By Vision
www.PuritySourceLabs.ru
There's a cycle concept that has seemed to put back up again and is going around "NANDROLONE DECANOATE" only..
This concept/protocol with Nadrolone "ONLY" is actually NOT old, at all.
Once upon a time in the golden era guys used to run deca and Dbol cycles and or Primo, from that all we really have is only anecdotal evidence. nothing more, aside from a small US military study.
When we peel bac the layers here, truly, there's something inherently estrogenic in nature about nandrolone that can't be mitigated with an AI, only a serm like Tamoxifen.
But, we'll get into that..
At one point in somewhat recent times there was a bunch of guys who are just entrepreneur living in Thailand trying to market themselves.
Some of the content was very entertaining, and some actually had some great findings citing some factiual data, and others - well, experiments are just that now aren't they?
Now let's talk about it!
I admire the approach of some that consider this idea and I do see and recognize the theory, yet I do not like the standpoint on how some are pressuring this protocol down the throats of users, advocating the superiority of it minimizing the importance of testosterone, and completely discrediting testosterone in general and overall health for that matter with no real follow-up protocol..
Now, where I stand on this, with simply just my opinion which means absolutely northing in the grand scheme of thing,
who am I? I'm just a man that admires science and biology especially data that has studies and trials at least with a foundation starting somewhere..
What troubles me most about this protocol, is some who stand behind this "Nandrolone only protocol" on occasions have regurgitated from somewhere
claiming that using test (androgens) is responsible for all or most estrogen??? Laughable..
Genetics, or the aromatases enzymes is not, or higher body fat composition (adipose tissue) isn't to blame ?!?!
How about drugs that can act is estro mimickers?
Last I recall the aromatase enzyme was responsible for this conversion, also lets talk about testosterone converting into DHT (in some users) by way of an enzyme called 5-alpha reductase, yielding DHT far more superior and androgenic as an agonist of the androgen receptor, thus being a chemical messenger that binds to a receptor and activates the receptor to produce a GREATER biological response over NANDROLONE (DHN)..
Testosterone has three courses of action, converting into estro, staying testosterone(it's main course of action) , or converts to DHT..
What does nandolone convert to? Hmmmmm
DHN... What's that?
This is a case to case basis, individual vs individual basis, not a one size fits all way of life.. Same guys stay dry as a bone on 1g of test, and others balloon up on 400mgs..Why is that? Genetics!!!!!
Let's think about this for a moment. Not trying to sound too conservative here, there's a few good reasons why it's not a bright idea. Test/estro ratio issues have been identified and tackled a thousands times over with a better biomedical perspective, compared to this bludgeoning, steadfast ideology, this "theory" has no real staple resource for its information that is collected and put together in the sake of what, because it "could be done, if dialed in correctly"?
That's silly sauce, for a bunch of goofy ganders acting like silly gooses..[/CENTER]
Deca only is not a protocol, it's merely a personal experiment with who's the lucky or "unlucky" bastard to enjoy the fruits of, deca only..
Progesterone blockers do not help against gyno due to nandrolone decanoate (Tamox will and its counter part Raloxifene would be the best targeting drug)
STUDY-
The progesterone blocker RU486 does not help against gynecomastia - in short: gyno - by nandrolone decanoate or other 19-nor-androgens. You can deduce that from some older research by the pharmaceutical company Theramex.
Nandrolone decanoate converts to estradiol five times more difficult than testosterone. We have known this since the 1950s, when one of the researchers drew up the table below based on test tube studies. [1] 19-nor-testosterone is nandrolone.
However, doping gurus know that steroids that are more difficult to convert into estradiol than testosterone, such as deca, can still cause gyno. And they also have an explanation for it. "These drugs sometimes work like progestagens," Nelson Montana writes, for example. [2] "They link to the progesterone receptor, and progesterone increases the breasts of women. It is therefore logical that progesterone-like steroids do the same for men. "
The solution, you would say, is the use of anti-progestagens such as RU486. This is the most powerful progesterone blocker on the market today and attaches so much importance to the progesterone receptor that it completely displaces progesterone. But years ago, Théramex discovered that progesterone blockers cannot prevent gyno due to 19-nor-androgens.
In a study published in 1995, the researchers tested the estrogenic effect of a series of progestagens, and included a set of derivatives of 19-nor-testosterone. Not so long ago [3] they have summarized the results from that research in the table below. The numbers indicate the estrogenic effect of 19-norT = nandrolone and NEL, NGM, LNG, NETA = nandrolone relatives. The table gives the estrogenic effect at two concentrations, and compares it with the estrogenic effect of estradiol. It is automatically set to 100.
