how soothing massages could be to the skin. In reality, a scalp massage could also help reduce hair loss. Essential oils should be used daily to massage the area.

There are a wide variety of treatments available for DHT hair loss. Ketoconazole and protein-rich shampoos or copper peptide topical solutions may form the multitude of medications. The most important thing to bear in mind is to seek proper consultation especially when the problem is severe enough for you to contain.
source of info :hairlossdomain.com

DHT Conversion

As we see from our discussion with estrogen, in considering the physiological effects of any steroid, we must look at all c;>f its active metabolites, and not just the initial compound. This includes not only estrogenic products, but androgenic metabolites as well. With this in mind, it is important to note that the potency of testosterone is considerably increased in many androgen responsive tissues when it converts to dihydrotestosterone. More commonly referred to by the three-letter abbreviation DHT, this hormone is, in fact, measured to be approximately three to four times stronger than testosterone. It is the most potent steroid found naturally in the human body, and important to discuss if we are to understand the full activity of testosterone, as well as other anabolic/androgenic steroids that undergo a similar conversion.

Testosterone is converted to dihydrotestosterone upon interaction with the 5-alpha reductase enzyme. More specifically, this enzyme removes the C4-5 double-bond of testosterone by the addition of two hydrogen atoms to its structure (hence the name di-hydro testosterone). The removal of this bond is important, as in this case it creates a steroid that binds to the androgen receptor much more avidly than its parent steroid.5-alpha reductase is present in high amounts in tissues of the prostate, skin, scalp, liver, and various regions of the central nervous system, and as such represents a mechanism for the body to increase the potency of testosterone specifically where strong androgenic action is needed. In these areas of the body little testosterone will actually make its way to the receptor without being converted to dihydrotestosterone, making DHT by far the active form of androgen here.
DHT and Androgenic Side Effects
In some regards this focal potentiation of testosterone's activity may be unwelcome, as higher androgenic activity in certain tissues may produce a number of undesirable side effects. Acne, for example, is often triggered by dihydrotestosterone activity in the sebaceous glands, and the local formation of dihydrotestosterone in the scalp is typically blamed for triggering male pattern hair loss. You should know that it is a terrible misconception among bodybuilders that dihydrotestosterone is an isolated culprit when it comes to these side effects. All anabolic/androgenic steroids exert their activities, both anabolic and androgenic, through the same cellular androgen receptor. Dihydrotestosterone is no different than any other steroid except that it is a more potent activator of this receptor than most, and can be formed locally in certain androgen-sensitive tissues. All steroids can cause androgenic side effects in direct relation to their affinity for this receptor, and DHT has no known unique ability in this regard.

Benefits of DHT
While a lot of attention is being paid to the negative side effects of the androgen dihydrotestosterone, you should know that there are some known benefits to the strong androgenic activity brought about by this hormone as well. For example, DHT plays an important role in the organization and functioning of the central nervous system. Many neural cells contain active androgen receptors, and it is thought that there may even be a specific importance of dihydrotestosterone in this area of the body. Studies have shown DHT to have a profoundly greater impact in these cells compared to testosterone. More specifically, animal models demonstrated that both testosterone and DHT would result in increased androgen receptor proliferation in neural cells three and seven hours after being administered, however only DHT was able to sustain this increase at the twenty-one hour mark.44 Although some might contend that this difference is simply due to DHT forming a more stable and lasting complex with the androgen receptor, others suggest that DHT and testosterone might even be affecting neural cells differently, such that the dihydrotestosterone-receptor complex and testosterone-receptor complex might be activating the transcription of different target genes.
The strong interaction between the central nervous system and skeletal muscles, collectively referred to as the Ineuromuscular system, is of key importance to thel athlete. There appears to be little doubt that the ability of! the body to adapt to training, and to activate nerve: endings in muscle tissue, is reliant on the interactions ofl the neuromuscular system. Inhibiting the formation of! DHT during a testosterone cycle may therefore inadvertently interfere with strength and muscle mass! gains. This would explain why bodybuilders commonlY!1
report a drop in steroid potency when they add the 5, alpha reductase inhibitor finasteride to a testosterone cycle. Many complain strength and even muscle mass gains slow significantly when this medication is added, which would not make sense if testosterone and androgen receptor activation in muscle tissue were solely responsible for growth. Clearly more is involved, and we cannot look at dihydrotestosterone simply as a side-effect hormone.

