first cycle 300mgs test/300 mgs deca?side affects

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    Quote Originally Posted by push400 View Post
    I am currently running a deca test cycle and noticed my nips puff up a little. i started taking arimidex which stopped it but theyre still there. im starting my pct of tamoxifen in one week and hoping this will help the situation. this is the firs side ive ever seen and i honestly would not recommend deca. Is tamoxifen the best pct for this cycle?
    Why wouldnt you reccomend deca? Just because YOU expierenced side effects from it? SO if I were to take test and get gyno i shouldnt reccomend it then? Thats the risk we all take, taking AAS... SIDE EFFECTS. Dont bash deca, its a great compound for those who dont abuse it, as with any AAS. Its a awesome bulking compound Deca>Test for mass IMO (If deca was ran alone, but dont do that)

    And if its Deca Induced Gyno, Nolvadex isnt going to do **** for that. U need Caber or Prami.

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    Quote Originally Posted by DetroitHammer View Post
    So until further notice the only way to block nandrolone’s very potent estrogenic effects is to block the androgen receptor, and with it any and all anabolic effect the drug may have.”
    That's inaccurate. Nandrolone has low affinity for the androgen receptor and most of its effects, positive and negative, are through other pathways.

    5a-reduction to Dihydronandrolone yields an enigmatic molecule with even less affinity for the androgen receptor.

    Binding to SHBG (of either) is practically nil.

    The only [well established] significant affinity of the molecule is for the progesterone receptor, and its modulation of that receptor is another matter of debate.

    It seems as though Big Cat is presenting the argument that Nandrolone acts as a partial agonist at the androgen receptor site. It's not an invalid hypothesis, but then the argument could be made that any compound scored lower than 100 on the androgen scale is a partial agonist.

    If estrogenic effects were experienced only when running Nandrolone by itself, it would be a plausible argument, as it would compete with your natural Testosterone and DHT for available receptors. Considering that estrogenic effects appear even in the presence of tremendous amounts of exogenous Testosterone, I must conclude he is mistaken.
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    Quote Originally Posted by KBD View Post
    Thats where ur wrong.

    Deca nor any other AAS suppresses exogenous test.
    I made no such claim.

    In most individuals, 300mg of Testosterone will not be sufficient to maintain libido in the presence of 300mg of Nandrolone. I suggested that Testosterone be proportionally favored, and I stand by it.
    The checks come to my government name, but Chemistry Man is what I'm known as.
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    Quote Originally Posted by Segugio View Post
    I made no such claim.

    In most individuals, 300mg of Testosterone will not be sufficient to maintain libido in the presence of 300mg of Nandrolone. I suggested that Testosterone be proportionally favored, and I stand by it.
    And why is that? Care to explain?

    It would be easy to maintain with prami or caber.
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    His complete text:
    Nandrolone was first made commercially available as a prescription synthetic anabolic by Organon as Deca-Durabolin, a brand of nandrolone decanoate, in 1962. It was almost immediately embraced by the athletic community, and rose to unseen popularity in the late 70’s, a status it maintained through most of the ‘90’s. Since then nandrolone has been distributed in several forms, by several companies, under a multitude of brand names, as demonstrated by the Table above.

    The popularity of nandrolone decreased severely during the nineties, although it remains one of the more popular drugs of choice because many falsely believe it to be a safe drug, or at the very least safer than alternatives. The decrease in popularity was partially the result of the many fakes produced during that time (nandrolone was in a sense becoming a victim of its own popularity) and of course the ban on steroid use and concomitant testing for anabolic androgenic steroids in many athletic federations, as of 1988. Nandrolone has easy to detect metabolites, and with methods for screening becoming more and more sensitive, for many athletes using this drug became an impossibility without risking getting caught and sanctioned.

    Around the same time as the time Organon was researching synthetic nandrolone as a commercial drug, researchers uncovered that nandrolone was also a naturally occurring metabolite in humans. There is still some confusion as to which came first actually, the synthetic nandrolone, or the discovery of natural nandrolone. There is also no clarity about the origin of nandrolone in the human body, although a study by Reznik et al22 using HCG to stimulate steroidogenisis shows a strong correlation between excretion of urinary nandrolone metabolites and the rise in plasma estradiol, the estradiol:testosterone ratio, but not to plasma testosterone. Data that may suggest that nandrolone is a by-product of the aromatization of testosterone to estradiol. At least two of the three proposed mechanisms for the final steps in the aromatization process in a study by Wright and Akhtar28 seem to support this notion if a small portion of the created radicals is not reactive enough to form a double bond, and instead attracts a hydrogen atom, leading to formation of nandrolone instead of estradiol.