As you can see, all androgens within the progestagens have an estrogenic effect. In some of them the effect exceeds that of estradiol. At extremely high concentrations, at least. The above involves tests with cells in a test tube, in which the researchers measured an enzyme that the cells started to produce after stimulating the estrogen receptor.
The researchers wondered what caused this estrogenic effect. [4] Did it have to do with the progesterone effect of the 19-nor drugs? To find out, they repeated the tests, but also put the RU486 progesterone blocker in the test tubes. They did the same with the anti-estrogen 4-hydroxy tamoxifen. The figure below shows what happens with the production of the enzyme. The 19-nor-androgen used was norethindrone.
As you can see, addition of the progesterone blocker did not affect the production of the enzyme. Progesterone activity therefore has nothing to do with the estrogenic effect of 19-nor-androgens. Addition of the anti-estrogen indeed reduced the production of the enzyme does .
The researchers repeated the tests with aminoglutethimide, a substance that is guaranteed to stop all aromatase. That had no effect. The estradiol effect therefore has nothing to do with aromatase.
But what causes the estrogenic effect? The researchers don't know. Not anymore, at least. In their 1995 publication, they suggest that it is caused by unknown metabolites of the androgens. In their more recent publication from 2003, however, they leave open the possibility that 19-nor-androgens can behave themselves as estrogens.
Anyway: the conclusion for athletes is clear. Anti-Prostegans do not help against Gyno by Deca. Antiestrogens such as tamoxifen do.
1. Kenneth Ryan. Biological Aromatization of Steroids. J. Biol. Chem., Feb, 1959; 234: 268 - 272.
2. Nelson Montana. Oh no! It's Gyno! What can you do about it? Testosterone Magazine via T-mag.com, nr 111, 30-6-2000.
2. J. Shields-Botella, I Duc, E. Duranti, F. Puccio, P. Bonnet, R. Delansorne, J. Paris. An overview of nomegestrol acetate selective receptor binding and lack of estrogenic action on hormone-dependent cancer cells. Journal of Steroid Biochemistry & Molecular Biology 87 (2003) 111-122.
3. J. Botella, E. Duranti, V. Viader, I. Duc, R. Delansorne, J. Paris. Lack of Estrogenic Potential or Progesterone-or 19-Nor-progesterone-derived Progestins as Opposed to Testosterone or 19-Nor-testosterone Derivatives on EndometrialIshikawa Cells. Steroid Biochem. Molec. Biol. Full. 55, no. 1, pp. 77-84, 1995.
[CENTER]Testosterone has three courses of action, converting into estro, staying testosterone (it's main course of action) , or converts to DHT..
What does nandolone convert to? Hmmmmm
DHN... What's that?
What people fail to understand is that DHN binds to the same receptor as DHT but very mildly, but once you remove DHT or "test" DHN now takes space in the receptors, and now that we're running nandrolone "ONLY" or no "DHT" derivatives this is were users will suffer from ED (and quite possible feminizing side effects), flooding our system with a synthetic progestin, it will increase prolactin serum levels having direct effects on progesterone receptors, pituitary related issues, etc etc
Further more Nandrolone does in fact covert into estrogen (factual), by way of many, many different courses of action, in ways that medical science has even been mislead and confused about, mistakenly citing that nandrolone doesn't convert into estrogen..[/CENTER]
Below is a read that may explain this subject a bit better, and shed some light on the topic that seems to always come back full circle, all because "they did it in the 70's"..
[CENTER][/CENTER]
Below is a read that may explain this subject a bit better, and shed some light on the topic that seems to always come back full circle, all because "they did it in the 70's"..Cool, and they churned butter in a wooden vat many moons ago, does that mean we still have to manufacture our butter through the same means and method? I high-lighted in red the go-to section to save you same reading time..
They did have a point (sorta), you don't really NEED test, but biologically it would help keep a male healthy and functioning, as intended from creation. These guys are putting more efforts into a theory using a substances that has been synthesized by man, that is also traced in extremely, small amounts in humans, knocking Testosterone out of the picture (which has been there in dominance for Hundreds and thousands of years of evolution) and now all the sudden suggest, naaah, you don't need it??
There's a perfectly good explanation for why test is needed.
