It is perhaps the most misunderstood steroid hormone, dihydrotestosterone (DHT). When the average bodybuilder hears those three letters, frantic thoughts of hair loss and exaggerated androgenic side effects usually come to mind. Questions like "does this steroid convert to DHT", or "is it DHT based" similarly arise often in steroid discussion. Although in some instances concerns about DHT conversion may be valid (in a technical sense only testosterone converts to DHT, although several testosterone and nandrolone derivatives do interact with the same enzyme to form new steroids), equating this steroid to a basic evil may in fact be a gross generalization. Indeed there is more to DHT than just side effects. And with the slated release of a DHT prohormone, the question arises: Is dihydrotestosterone the enemy to a happy and healthy cycle, or does it actually serve a purpose to the athlete?
The relation between DHT and Side Effects
Dihydrotestosterone is the most potent androgen found in the human body. It is roughly three to four times stronger an agonist of the androgen receptor than testosterone, and is produced from testosterone (via interaction with the 5-alpha reductase enzyme) in specific target tissues as a way to mediate androgen activity in the body where strong stimulation is needed. This includes areas of the skin, scalp, prostate and central nervous system. It is this process where one sees the obvious correlation between DHT and androgenic side effects; as such tissues are those that appear to be most sensitive in terms of producing such effects. The sebaceous glands responsible for secreting oils for instance are found in areas of the skin, which when over stimulated may cause acne to develop. Hair follicles in the scalp are also sensitive to androgens, and for those with a genetic predisposition, androgens will likely play a role at some point in promoting male pattern hair loss. Prostate tissues are also highly sensitive to androgens, and diseases such as benign prostatic hypertrophy (BPH) and prostate cancer are similarly responsive to androgens.
Clearly the local production of DHT in target tissues is relevant to the incidence of side effects with a drug such as testosterone. That however should not to mislead us into thinking that DHT is an isolated culprit, or that it serves no valuable purpose. Clearly all agonists of the androgen receptor share similar ability to promote androgenic activity in these tissues. If we block the 5-alpha reductase enzyme with an inhibitor for example, testosterone will still be able to activate the androgen receptor. Although testosterone is of course less active than DHT, in a sufficient dosage side effects will still result. A big misconception among athletes is that the use of finasteride, a 5-AR inhibitor, will block any chances for noticing hair loss with testosterone therapy. While it does offer help by means of lowered androgenic activity in the scalp, it is certainly not a cure-all for the balding steroid user.
DHT and the neuromuscular system
It has been suggested that inhibiting the reduction of testosterone to DHT may not always be a good thing in terms of performance enhancement. It seems clear that DHT plays a vital role in the organization and functioning of the central nervous system, effects mediated by androgen receptors in neural cells. The specific importance of DHT in this area is evidenced by studies showing this hormone has a profoundly greater impact in neural cells compared to testosterone. In one such study it was demonstrated that both testosterone and DHT would result in increased androgen receptor proliferation in neural cells at 3 hours and 7 hours post administration, however only DHT sustained this increase at 21 hours. This strong difference lends support to suggestions that DHT and testosterone effect neural cells differently, perhaps such that the dihydrotestosterone-receptor complex and testosterone-receptor complex might even activate the transcription of different target genes. Others maintain that such a difference in effect would only be due to DHT forming a more stable and lasting complex with the androgen receptor, but the vital importance of DHT still remains evident.
The strong interaction between the central nervous system and skeletal muscles may be of key importance to the athlete, as these two areas interact to form what is referred to as the neuromuscular system. Clearly the ability of the body to adapt to training and better call upon nerve endings in muscle tissue is reliant on the functioning of the central nervous/neuromuscular system. Inhibiting the formation of DHT during a testosterone cycle may therefore inadvertently cause less to be achieved in terms of strength and muscle mass gains. We might also take note of the fact that while the anabolic steroid nandrolone is a stronger agonist of the androgen receptor than testosterone, it is much less effective at promoting strength and muscle mass increases in comparison. It seems logical that the loss of DHT (nandrolone actually reduces to a weaker steroid upon interaction with the 5-alpha reductase enzyme) may have something to do with this outcome. What is obvious is that were androgen receptor stimulation in muscle tissue solely responsible for strength and muscle growth, nandrolone would be a more potent drug than testosterone. Yet testosterone compounds remain the primary mass and strength agents among bodybuilders.
DHT and Androgen/Estrogen action on body fat
Androgens and estrogens both play important roles in mediating the disposition of body fat and lean muscle mass. Their respective roles however appear to be very different. While androgens are the primary hormones responsible for muscle growth, they also seem to play a part in promoting fat loss. Results obtained during numerous androgen replacement studies for example strongly support a loss of body fat when androgen levels rise. The specific mechanism involved may be the support of catecholamine-induced lipolysis, caused by the androgen increasing the number of beta-adrenergic receptors (the primary triggers for fat mobilization) on the membrane surface of fat cells, an effect clearly demonstrated in animal models.