    Nandrolone differs in structure from testosterone, the principle natural androgen, only by the omission of the 19th carbon (the methyl group attached to carbon 10), hence the name 19-Nor testosterone.

    Characteristics

    Anabolic Characteristics : Nandrolone is often characterized as being more anabolic than testosterone. This assumption is however usually based on either the binding affinity of nandrolone relative to testosterone at the androgen receptor, and the anabolic:androgenic ratio of the product. Neither of these however can be directly extrapolated to predict the anabolic activity of nandrolone.

    The anabolic:androgenic ratio determines the difference between the increase in weight in a smooth muscle (usually the levator ani) and the increase in weight in an androgen responsive target tissue, namely the ventral prostate. This ratio is meant to indicate the difference of the drugs anabolic activity, relative to its virilizing capabilities, in contrast to that of testosterone, given the arbitrary value of 1:1. It does however not say anything about the absolute ability of a product to increase weight in a striated muscle cell. The anabolic:androgenic ratio of many products can be found in a multitude of ancient studies, but many agree this ratio has lost any and all meaning. Secondly it is worth noting that the anabolic:androgenic ratio of a product can differ strongly with the length of the ester attached to it15,16. Ranging from 7:1 for nandrolone butyrate to 32:1 for nandrolone undecanoate. Given that the ratio can differ for different pharmacokinetic values and that neither value is truly indicative of androgenic potential on the one hand, or muscle-building properties on the other hand, any and all assumptions based on this ratio can be discarded.

    The binding affinity, at first glance, seems to hold more promise. Since in striated muscle both nandrolone and testosterone bind unaltered to the androgen receptor. And nandrolone seems to do so with anywhere from 1 to 2.4 times the affinity of testosterone1,2. Given that number some have stated that nandrolone is up to 2.4 times more anabolic than testosterone. Experience teaches us otherwise. The same study1 seems to shed some extra light on this as it was primarily intended to demonstrate that different patterns of metabolism can influence the anabolic activity of products. But since both steroids bind to the AR unaltered in striated muscle cells one cannot account for a 2.4 time increase by referring to differences in metabolism to estrogens and so on. More likely the answer is to be found in the distinct activation profiles of androgen responsive promoter constructs17. While the study, previously discussed in depth, only shows how different anabolics react differently in activating DNA promoter constructs after binding the AR in a purely theoretical model, there is one thing that can be noted when looking at all three tested constructs. Namely that testosterone is a much more potent activator of most if not all constructs at any given dose. This could explain why testosterone is a much more potent anabolic in vivo than in vitro binding assays may allude to. Given this, one should also question the anabolic properties of a drug based on relative binding affinity comparative to other drugs.

    So is there actual scientific data that can give us exclusion about the exact anabolic nature of nandrolone ? Alas, no. Extensive experience with the drug in bodybuilding circles has given us the chance to estimate the phenotypical anabolic properties of the drug at some 60-70% that of testosterone. So contrary to what you may hear or read from some sources, nandrolone is not a more anabolic drug than testosterone, at least not in muscle. Such claims are all too often based on data that cannot be extrapolated to proper real-life situations.

    Androgenic Characteristics : Nandrolone is often falsely perceived as a ‘safe’ drug because of its low androgenic potential. Whilst again, anabolic:androgenic ratio’s do not accurately reflect the androgenic potential, it is however still a safe bet to classify nandrolone as low androgenic. It is rapidly deactivated by the 5-alpha-reductase enzyme to 5-alpha-dihydronandrolone. 5-alpha-reductase is present in high concentration most androgen responsive tissues like prostate, scalp, skin, genitalia, etc. Dihydronandrolone has 3-4 times less affinity for the androgen receptor than nandrolone2 itself does. This is sharp contrast to what occurs with testosterone under similar conditions. Testosterone is altered to 5-alpha-dihydrotestosterone (DHT) by the same enzyme, and DHT is several times more androgenic than testosterone. Because of the difference between DHT and DHN given the same binding of testosterone and nandrolone in said tissues2 one could easily classify nandrolone as being 10 times less androgenic than testosterone.

    However the relevance of such a figure can be called into question. Under medical conditions this can make a major difference, as it often concerns treating females, children, or the elderly, with pharmaceutically effective doses for the duration of a single cycle, people who are usually more responsive to androgenic side-effects. For a healthy male bodybuilder under the age of 45 the androgenic activity of commonly used steroids in effective doses for muscle building never exceeds acceptable levels.

