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08/12/2018 1:05 pm
Yes but MT is far more androgenic than estrogenic. If the action of one compound is MORE estrogenic than androgenic/anabolic it should not be classified as an AAS. Even if MT is more estrogenic than T, given to a woman its action will be androgenic/anabolic/anti-e.
Androgenic and anabolic aren't necessarily associated.
It is also a hard statement to call it like that, given that you can't quantify when a product is more estrogenic than androgenic. A product like tamoxifen will be, compared to estrogen, less estrogenic and more androgenic, despite no androgenic effects and an anti-estrogenic effect, even in men. Yet no one will classify it as an androgen.
In my humble opinion, we are talking about terminology we can't properly classify.
Your statement was that is something is anabolic, androgenic, and a steroid, it is automatically anti-estrogenic ... , but estrogen itself has been demonstrated, in the strictest sense of the word, to be all three, and estradiol is not an anti-estrogen ....
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
08/12/2018 1:39 pm
Androgenic and anabolic aren't necessarily associated.
In an AAS they are.
Because the term AAS only design a category of steroids, not all, called T analogs or derivatives. To be an AAS the compounds must have good similarities with T in their chemical structures and to exhibit androgenic and anabolic properties. That's mean 3 criteria.
And because in lot of tissues (but not all) androgenic action counterbalance estrogenic action, they are all in some extent anti-e.
08/12/2018 2:36 pm
[B]In an AAS they are.
Not at all, or we wouldn't have a need to have anabolic:androgenic dissociation values if anabolism and androgenic activity were highly correlated. In AAS we see both androgenic effects and anabolic effects, or they wouldn't be called AAS, but androgenism and anabolism aren't always associated.
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Because the term AAS only design a category of steroids, not all, called T analogs or derivatives. To be an AAS the compounds must have good similarities with T in their chemical structures and to exhibit androgenic and anabolic properties. That's mean 3 criteria.
And because in lot of tissues (but not all) androgenic action counterbalance estrogenic action, they are all in some extent anti-e.
The first criterium is not a necessity. In fact many estrogens and progestins show far more likeness with Testosterone than some AAS, like fluoxymesterone or formebolone for instance.
If it is a steroid, and posseses anabolic and androgenic characteristics, it is an AAS. In the truest sense of the word. If you wish to attach other criteria to that for your own use that is fine, but it will draw a very difficult line to follow with some compounds, like for example that Methoxy-TRN stuff. It is by all rights a progestin, but it shows moderate androgenic activity and is sold as an anabolic substance.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
08/12/2018 3:07 pm
Not at all, or we wouldn't have a need to have anabolic:androgenic dissociation values if anabolism and androgenic activity were highly correlated. In AAS we see both androgenic effects and anabolic effects, or they wouldn't be called AAS, but androgenism and anabolism aren't always associated.
But in AAS they are ...
The first criterium is not a necessity. In fact many estrogens and progestins show far more likeness with testosterone than some AAS, like fluoxymesterone or formebolone for instance.
Depending of which progestins you speak about, but some are 19-nor derivatives. I think to compare we must remember that the principal characteristics of androgens are the 3=O and 17-OH groups.
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If it is a steroid, and posseses anabolic and androgenic characteristics, it is an AAS. In the truest sense of the word. If you wish to attach other criteria to that for your own use that is fine
Not only me, I quote and translate from my school book AAS are synthetic analogues of the male hormone "testosterone" with anabolic and androgenic effects.
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but it will draw a very difficult line to follow with some compounds, like for example that Methoxy-TRN stuff. It is by all rights a progestin, but it shows moderate androgenic activity and is sold as an anabolic substance.
And will you class it in the AAS family ?
08/12/2018 3:42 pm
I have used many compounds and I have to say Mestanolone is my fav. Its the best cutting agent I have used because I believe that it is in some respects anti estrogenic. I believe this because the only time I can reduce my estrogenic fat stores such as on the back of my delts and tris and love handles is when I am running this compound.
08/12/2018 4:43 pm
[B]But in AAS they are ...
No they are not. If they were associated, we wouldn't need A:A dissociation constants. You do understand what association and dissociation means right ? And you do know they are contradictory ?
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Depending of which progestins you speak about, but some are 19-nor derivatives. I think to compare we must remember that the principal characteristics of androgens are the 3=O and 17-OH groups.
Why ? Several SARMS don't even have a steroidal structure. What about Stanozolol ? DMT ? androstenedione ? Quinbolone ? You see, you are messing with an imaginary line. You can make up as many criteria as you like, but they are all arbitrary. The only thing absolute about Anabolic androgenic steroids is that they are :
Anabolic
Androgenic
Steroids
And like I said, the difference between testosterone and estradiol is a lot smaller than the difference between testosterone and some AAS.
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Not only me, I quote and translate from my school book AAS are synthetic analogues of the male hormone "testosterone" with anabolic and androgenic effects.