Anti-Estrogens and the Athlete

So what does this all mean to the bodybuilder looking to gain optimal size? Basically I think it calls for a cautious approach to the use of estrogen maintenance drugs if mass is the key objective (things change, of course, if we are talking about cutting). Obviously, anti-estrogens
should be used if there is a clear need for them due to the onset of estrogenic side effects, or at the very least, the drugs being administered should be substituted for nonestrogenic compounds. Gynecomastia is certainly an unwanted problem for the steroid user, as are noticeable fat mass gains. But if these problems have not presented themselves, the added estrogen due to a cycle of testosterone or Dianabol, for example, might indeed be aiding in the buildup of muscle mass, or keeping you energetic. An individual confident they will notice, or are not prone to getting, estrogenic side effects, may therefore want to hold off using estrogen maintenance drugs so as to achieve the maximum possible gains in tissue mass.

Estrogen Aromatization

Testosterone is the primary substrate used in the male body for the synthesis of estrogen (estradiol), the principal female sex hormone. Although the presence of estrogen may seem quite unusual in men, it is structurally very similar to testosterone. With a slight alteration by the enzyme aromatase, estrogen is produced in the male body. Aromatase activity occurs in various regions of the male body, including adipose, liver, gonadal, central nervous system, and skeletal muscle26 tissues. In the context of the average healthy male, the amount of estrogen produced is generally not very significant to one's body disposition, and may even be beneficial in terms of cholesterol values (See Side Effects: Cardiovascular Disease). However, in larger amounts it does have potential to cause many unwanted effects including water retention, female breast tissue development (gynecomastia), and body fat accumulation. For these reasons, many focus on minimizing the build-up or activity of estrogen in the body with aromatase inhibitors such as Arimidex and Cytadren, or antiestrogens such as Clomid or Nolvadex, particularly at times when gynecomastia is a worry or the athlete is attempting to increase muscle definition.

We must, however, not be led into thinking that estrogen serves no benefit. It is actually a desirable hormone in many regards. Athletes have known for years that estrogenic steroids are the best mass builders, but it is only recently that we are finally coming to understand the underlying mechanisms why. It appears that reasons go beyond the simple size, weight, and strength increases that one would attribute to estrogen-related water retention, with this hormone actually having a direct effect on the process of anabolism. This is manifest through increases in glucose utilization, growth hormone secretion, and androgen receptor proliferation.

Glucose Utilization and Estrogen

Estrogen may playa very important role in the promotion of an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering of the level of available glucose 6-phosphate dehydrogenase, an enzyme directly tied to the use of glucose for muscle tissue growth and recuperation.27 28 More specifically, G6PD is a vital part of the pentose phosphate pathway, which is integral in determining the rate nucleic acids and lipids are to be synthesized in cells for tissue repair. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically, which isbelieved to represent a mechanism for the bo.dy to enhance recovery when needed. Surprisingly, we find that estrogen is directly tied to the level of G6PD that is to be made available to cells in this recovery window.The link between estrogen and G6PD was established in astudy demonstrating levels of this dehydrogenaseenzyme to rise after administration of testosteronepropionate. The investigation further showed that the aromatization of testosterone to estradiol was directly responsible for this increase, and not the androgenic action of this steroid. The non-aromatizable steroids dihydrotestosterone and fluoxymesterone were tested alongside testosterone propionate, but failed to duplicate the effect of testosterone. Furthermore, the positive effect of testosterone propionate was blocked when the aromatase inhibitor 4-hydroxyandrostenedione (formestane) was added, while 17-beta estradiol administration alone caused a similar increase in G6PD to testosterone propionate.The inactive estrogen isomer 17alpha estradiol, which is unable to bind the estrogen receptor, failed to do anything. Further tests using testosterone propionate and the anti-androgen flutamide showed that this drug also did nothing to block the positive action of testosterone, establishing it as an effect independent of the androgen receptor.

Estrogen and GH/IGF·l

Estrogen may also play an important role in the production of growth hormone and IGF-1. IGF-1 (insulin-: like growth factor) is an anabolic hormone released in the liver and various peripheral tissues via the stimulus of growth hormone (See Drug Profiles: Growth Hormone). IGF-1 is responsible for the anabolic activity of growth hormone such as increased nitrogen retention/protein synthesis and cell hyperplasia (proliferation). One of the first studies to bring this issue to our attention looked at I the effects of the anti-estrogen tamoxifen on IGF-1 levels, demonstrating it to have a suppressive effect.30 A second, perhaps more noteworthy, study took place in 1993,

which looked at the effects of testosterone replacement therapy on GH and IGF-1 levels alone, and compared them to the effects of testosterone combined again with tamoxifen.3' When tamoxifen was given, GH and IGF-l levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300 mg of testosterone enanthate weekly to cause a slight IGF-l increase in normal men. Here the 300 mg of testosterone ester caused an elevation of estradiol levels, which would be expected at such a dose. This was compared to the effect of the same dosage of nandrolone decanoate; however, this steroid failed to produce the same increase. This result is quite interesting, especially when we note that estrogen levels were actually lowered32 when this steroid was given. Yet another demonstrated that GH and IGF-l secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-l secretion.