    Nonetheless, scaremongering by guru’s in the late ‘70’s and early ‘80’s, based on wrongfully extrapolated data from medical settings, has scared most of the bodybuilding community into over-exaggerating the androgenic risk involved with steroid use. This has lead to nandrolone being adopted as the number 1 drug of use/abuse among both competitive and non-competitive athletes from the late 1970’s up until the late ‘90’s. Even after that it remained unseemingly popular with most non-competitive athletes. However as will soon become evident when reading this profile, unlike in most medical settings, nandrolone is everything but a good choice for the bodybuilder.

    Estrogenic/Progestagenic Characteristics : The estrogenic and progestagenic nature of nandrolone have been a topic of much debate over the years. Estrogen-sensitive nandrolone users have always complained about inexplicable estrogen-like symptoms that cannot be treated with conventional anti-estrogen therapies. Because of its more estrogen-like structure due to the lack of a 19th carbon atom, nandrolone shows considerably less affinity than testosterone for the aromatase enzyme that converts androgens to estrogens. Nandrolone has only approximately 1/5th the affinity for aromatase of testosterone in vitro18. There is more than ample evidence to suggest that in vivo this is probably a lot less. As occurs with all steroids that do not readily form estrogen or estrogen metabolites yet somehow seem to display what is perceived as estrogenic characteristics, a multitude of wild and unsubstantiated theories soon sprang up. This has caused and still causes great confusion amongst most steroid users.

    One such theory blamed a feminizing hormone called prolactin. However that theory never really held up since potent androgens tend to decrease prolactin and prolactin sensitivity whereas estrogens seem to increase its activity. There was also no evidence to assume that prolactin played any significant role in the most common of estrogenic side-effects in the absence of estrogen, which would fail to explain why conventional anti-estrogenic therapy did not work with nandrolone use/abuse, given that nandrolone aromatized considerably less and blood profiles of users generally showed low estradiol and estrone levels in the blood after several weeks of use. Fortunately this theory was only shortlived, and only maintained by a few obscure guru’s eager to draw attention to themselves by claiming to have found a solution, where there wasn’t a problem.

    Another theory, that has persisted very long, and remains the most popular belief today was that nandrolone’s progestational activity lay at the base of the perceived estrogenic effects. This theory again held very little ground, but is commonly accepted because it was never thoroughly refuted since the rumour first started circulating. Indeed, nandrolone3 and several of its metabolites4,5 have been identified as being progestins. Meaning they can bind and activate the progesterone receptor. And equally supportive of the theory, studies have demonstrated that progestagenic activity can both stimulate and suppress estrogenic activity6. Whether that holds true for the more common estrogenic side-effects is not really known, but it leant a validity to this theory. However, again, progestins have never been shown to cause estrogenic side-effects in the absence of estrogen. So once again, this did not account for the lack of effect with conventional anti-estrogens.

    A third and last theory that has only been circulating of late is that nandrolone was directly estrogenic, binding and activating the estrogen receptor (ER) without metabolizing. Most likely the rumour initiated after the proposed theory that oxymetholone, another non-aromatizing drug, may me directly estrogenic. It was a theory first proferred by Bill Llewellyn7, and found support with people like myself and organic chemist Patrick Arnold. A dutch pseudo-guru even suggested he had found proof in the fact that studies demonstrated that nandrolone bound the estrogenic receptor8. This infamous study however demonstrated that nandrolone had a more estrogenic effect at the ER than testosterone in millimolar doses. However testosterone is not a potent ER activator, nor are millimolar in vitro doses indicative of what a typical steroid user would have in his blood.

    All of these theories were shot down by two other studies9,10. The first study is not immediately relevant, but that it contained a table with results from an older study, showing the relative estrogenic properties of several progestins, compared to estradiol.




    As you can see from the table above, taken from that study, nandrolone was about 60% as estrogenic in nature as estradiol itself. So far nothing special. All this tells us is that nandrolone has very potent estrogenic action that cannot be explained by aromatization, which is what we already knew. At best this has some shock value by demonstrating just HOW estrogenic it really is. The second study however was undertaken by the same researchers to hopefully shed some light on the situation. It did not. But it disproved all commonly accepted theories supported to date. In the study the researchers administered nandrolone with either an aromatase blocker, a progesterone receptor blocker or an estrogen receptor blocker. As was to be expected the aromatase blocker had no effect whatsoever on the estrogenic activity of nandrolone. More surprisingly, neither did the progesterone receptor blocker. Which also strikes a blow for basically any involvement of progestational activity in the development of common estrogenic side-effects associated with AAS use. And lastly, and even more surprisingly, the estrogen receptor blocker’s effect on the estrogenic activity was just barely significant. This suggests that nandrolone’s direct binding (or that of its metabolites) to the estrogen receptor played a very limited role. At the end of that all we could state was that nandrolone was 60% as estrogenic as estradiol itself, but more than 55% of that could not be explained.