Exogenous testosterone is NOT our own, some people will react poorly to it, some having an immune (allergic like) response to certain esters but that's a different topic. Think of exogenous test like its a glove, it fits on your hand, it can move with your hand - like a hand - but it's not your real hand, yet the glove doesn't have a KEY "signature" trait to it, like finger prints.. These fingerprints I speak of is what our OWN natty test has, its an ability to send different chemical messages relaying different responses because its your own natty test. Think of people getting a transplant and a body rejecting it, because it's not theirs, some it can work for, some it will not.
Don't take your bodies bacon or the honey be from nature.. Seriously.. LOL.. What does Vision mean by that?
Keep reading -
My last though on this topic before we get the the best part.. Removing Test is equivalent to removing a Bee from nature.
There's is simply no real upper hand advantage for people to run Nandrolone only at supratherapeutic dosages with shutting themselves down without exogenous T included. If anything a SARMS stack would be the next best thing if someone considered NOT using test, without any other AAS.
IMO I believe we should greatly consider that hormones especially testosterone are "chemical messengers" that rely messages to cells that display specific receptors for each hormone and respond to the signaling.. Depending on the hormones and the individuals metabolization ratio with the hormone they can/may make changes directly to a cell, by changing the genes that are activated, or by making changes indirectly to a cell by stimulating other signaling pathways inside a specific cell group that is effected and effect other processes, this can "initiate" an intracellular cascade of events, hormones/TESTOSTERONE have various biosynthetic pathways and nothing can simulate it or duplicate it, although some are synthesized to try and mimic however they can never play the role that testosterone has. Even at just a replacement dose, your body needs T in order to have proper Homeostasis.. Balances within the system and checks. Now removing something entirely is equivalent to removing a Bee from nature.
You'll see different effects that will vary greatly by individual instances, as genetics, age or even ethnicity (in some cases),
Hormones have various biosynthetic pathways occurring in the endorcrine,
some either or before reaching their target tissue (to control plasma levels or active compounds),
or at times after termination of their actions (inactivation and elimination)..
However, many of hormones are metabolized within their target tissue,
in which a complex interplay between activation and inactivation mechanisms serve to regulate the specificity and the amplitude of the hormonal response..
Always employ T even at a replacement level or slightly lower, while you allow the other compounds to be the horse.
Removing T and using something else in place of, is like throwing some nice crispy bacon in the trash and trying to make some artificial synthetic bacon.. Why??? You love bacon right? well you endocrine loves T... Don't take your bodies bacon.
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Written by Dan Gwartney, MD
Most anabolic steroid (AAS) users are not extreme in their practices. While people find it interesting to discuss the cycles of professional athletes, amazed by the number and amount of drugs used to achieve elite levels of mass and power, the common user tends to plan cycles chosen for convenience and reliability. Though it is often passed over due to its familiarity, the classical cycle for decades was “Deca & D-bol,” referring to nandrolone decanoate and methandrostenolone (Deca-Durabolin and Dianabol). Dan Duchaine (deceased), renowned author of The Underground Steroid Handbook and former AAS guru to many top bodybuilders, once commented that if someone doesn’t grow on Deca and Dianabol, nothing will work.1
Deca and D-bol is considered a near-ideal cycle by many recreational AAS users, as it is convenient, inexpensive, effective and relatively free from side effects. [Note: methandrostenolone is no longer sold under the trade name Dianabol] D-bol (a term used generically to refer to all methandrostenolone products) provides rapid gains in strength and mass, though this is accompanied by a significant increase in body water and side effects (acne, irritability, hair loss) are common with higher dose use. D-bol use by women holds a very high risk of hirsute (masculinizing) side effects, including: facial hair, deepening voice and clitoral hypertrophy. It is also important to note that D-bol is a 17á-alkylated steroid, which means that it can cause liver damage at moderate dosages; rarely, cases of liver tumors, malignant cancers, or blood-filled cysts have been reported, posing serious, even fatal threats to a user’s health.2
Deca (again, a term used generically for many nandrolone products) is very nearly the opposite. It is slow to act, requiring two weeks or longer to generate noticeable gains, but the gains are usually of higher quality even though they are not as pronounced. Deca does not carry as high a risk of androgenic effects in males even though it binds tightly to the androgen receptor. In fact, Deca is actually converted into a less androgenic metabolite by the enzyme 5á-reductase (the enzyme that converts testosterone to DHT and thought to be responsible for hair loss and prostate enlargement). Impotence and loss of libido is infrequently associated with Deca; many AAS users combine Deca with an androgenic AAS such as D-bol to prevent these changes in sexual drive or function. The combination of Deca and D-bol is considered an ideal balance of two complementary drugs by most users.3