Estrogen and the Androgen Receptor

It has also been demonstrated that estrogen can increase the concentration of androgen receptors in certain tissues. This was shown in studies with rats, which looked at the effects of estrogen on cellular androgen receptors in animals that underwent orchiectomy (removal of testes, often done to diminish endogenous androgen production). According to the study, administration of estrogen resulted in a striking 4800/0 increase in methyltrienolone (a potent oral androgen often used to reference receptor binding in studies) binding in the levator ani muscle.34 The suggested explanation is that estrogen must either be directly stimulating androgen receptor production, or perhaps diminishing the rate of receptor breakdown. Although the growth of the levator ani muscle is commonly used as a reference for the anabolic activity of steroid compounds, it is admittedly a sex organ muscle, and different from skeletal muscle tissue in that it possesses a much higher concentration of androgen receptors. This study, however, did look at the effect of estrogen in fast-twitch skeletal muscle tissues (tibialis anterior and extensor digitorum longus) as well, but did not note the same increase as the levator ani. Although discouraging at first glance, the fact that estrogen can increase androgen receptor binding in any tissue remains an extremely significant finding, especially in light of the fact that we now know androgens to have some positive effects on muscle growth that are mediated outside of muscle tissue.

Estrogen and Fatigue

"Steroid Fatigue" is a common catchphrase these days, and refers to another important function of estrogen in both the male and female body, namely its ability to promote wakefulness and a mentally alert state. Given the common availability of potent third-generation aromatase inhibitors, bodybuilders today are (at times) noticing more extreme estrogen suppression than they had in the past. Often associated with this suppression is fatigue. Under such conditions, the athlete, though on a productive cycle of drugs, may not be able to maximize his or her gains due to an inability to train at full vigor.This effect is sometimes also dubbed "steroid lethargy." The reason is that estrogen plays an important supporting role in the activity of serotonin. Serotonin is one of the body's principle neurotransmitters, vital to mental alertness and the sleep/wake cycle.35 36 Interference with this neurotransmitter is also associated with chronic fatigue syndrome,37 38 so we can see how vital it is to fatigue specifically. Estrogen suppression in menopause has also been associated with fatigue,39 as has the clinical use of newer (more potent) aromatase inhibitors like anastrozole,4o letrozole,41 exemestane,42 and fadrozole43 in some patients. These things may be important to consider when planning your next cycle. Although not everyone notices this problem when estrogen is low, for those that do, a little testosterone or estrogen can go a long way in correcting this. It is also of note that the use of strictly non-aromatizable steroids sometimes causes this effect as well, likely due to the suppression of natural testosterone production (cutting off the main substrate used by the male body to make estrogen).

Introduction to Testosterone

Anabolic steroids are a class of medications that contain a synthetically manufactured form of the hormone testosterone, or a related compound that is derived from (or similar in structure and action to) this hormone. In order to fully grasp how anabolic steroids work, it is, therefore, important to understand the basic functioning of testosterone.

Testosterone is the primary male sex hormone. It is manufactured by the Leydig's cells in the testes at varying amounts throughout a person's life span. The effects of this hormone become most evident during the time of puberty, when an increased output of testosterone will elicit dramatic physiological changes in the male body. This includes the onset of secondary male characteristics such as a deepened voice, body and facial hair growth, increased oil output by the sebaceous glands, development of sexual organs, maturation of sperm, and an increased libido. Indeed the male reproductive system will not function properly if testosterone levels are not significant. All such effects are considered the masculinizing or "androgenic" properties of this hormone.

Increased testosterone production will also cause growth promoting or"anabolic" changes in the body, including an enhanced rate of protein synthesis (leading to muscle accumulation). Testosterone is the reason males carry more muscle mass than women, as the two sexes have vastly contrasting amounts of this hormone. More specifically, the adult male body will manufacture between 2.5 and 11 mg per day' while females only produce about 1/4mg. The dominant sex hormone for women is estrogen, which has a significantly different effect on the body. Among other things, a lower androgen and higher estrogen level will cause women to store more body fat, accumulate less muscle tissue, have a shorter stature, and become more apt to bone weakening with age (osteoporosis).