    Yours truly dug a little deeper and actually found the answer in a synthetic nandrolone metabolite, named estren (19-Nor-4-androstene-3α,17β-diol)11. Estren was found to only weakly bind the estrogen receptor, showing no real activity at that site and possessing a 300-fold lower binding affinity. Yet it mimicked the actions of estrogens in osteoblasts. Estren was however shown to be as active as DHT at activating certain androgen receptor related transcripts. The same study also demonstrated that estren was capable of activating estrogen specific constructs in the DNA through the androgen receptor. Estren is a metabolite of nandrolone through the 3α-HSD enzyme. So in first instance one might suggest we start looking for something that blocks this enzyme. However I mentioned that this steroid was synthetic. Nandrolone is a natural androgen. So why does estren not appear naturally in the body ? Well mostly because it is a very labile structure, that is quickly converted back to nandrolone. The problem however is that the researchers noted that despite similar activity on several constructs as DHT, it bound with a 200-fold lower activity to the androgen receptor. The researchers found that the high androgenic potency of estren resulted in its conversion to the more stable molecule nandrolone, almost 50% in 4-6 hours, and no less than 95% within 24 hours. From this it can be concluded that the effects of estren via the AR are mediated by its metabolite nandrolone, and it is in fact nandrolone that activates estrogen specific transcripts via binding and activating the androgen receptor. Now the study also noted that binding of DHT activated estrogen-related transcripts, so this is not uncommon, but DHT did so with a 30 to 100-fold lower potency than estren. The authors concluded :

    “Finally, the unexpected estren-dependent activation(and by extension nandrolone-dependent activation) of ERE-driven gene expression in cells that express AR, which occurs with far greater potency relative to DHT, predicts the possibility of some troublesome feminizing effects in males, which still await examination."

    This is indeed a further blow to nandrolone’s already damaged image as being a safe steroid. As my co-author astutely pointed out, one could potentially treat this problem with the addition of chemicals that block the estrogen response element, such as piperidinediones12. However I’m not aware of any commercial preparations with such products, and finding them may prove difficult. So until further notice the only way to block nandrolone’s very potent estrogenic effects is to block the androgen receptor, and with it any and all anabolic effect the drug may have.

    Water-retention and blood Pressure : Blood pressure is rarely a concern with the use of nandrolone. Monitoring blood pressure continuously through the use of any cycle with anabolic androgenic steroids is of course advisory.

    Water retention with nandrolone is quite frequently noticed. In fact in the past it has often been an excuse for athletes to incorporate nandrolone in their cycles. Nandrolone is reported to increase water in the synovia of joints, and have a ‘lubricating’ effect offering the bodybuilder a more pain and trouble free workout when lifting very heavily. This practice is of course advised against, as is any of the like, because such properties can mask underlying injuries and leave the athlete with severe damage to his person as the result of his heavy lifting. Water retention is often wrongfully associated with estrogen, quite possibly because it is often seen with aromatizing steroids. However several AAS have more direct effects on water retention, such as agonizing aldosterone, as is the case with nandrolone13. The increased activity of aldosterone results in more sodium and conversely more water being retained by the body.

    Therefore it is never advisory to treat water retention, if that is the main problem, with an anti-estrogen. That is the Anabolic steroid equivalent of chasing a mosquito with a bazooka. Especially in the case of nandrolone, where irrelevant of how much of water retention is caused by estrogenic effects, and anti-estrogen would serve no purpose at all. A much better approach is to treat it with products specifically designed for the purpose, such as ACE-inhibitors (Captopril, Capoten) or mild diuretics. One might proffer this is dangerous, but under the care of a physician any and all risk is eliminated. The dangers of these products lay mostly in the acute risk of misusing the products, dangers that are easily circumvented with proper use and supervision. With most anti-estrogens nothing is known about their long term and repetitive use and the effect on our health. So using anti-estrogens as preventive measures in people most likely not suffering estrogenic side-effects, or treating something that is best treated another way, is highly advised against by all health professionals.