One side effect that is not uncommon in many AAS cycles, including the venerable Deca and D-bol cycle is gynecomastia (“bitch tits”).4 Gynecomastia is the growth of breast tissue in a male. This condition is relatively common during puberty and later in life; it is also seen in severe cases of obesity and with the use of certain drug therapies, including: antipsychotics, anti-androgens used during prostate cancer treatment and AAS excess. When gynecomastia occurs during a cycle that includes Deca, the condition is often blamed on other drugs in the cycle, as Deca is commonly believed to be resistant to aromatization. In the case of the prototypical Deca and D-bol cycle, this is reasonable, as one metabolic by-product of methandrostenolone (D-bol) is a potent estrogen, 17á-methylestradiol.2 However, the pristine reputation of nandrolone may be unwarranted and incorrect. Deca is rarely used in one-drug cycles, as it is fairly mild in regard to size or strength gains, particularly in comparison to most other AAS. When used without stacking with other AAS, Deca cycles are generally low to moderate in dose (200mg-600mg/week). It is rare for an adult male to report any significant side effects, with the possible exception of impotence and a reduction in libido (sex drive). This occurs because nandrolone interacts with the androgen receptor and progesterone receptors.5 Progesterone is a female sex hormone, much like estrogen. Many of the steroid-based contraceptives for men being developed within the pharmaceutical industry combine an androgen (such as a long-acting testosterone) along with a progestin.6 While high doses of androgens do lower sperm counts dramatically, to completely shut down sperm production, extremely high concentrations of testosterone are required and the effect is not uniform among all men. Additionally, the concentrations of androgen-only contraception required for effective contraception would result in significant side effects in many people. By combining an androgen and a progestin, researchers have found that fairly consistent contraceptive results can be achieved without introducing significant side effects. As nandrolone is capable of activating both androgen and progestin receptors, it is easy to see how fertility and sex drive could be affected when anabolic (supraphysiologic) doses are used. In fact, natural testosterone production is quickly suppressed and it may take several weeks to months after nandrolone use ends before normal testosterone production is restored. Thus, most experienced AAS users include post-cycle support at the end of a Deca-inclusive cycle, such as hCG and/or Clomid.3
Not only does nandrolone directly interact with androgen and progestin receptors, it also holds the potential of being converted into estradiol (the most potent natural estrogen, commonly a metabolite of testosterone). Herein lies a matter of much confusion. Only recently have the steps involved in the aromatase reaction been defined in sufficient detail to discuss and analyze.7 While testosterone and androstenedione are both natural substrates (starting blocks) for the aromatase reaction, nandrolone is not normally formed in human males in significant amounts.8 In fact, only recently has it been proven that metabolites of nandrolone may be present in athletes absent of the use of anabolic steroids, though again, only trace amounts were produced— below the limits allowed by most drug tests.8 Nandrolone appears to be a very minor by-product of the aromatase reaction that does not accumulate under normal physiologic conditions. Nowhere in the string of reactions involved in classic aromatization is 19-nortestosterone (nandrolone) formed. It is likely that the nandrolone metabolites detected in human males under hCG stimulation represent an overload of the aromatase system with nandrolone being a flawed product, similar to a factory reject.
Confusion prevails regarding the aromatization of nandrolone associated with steroid use. It has been reported by many sources, including respected researchers in prestigious scientific journals, that nandrolone is a non-aromatizable steroid.9 A close examination of related research reveals possible sources for the confusion and provides a concrete answer to the question.
The aromatase reaction is a complex, multi-step pathway involving a number of enzymatic reactions.7 It is present in many different tissue types (brain, ovary, adipose, placenta, etc.) and across many different species (human, horse, pig, etc.).10-13 In fact, even certain bacteria are capable of aromatizing androgens.7 In part, solving the hypothesis regarding any possible interaction of nandrolone with the aromatase reaction has been muddied by studying the enzyme system using vastly different sources. It is known that the aromatase enzyme (cytochrome p450arom) varies greatly. Bacterial aromatase has little similarity to mammalian aromatase. Among animals, there are distinct differences between pigs, horses and man that make translating results from one species to the others difficult.7,10,11,14 Further, it has been shown that even within a single species, there are different promoters (signals that “turn on” enzyme production) in different tissues.12 Conditions that may promote aromatization in the testes are different from those of fat cells.