On the other hand we see that estrogens may act to promote the storage of body fat, an effect known to be particularly pronounced in men when given supraphysiological doses of estrogens. And as testosterone and several other anabolic steroids readily aromatize (convert to estrogens) in the body, such activity may be important to consider during a steroid cycle. The buildup of estrogens may likewise represent a counter balance during steroid use. In many instances an athlete will report increases in body fat when taking aromatizable compounds for example, presumably due to the buildup and activity of supraphysiological estrogen levels. While the androgenic activity may be promoting fat loss, the countering estrogenic activity may dominate the metabolism and new fat will be deposited.
It is for the purpose of fat loss that a non-aromatizable androgen such as DHT might prove most useful. Since DHT cannot be aromatized, its activity in the body is purely androgenic. As a result a notable shift in androgen/estrogen ratio would result with use, which can prove to be very beneficial in fostering a fat burning metabolism. As the ratio of androgenic to estrogenic action rises, so should the level of fat loss achieved. It is for this reason that many competitive bodybuilders will use non-aromatizable compounds such as stanozolol, methenolone, trenbolone, fluoxymesterone, Proviron (mesterolone; 1-methyl DHT) and Masteron (drostanolone; 2-methyl DHT) exclusively during contest season. Some will go so far as to avoid the milder anabolics nandrolone and boldenone at this point, as even the low amount of estrogen produced from these steroids could be unwanted if an extremely shredded look is desired.
Studies also suggest that DHT acts as an anti-aromatase in the body, further combating estrogenic action and supporting the desired state of metabolism. It is believed that this occurs by DHT having some affinity to interact with the aromatase enzyme, yet due to its structure is incapable of being altered by it (no estrogen is produced). As the enzyme's binding site is temporarily occupied by DHT, other substrates such as testosterone will not be able to bind to it, and an anti-aromatase effect is achieved. It is to this end in which Proviron (mesterolone; 1-methyldihydrotestosterone) is typically utilized by the athlete, although again, this oral DHT preparation is also popular as a non-aromatizable cutting steroid. Some studies suggest that DHT may even interfere with aromatase activity through other, non-competitive means as well.
DHT and free testosterone
In the human body only a very small percentage of testosterone (our primary anabolic hormone) is free at any given time to interact with cellular receptor sites. This is because the vast majority (98%) will form temporary complexes with the plasma binding proteins Sex Hormone Binding Globulin (SHBG) and albumin (the distribution between the two is roughly equal), which prevent the hormone from exerting activity in the body. It is here that dihydrotestosterone differs from testosterone in another important way, in that it binds several times more avidly to SHBG in comparison. In terms of bodybuilding, administration of these two compounds could likewise produce a synergistic effect. As the level of DHT rises in the body, so would the amount of free testosterone, as the former hormone will be out competing the latter for binding to SHGB. This would occur in a dose dependent manner, the greater the ratio of DHT to testosterone the better the effect achieved. This is an excellent, though previously not suggested, use for our oral DHT preparation Proviron, as due to its slightly altered structure it binds even more avidly to SHBG than dihydrotestosterone.
BPH and DHT as an androgen replacement
A common worry among males, particular as we age, is the possible development of prostate diseases. Prostate cancer and benign prostatic hypertrophy for example, are partially androgen dependent conditions that clearly respond to the high presence of DHT in prostate tissues. Initially the reduction of testosterone to DHT was targeted with the drug finasteride in such cases, the intention to minimize androgen action in the prostate and interfere with the progress of the disease. However we find this therapy less that ideal because on one hand testosterone is still capable of maintaining androgen action in the absence of DHT, and on the other we have come to find that both androgens and estrogens play synergistic roles in the induction of BPH. Today estrogen is often targeted in conjunction with the testosterone to DHT reduction when treating this condition. In terms of androgen replacement for an aging male at possible risk for BPH, we find that DHT may even make a better drug of choice over testosterone. Although no form of androgen replacement can be considered safe with a disease responsive to these hormones, due to the non-aromatizable nature, as well as anti-aromatase and estrogen suppressing action of DHT, it may represent a safer alternative to testosterone when such therapy is indicated.
Clearly we should realize that there is a lot more to dihydrotestosterone than just side effects. The formation of this hormone in the human body plays a crucial role in several areas, including sexual functioning, the maintenance and functioning of the central nervous system, and support of bone density and muscle mass. Admittedly DHT is a poor anabolic itself, as it seems to be much more rapidly metabolized to inactive form in muscle tissues compared to testosterone. This is not to say however that its presence in the body serves the athlete no purpose, or that it does not support muscle growth. Indeed inhibiting its formation may have strong consequences in terms of muscle mass and strength gains when undergoing therapy with a testosterone. Unmistakably there are two sides to this androgen, and as users of the oral DHT preparation Proviron typically report, one of them appears to be that of a useful compound in terms of performance enhancement.
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