    Effects of nandrolone on Immune response : Sex steroids promote very different effects on the immune response, and this may account for the gender difference seen in the prevalence of auto-immune diseases27. This same study indicates there are two main ways of responding to an immune challenge (in reality immunology is a more complicated and intricate interplay of immune cells and their secretion of cytokines), namely a T-helper1 cell response and a T-helper2-cell response (depending on which one predominates). Each establishes a different pro-inflammatory response. Men tend to produce the latter response more often, and women the former. Of note in this case is that women during gestation exhibit a more male response. This is because progesterone, which is the more abundant hormone during gestation, elicits a similar response to testosterone, whereas estradiol seems to be more prone to cause the other reaction.
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    Cont...
    This was pointed out to me by my colleague when reading the comments regarding nandrolone and pain-free workouts (see above) in the first draft of this profile. He had previously theorized that another key element in the observation that nandrolone offers more pain-free workouts could be that it is both androgenic and progestagenic in nature, and therefore strongly promotes one immune response over the other. Now in regard of the more recent discoveries into nandrolone’s estrogenic potential, one might wonder how this theory can still hold up. Well in their study Centrella et al11 did note that the estrogenic transcripts activated by estren (and thus nandrolone) through the androgen receptor were different from those of estradiol. For instance, estren was not capable of stimulating runx2. This leaves the possibility open that nandrolone can cause severe estrogenic side-effects through AR-mediated estrogenic transcription, and still have little or none of estradiol’s effects on immunity.

    Effects of nandrolone on pain and perception thereof : We already touched on this subject twice. Once when we referred to nandrolone’s effect on retention of water in joints, and once when we alluded to a possible different modulation of the immune system by nandrolone in the two paragraphs above. Another rarely looked at fact is that nandrolone is a less potent glucocorticoid antagonist than most other androgens29. Since it is known to bind the glucocorticoid receptor, this theory is often cast aside, since it is believed to have inhibiting effects on the anti-inflammatory response by glucocorticoids. But as Mayer and Rose aptly point out, most androgens bind the glucocorticoid receptor somewhat, and in that list nandrolone is one of the weaker competitors. This would allow more of an anti-inflammatory response than would be the case with most androgens.

    All these factors combined probably lead to a reduced perception of pain in joints when working out. But as pointed out in the paragraph of water retention, a reduced perception of pain does not mean that the underlying injury is gone, and such use of any compound can lead to increased damage in the end. Such practices should be strongly avoided, and an injury should be properly treated by a physician and subjected to rest until it is completely healed.

    Libido : Nandrolone still instills some fear in users when it concerns the dreaded ‘Deca ****’ (Deca stemming from Deca-Durabolin, a popular brand name for nandrolone decanoate), which is the loss of libido, or the ability to maintain an erection as the result of nandrolone use. Most studies using clinically acceptable doses (50-200 mg/ week) showed no diminished libido in test subjects19,20. So quite likely the problem only occurs in higher doses of nandrolone, which for many reasons cited here, are definitely not recommended for the health-conscious athlete. Because no studies have clearly documented a loss of libido, probably due to the use of much lower doses, there is also no real explanation for the loss of libido. The problem is however easily countered by the addition of a product that boosts libido, such as testosterone, androstanolone or several DHT-derivatives.

    Detection of metabolites : Nandrolone fell of its pedestal during the 90’s as the drug of choice for all athletes. As of 1988 the use of anabolic androgenic steroids was outlawed by most athletic federations, and nandrolone was a rather easy to discover substance of abuse. With increasing sensitivity of detection and more positive cases being uncovered, the use of nandrolone, and later AAS in general, in professional and semi-professional sports cleared the way for less detectable, but alas often more dangerous drugs.

    Nandrolone is usually synthetized with long-acting esters that have a long half-life and remain detectable for a very long time. On top of that nandrolone readily reesterifies, leaving trace amounts of the drug in the body for much longer than the normal clearance time. Another problem is that nandrolone shows considerably less affinity for sex-hormone binding globulin26. SHBG is needed for transport and clearance of steroids. And last but not least, a study by Baume et al23 showed that in some test subjects receiving an orally ingested dose of 25 mg of unesterified nandrolone sometimes allowed for the detection of nandrolone metabolites in concentrations higher than 100 micrograms per liter AFTER 5 DAYS. To compare, the cut-off for doping tests is a mere 2 micrograms per liter, and normal excretion rates of norandrosterone (the principle detected urinary metabolite) in non steroid users have never exceeded 0.7 micrograms per liter in any of the literature I found. Imagine then how long a large, intramuscularly injected esterified dose would remain detectable for. The current sensitivity claims detection 18-24 months after last use, depending on person and dose.