The actual mechanism in which testosterone elicits these changes is somewhat complex. When free in the blood stream, the testosterone molecule is available to interact with various cells in the body. This includes skeletal muscle cells, as well as skin, scalp, kidney, bone, central nervous system, and prostate tissues. Testosterone binds with a cellular target in order to exert its activity, and will, therefore, effect only those body cells that posses the proper hormone receptor site (specifically the androgen receptor). This process can be likened to a lock and key system, with each receptor (lock) only being activated by a particular type of hormone (key). During this interaction,the testosterone molecule will become bound to the intracellular receptor site (located in the cytosol, not on the membrane surface), forming a new "receptor complex." This complex (hormone + receptor site) will then migrate to the cell's nucleus, where it will attach to a specific section of the cell's DNA, referred to as the hormone response element. This will activate the transcription of specific genes, which in the case of a skeletal muscle cell will ultimately cause (among other things) an increase in the synthesis of the two primary contractile proteins, actin and myosin (muscular growth). Carbohydrate storage in muscle tissue may be increased due to androgen action as well.

Once this messaging process is completed, the complex will be released, and the receptor and hormone will disassociate. Both are then free to migrate back into the cytosol for further activity. The testosterone molecule is also free to diffuse back into circulation to interact with other cells. The entire receptor cycle, including hormone binding, receptor-hormone complex migration, gene transcription and subsequent return to cytosol is a slow process, taking hours, not minutes, to complete. For example, in studies using a single injection of nandrolone, it is measured to be 4 to 6 hours before free androgen receptors migrate back to the cytosol after activation. It is also suggested that this cycle includes the splitting and formation of new androgen receptors once returned to cytosol, a possible explanation for the many observations that androgens are integral in the formation of their own receptor sites.

In the kidneys, this same process works to allow androgens to augment erythropoiesis (red blood cell production).3 It is this effect that leads to an increase in red blood cell concentrations, and possibly increased oxygen transport capacity, during anabolic/androgenic steroid therapy. Many athletes mistakenly assume that oxymetholone and boldenone are unique in this ability, due to specific uses or mentions of this effect in drug literature. In fact, stimulation of erythropoiesis occurs with nearly all anabolic/androgenic steroids, as this effect is simply tied with activation of the androgen receptor in kidney cells. The only real exceptions might be compounds such as dihydrotestosterone and some of its derivatives,4 which are rapidly broken down upon interaction with the 3alpha-hydroxysteroid dehydrogenase enzymes (kidney tissue has a similar enzyme distribution to muscle tissue, see "anabolic/androgenic dissociation" section), and therefore display low activity in these tissues.

Adipose (fat) tissues are also androgen responsive, and here these hormones support the lipolytic (fat mobilizing) capacity of cells.5 This may be accomplished by an androgen-tied regulation of beta-adrenergic receptor concentrations or general cellular activity (through adenylate cyclase).6 We also note that the level of androgens in the body will closely correlate (inversely) with the level of stored body fat. As the level of androgenic hormones drops, typically the deposition of body fat will increase.? Likewise as we enhance the androgen level, body fat may be depleted at a more active rate. The ratio of androgen to estrogen action is in fact most important, as estrogen plays a counter role by acting to increase the storage of body fat in many sites ofaction.8 Likewise, if one wished to lose fat during steroid use, estrogen levels should be kept low. This is clearly evidenced by the fact that non-aromatizing steroids have always been favored by bodybuilders looking to increase the look of definition and muscularity while aromatizing compounds are typically relegated to bulking phases of training due to their tendency to increase body fat storage. Aromatization is discussed in more detail in a following section (see: Estrogen Aromatization).As mentioned, testosterone also elicits androgenic activity, which occurs by its activating receptors in what are considered to be androgen responsive tissues (often through prior conversion to dihydrotestosterone. See: DHT Conversion). This includes the sebaceous glands, which are responsible for the secretion of oils in the skin. As the androgen level rises, so does the release of oils. As oil output increases, so does the chance for pores becoming clogged (we can see why acne is such a common side effect of steroid use). The production of body and facial hair is also linked to androgen receptor activation in skin and scalp tissues. This becomes most noticeable as boys mature into puberty, a period when testosterone levels rise rapidly, and androgen activity begins to stimulate the growth of hair on the body and face. Some time later in life, and with the contribution of a genetic predisposition, androgen activity in the scalp may also help to initiate male-pattern hair loss. It is a misconception that dihydrotestosterone is an isolated culprit in the promotion of hair loss, however; as in actuality it is the general activation of the androgen receptor that is to blame (see: DHT Conversion). The functioning of sex glands and libido are also tied to the activity of androgens, as are numerous other regions 0 the central nervous/neuromuscular system.