In mammals, the aromatase reaction involves two separate enzymes that are jointly involved in converting androgens into estrogens.7,12 The first, the hemoprotein CYParom encoded by the CYP19 gene (for those of you who need that kind of information), is the catalyst. It attacks the 19-carbon in two steps and the nearby 1-carbon by oxidizing the androgen molecule at those points. The resulting response and actions of the second enzyme (NADPH-cytochrome P450 reductase) cause the loss of the 19-carbon and the simultaneous generation of a phenolic A-ring (a defining feature of an estrogen). In the absence of a 19-carbon, such as in nandrolone, the reaction would be much less efficient if it was even able to function.
Many medico-scientific journals have noted nandrolone to be a non-aromatizable AAS. Studies using brain cells have shown nandrolone to be more neurotoxic (damaging to nerve cells) because it is not aromatized. It is true that nandrolone is not a candidate for classic aromatization, as the 19-carbon that is missing from nandrolone is the starting point for the entire aromatase reaction. Interestingly, nandrolone stimulates aromatase in rat models, even though it does not participate in the reaction. This would accelerate the conversion of other androgens (testosterone, D-bol, etc).
Yet, the results of a recent study published in the Climacteric prove that nandrolone and other 19-nortestosterone-derived steroids can be converted into estrogenic steroids through a series of enzymatic reactions that take place in the human liver.15 The catalytic (accelerating) first enzyme, CYP 450arom, is not present in the adult human liver, though CYP 450arom is present in certain liver diseases and tumors. However, another enzyme called CYP 450 monooxygenase is able to attack the 2-carbon of the nandrolone and begin the generation of the phenolic A-ring…the definitive step in converting an androgen (or 19-norandrogen in this case) into an estrogen.
Recall that the CYP 450arom played a catalytic role, speeding up the classic aromatase reaction. CYP 450 monooxygenase is much slower and less efficient. This accounts for the comments that nandrolone aromatizes at a rate of 20 percent of testosterone or androstenediol.3 In fact, the rate may be much less. Realizing that Deca is injected intra-muscularly and disperses slowly, and the enzyme system discussed in the Climacteric article was specific to the liver, it is unlikely that standard nandrolone-containing cycles would see a major contribution to feminizing effects from nandrolone being aromatized. However, oral norandrogen-precursors were prominently marketed during the prohormone glory days and an oral norandrogen (7á-methylnortestosterone) is being developed as a potential male contraceptive. It is possible, especially at abusive doses, that such oral norandrogens may elevate estrogen levels sufficiently to cause gynecomastia or other estrogen-related problems. In women provided with oral norandrogens for menopause, researchers speculate that the drugs may hold the potential of increasing estrogen and thus, risk for blood-clotting problems or estrogen-sensitive cancers.15
Nandrolone is considered a relatively safe AAS and has been used extensively by recreational bodybuilders and power athletes. It has rarely been considered to increase the risk of estrogen-related problems, as steroids missing the 19-carbon are not substrates for the classic aromatization reaction. However, in addition to its capacity to stimulate progesterone receptors (a related group of feminizing sex steroid hormones), nandrolone may also increase estrogen levels via a secondary aromatase reaction, promoting the development of gynecomastia and prolonging the delay in restoring natural testosterone production post-cycle. Classic aromatization of testosterone or other androgens may also be accelerated by nandrolone. Oral forms of nandrolone, including prohormones, likely have a much higher estrogenic index and a higher risk of estrogenic side effects due to hepatic (liver) first pass clearance.
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Sponsored by PSL
Vision
TestE/Deca Blend 450
This Blend with Test/deca 450mg has been a highly favored cocktail in the market for years, this mixture has been produced by many compounding competitors for great reason. For one, its highly regarded by many users would wide, delivering a nice dose of testosterone and nandrolone decanoate in 1mL making it extremely convenient to add in just about any cycle. Compared to most traditional single doses of the same hormones all the while needing more oil volume, where this high concentration is used to minimize oil volume by providing convenience for all users. This can fit well with other compounds being used in the same cycle..
This specially compounded formula is designed for serious users. It contains the following ratios totaling 450mg/mL
Testosterone Enanthate 250mg/mL
Nandrolone Decanoate 200mg/mL
This is a very unique blend that can assist with many goals especially encouraging muscle growth and size, or a singular dose for therapeutic purposes such as joint pain relief or cruising/maintaining between blasts.
This blend has always held the reputation as being a great mass builder when combined with dbol or drol. This blend could display estrogenic side effects in some users, therefore the use of AI's, SERMS or prolactin ancillaries may be necessary.to minimize side effects.