    Supression of natural androgens and maintenance of mass : As can be easily deducted from all the data gathered up to this point, nandrolone is particularly suppressive of one’s own natural testosterone levels. With 60% the estrogenic activity compared to estradiol itself, being a powerful androgen, having progestational activity, the long half-life of its most common esters and the long stay of nandrolone metabolites in the body one could easily state that out of the more well-known anabolic androgenic steroids, nandrolone is by far the most suppressive of the Hypothalamic-pituitary gonadal axis. This not only poses a problem with recovery of natural endocrine response after use of nandrolone, but also with respect to maintaining whatever mass was gained.

    Prolonged periods of low natural testosterone in the period that nandrolone levels drop, but one in a hypogonadale situation that is ill suited for the maintenance of muscle mass. That makes it extremely difficult for users to maintain their gained mass. More often than not the user will however blame the fact that most of his weight was water, and that he lost little or no real mass.

    Fat Gain : A lot of drugs with considerable estrogenic activity are often accused of causing fat gain in athletes. This is however simply flawed perception. During a cycle such drugs often cause mild water retention, and smoothing out, leaving a user thinking he is less defined and possibly gaining fat. For this reason such drugs are often used in mass cycles, when a high amount of calories is used as well. The high amount of calories however can increase adipose tissue weight during that period, leaving the user fatter than he was. Not willing to admit to less than perfect diet habits, it is then easy to blame it on the product used.

    With nandrolone however fat gain is a possibility. The theory behind fat gain from estrogenic drugs is oftens substantiated by pointing out that women have a higher body-fat percentage than men. But as my esteemed co-author once noted in a previous article, the culprit for increased gluteofemoral fat in women was found to be progesterone24,25.

    Since nandrolone and several of its metabolites are known progestins3,4,5 the risk is therefore somewhat greater that it may exert a direct influence on adipose gain.

    Pharmacokinetic information

    I know most readers were probably hoping for absolute pharmacokinetic answers, such as definitive half-life times and such. I know data like that often makes for heavy discussions on web-boards and in many a gym, with regards to the stability of blood levels and the frequency of injection, but sadly I have to disappoint you. Minto et al21 demonstrated that the pharmacokinetics of nandrolone (and by extension probably most esterified steroids) esters will vary greatly depending on variables such as site and depth of injection, pH, osmolarity of the solution, vehicle used, amount of vehicle used and type of ester. In their study they also compared four 100 mg injections. Nandrolone phenylpropionate in 4 ml of oil injected in the gluteus (NP), Nandrolone decanoate in 4 ml of oil injected in the gluteus (NDG), Nandrolone decanoate in 1 ml of oil in the gluteus (ND1) and nandrolone decanoate in 4 ml of oil, injected in the deltoid (NDD). Between esters (NP vs NDG) the researchers noted that despite a similar yield of free nandrolone from either ester (see table above), that half-life was considerably lower for NP (2.4 days as opposed to 7.0 days for decanoate). Between injections in 1 or 4 ml of vehicle (ND1 vs NDG) there was no significant difference in half-life time but a small increase in peak concentration in the lower volume. And finally between injections in the glute or the deltoid, researchers determined that retention in the deltoid, and thus half-life, was greater with injection in the deltoid.

    What we can determine from this is that for every preparation, person and injection site, pharmacokinetics of a nandrolone injection can vary a great deal. Since most commonly used nandrolone injections are usually in higher concentrations, and thus relatively lower depots, we can always expect a faster release time and half-life for higher concentrations of drug. Given the results obtained with nandrolone decanoate in this study that means that likely half-life will be similar, around 7 days. Suggesting a single weekly dose is sufficient, but also needed. Among bodybuilders it is often the question wether or not to inject more often. This data corroborates the belief that more than one injection weekly is certainly not needed. In clinical settings it is often the practice to inject less often, and as this data shows, if the aim is to maintain stable blood levels, bi-weekly, or tri-weekly injections (as is common practice) will simply not do.

    The data also speak in favour of nandrolone decanoate over nandrolone phenylpropionate if a choice has to be made among these two most found forms of nandrolone. The phenylpropionate, despite a similar or greater lipophillicity, and similar molecular weight, has a much shorter half-life and calls for more frequent injections. Peak concentrations were much higher, and both time to peak and clearance time were significantly higher as well, suggesting a notably faster release for phenylpropionate.

    Discussion

    It should be obvious that nandrolone should not be the first choice for most athletes. Given its unpredictable and hard to treat estrogenic effects it should definitely be avoided by people who have reason to believe they are very sensitive to estrogenic side-effects, and if used, low doses are advisable.

    For some people nandrolone may still hold benefits. Older men fearing problems with their prostate, and especially women (though I highly advise against women using anabolic androgenic steroids) might find the low virilizing effect of nandrolone an attractive feature. Though best avoided, if this drug is to be used, some precautions and preventive measures can be taken to ensure minimal problems.

    First of all one should use it in a low dose and stacked with some form of testosterone. The low dose as well as the additional testosterone will avoid problems with libido. Adding a small amount of testosterone to mimic natural testosterone levels is also a good move in regard to general health. In longer stacks, nandrolone use is best discontinued some 2 weeks before other products are stopped. This in order to clear the bulk of the nandrolone and its metabolites by the end of the cycle, which will help maintain mass and hasten recovery of natural testosterone production. Avoid using it with other drugs that are estrogenic in nature, such as methandrostenolone and oxymetholone as this can highly increase the chance of estrogenic side-effects, that might possibly be quite hard to treat. Avoid using this drug during periods when maintaining a lean physique is of crucial importance, as there is the possibility that nandrolone may increase fat gain or hinder fat loss. And lastly, avoid nandrolone like the plague if you are a tested athlete.
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    Last paragraph...
    As was evident from the work done by Minto and his colleagues21 it is best to opt for nandrolone decanoate over nandrolone phenypropionate, and to inject it in the glute. In the study this correlated with a 7-day half-life time, and single weekly injections would then be favoured. I also personally favour the decanoate version over the other versions, since all the others with the exception of cypionate are longer acting esters, which may compound some of the problems described with endogenous testosterone suppression and maintenance of mass.
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    Quote Originally Posted by KBD View Post
    And why is that? Care to explain?

    It would be easy to maintain with prami or caber.
    It would be. I was not aware that he was in possession of a Dopamine Agonist, or that he had any interest in using one.
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    Quote Originally Posted by Segugio View Post
    It would be. I was not aware that he was in possession of a Dopamine Agonist, or that he had any interest in using one.
    Even without one he would be fine.

    Testosterone isnt a anti-prolactin.

    So if your taking 400mg of deca and 600mg of test compared to 250mg of test, libido would still be affected by prolactin regardless of the test dose.

    But nandrolones and other AAS cannot suppress exogenous test.

    If your suffering libido issues on deca/tren you need a anti-prolactin. Doubling the test dose will just raise estrogen levels more. And high estrogen and high prolactin arent friendly on your sex drive at all.

    Me and a couple other buddies can take tren and have a higher libido than we do on test. But in others it kills sex drive because of prolactin, not because of a testosterone dose.

    The reason i come to believe tren raises sex drive is its extremely high androgenic ratio.

    Deca raises prolactin with a very LOW androgenic ratio. Hence why deca **** could be worse than tren ****.
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    "The anabolic:androgenic ratio of many products can be found in a multitude of ancient studies, but many agree this ratio has lost any and all meaning. Secondly it is worth noting that the anabolic:androgenic ratio of a product can differ strongly with the length of the ester attached to it15,16."

    Do you have a link to his citations (15, 16)? I am extremely curious as to where this information was derived.
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    Quote Originally Posted by Segugio View Post
    "The anabolic:androgenic ratio of many products can be found in a multitude of ancient studies, but many agree this ratio has lost any and all meaning. Secondly it is worth noting that the anabolic:androgenic ratio of a product can differ strongly with the length of the ester attached to it15,16."

    Do you have a link to his citations (15, 16)? I am extremely curious as to where this information was derived.
    Did i post up an androgenic ratio? No, but anyone whos taken tren will vouch it is MUCH MORE androgenic than testosterone and if you have taken tren and dont notice that, then your tren is bunk. Androgens tend to make me very vascular hard, sex drive extremely high and aggressive and oily ass skin.

    Ive seen the Anabolic Androgenic Ratio list, while i may not believe those numbers are EXACT. I do know Tren is the highest ****in androgenic steroid ive ever taken.
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    Quote Originally Posted by KBD View Post
    Even without one he would be fine.

    Testosterone isnt a anti-prolactin.

    So if your taking 400mg of deca and 600mg of test compared to 250mg of test, libido would still be affected by prolactin regardless of the test dose.

    But nandrolones and other AAS cannot suppress exogenous test.

    If your suffering libido issues on deca/tren you need a anti-prolactin. Doubling the test dose will just raise estrogen levels more. And high estrogen and high prolactin arent friendly on your sex drive at all.

    Me and a couple other buddies can take tren and have a higher libido than we do on test. But in others it kills sex drive because of prolactin, not because of a testosterone dose.

    The reason i come to believe tren raises sex drive is its extremely high androgenic ratio.

    Deca raises prolactin with a very LOW androgenic ratio. Hence why deca **** could be worse than tren ****.
    I'm not at all in disagreement. Controlling prolactin is far more effective than increasing androgens. I just did not see any indication that he was in possession of either Pramipexole or Cabergoline.

    If your ingredients are Test and Deca, the best you can do is increase the amount of the stronger androgen. I was under the impression that he had only those two items.
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    Quote Originally Posted by Segugio View Post
    I'm not at all in disagreement. Controlling prolactin is far more effective than increasing androgens. I just did not see any indication that he was in possession of either Pramipexole or Cabergoline.

    If your ingredients are Test and Deca, the best you can do is increase the amount of the stronger androgen. I was under the impression that he had only those two items.
    Idk if he has them or not, but why are you believing increasing the androgen will solve the problem?
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    Quote Originally Posted by KBD View Post
    Idk if he has them or not, but why are you believing increasing the androgen will solve the problem?
    It doesn't "solve" anything. I said it was an action favorable to libido, given that those are the only two compounds he possesses.

    If everything acted through a single consistent mechanism, there would be no need to research. Androgens increase libido through pathways that do not involve prolactin.

    Just because a Dopamine Agonist increases libido doesn't mean that it is some sort of antidote to Nandrolone, or that it has any effect on the estrogenic expression of said compound.

    One could just as easily claim that Nandrolone increases PDE5 expression, because Cialis works, or that it decreases Melanocortin expression, because Bremelanotide works. They're all completely unrelated (as far as today's science knows). There is a more substantial relationship between Androgens, Estrogens, and Prolactin, but it is still not a clean cut cause-and-effect.
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    Quote Originally Posted by Segugio View Post
    It doesn't "solve" anything. I said it was an action favorable to libido, given that those are the only two compounds he possesses.

    If everything acted through a single consistent mechanism, there would be no need to research. Androgens increase libido through pathways that do not involve prolactin.

    Just because a Dopamine Agonist increases libido doesn't mean that it is some sort of antidote to Nandrolone, or that it has any effect on the estrogenic expression of said compound.

    One could just as easily claim that Nandrolone increases PDE5 expression, because Cialis works, or that it decreases Melanocortin expression, because Bremelanotide works. They're all completely unrelated (as far as today's science knows). There is a more substantial relationship between Androgens, Estrogens, and Prolactin, but it is still not a clean cut cause-and-effect.
    I agree with what your saying, but to be honest i dont notice a difference between 300mg and 600mg of test when it comes to libido. actually, the higher my test is, the lower my libido gets due to high estrogen, i believe a good dose of deca/tren(400mg a week) with a trt dose of test (250mg) a week, is enough to maintain sex drive. Not arguin brotha, just learnin.. just learnin
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    How much nolva would you take per day for pct ?
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    Hi guys, I am 34 and just stared my first cycle 3 weeks ago. I take 250 deca and 250 testogel every week for 10 weeks. I just stared feeling the sensitiveness in my nipples and my right side kind of felt sore today so it freaked me out a little bit. I have nolva in hand and just ordered liquidex and letro, they should be here in couple of days. My question is am i taking the right dose of deca and test? Is it normal to feel sensitive in the early stage of cycle? If it is the initiation of gyno, which route to take? Is it ok to take nolva during cycle or just take A.i or letro during and keep the nolva for pct? Am i too late for A.i or letro? I guess i m prone to gyno Please help!!!...Thanks...
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    Provided it's from the test an AI should suffice. Armidex or aromasin are the popular ones but letro will kill it faster than the others. If it's from the deca (progesterone related) you'll need caber or prami. There is one other thing that it could be from and that is a raise in estren levels and as far as I know the only thing that can reverse estren related gyno is cessation of use from deca. More than likely tho at 250mg deca it shouldn't be a problem and it'll be from the test. Trial and error is how you'll find out for sure tho
  

  
 

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