Sure, and if you look at another book or study, they will describe it in another way. As I just said, its an arbitrary line which criteria you choose to apply. But in the broad sense of the word there are only 3 criteria that are unique to AAS in all definitions : Anabolic, Androgenic, steroids.
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And will you class it in the AAS family ?
I don't, some do. But you see, for me, my definition of AAS includes that they are substances with possible use for increasing muscle mass. A criterium also not shared by everyone.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
08/12/2018 5:37 pm
No they are not. If they were associated, we wouldn't need A:A dissociation constants. You do understand what association and dissociation means right ? And you do know they are contradictory ?
But they are associated. No T derivative is a pure anabolic agent. We speak about two (at least in a certain extent) AR-mediated effects.
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Why ? Several SARMS don't even have a steroidal structure.
SARM are not AAS.
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What about stanozolol ? DMT ? androstenedione ? Quinbolone ? You see, you are messing with an imaginary line. You can make up as many criteria as you like, but they are all arbitrary.
I was absolutely sure, you will answer this And yes some AAS lack them. But stanozolol remain a DHT derivative.
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The only thing absolute about Anabolic androgenic steroids is that they are :
Anabolic
Androgenic
Steroids
Yes I can agree. The thing is that they are in fact T derivatives ...
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And like I said, the difference between testosterone and estradiol is a lot smaller than the difference between testosterone and some AAS.
I disagree. All chemical modifications are not equal. You must not only compute the number of structural alterations. Because its aromatic A-ring, E2 is a very different compound that its precursor (T), it exerts its action via a different receptor.
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Sure, and if you look at another book or study, they will describe it in another way.
I agree, but just to say that it is not only mine definition. But the definition of many authors.
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As I just said, its an arbitrary line which criteria you choose to apply. But in the broad sense of the word there are only 3 criteria that are unique to AAS in all definitions : Anabolic, Androgenic, steroids.
Ok.
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I don't, some do. But you see, for me, my definition of AAS includes that they are substances with possible use for increasing muscle mass. A criterium also not shared by everyone. [/B]
Anabolic by itself does not mean possible use for increasing muscle mass ?
08/12/2018 6:10 pm
[B]But they are associated. No T derivative is a pure anabolic agent. We speak about two (at least in a certain extent) AR-mediated effects.
It is perfectly possible for 1 receptor to mediate different pathways, with different co-factors. In fact most receptors do act this way, which is why it is possible for 2 ligands to mediate different effects. This is also the case for AAS.
No T derivative is a pure anabolic agent, but the fact that they all have both anabolic and androgenic effects (or they wouldn't be AAS would they ?) doesn't mean they are in any way associated. In fact I will repeat for the fourth time, they are DISSOCIATED. That was the whole point of the AAS development boom in the 60's and 70's : The DISSOCIATION of anabolic and androgenic effects. The fact that they have both, and both are mediated by the same receptor doesnot mea, they are "associated".
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SARM are not AAS.
Not all SARMS are AAS, but some AAS are SARMS. In fact, nandrolone is the typical SARM, as it mediates tissue specific effects where it causes less effect in androgenic target tissues, and more effect in muscle for a given dose.
The reason the latest wave of SARMS are not AAS is simply because they do not fit the third criterium : they are not steroids.
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I was absolutely sure, you will answer this And yes some AAS lack them. But stanozolol remain a DHT derivative.
Of course it is. It was you who said that to be an AAS it had to have a 3-keto and a 17b-hydroxy group, not me. I say that to be an AAS it has to be
Anabolic
Androgenic
Steroid
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Yes I can agree. The thing is that they are in fact T derivatives ...
So is estradiol. It is derived from testosterone. In fact it is more literarally derived from testosterone, since this conversion occurs in vivo as well.
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I disagree. All chemical modifications are not equal. You must not only compute the number of structural alterations. Because its aromatic A-ring, E2 is a very different compound that its precursor (T), it exerts its action via a different receptor.
I contest that because of its pyrazol ring, stanozolol is a very different compound from testosterone.
I also contest that progesterone is very similar in structure to testosterone and exerts its effect via a different receptor as well, same for cortisol.
I contest that 19-Nor-4,9-androstadiene-3-one-17b-ol is IN FACT a stronger progestin than progesterone, and a much weaker androgen than testosterone, this despite the fact that is classified in all sources as an AAS and structurally not even you can denie it since it is one double bond removed from both nandrolone and trenbolone,both typical AAS.
So your whole argument holds no ground.
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I agree, but just to say that it is not only mine definition. But the definition of many authors.
Correction, the "arbitrary" definition of "some" authors.
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Anabolic by itself does not mean possible use for increasing muscle mass ?
Most definitely not. Look up the definition of anabolic, you will find it has nothing to do with muscles.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
08/12/2018 7:08 pm
No T derivative is a pure anabolic agent, but the fact that they all have both anabolic and androgenic effects (or they wouldn't be AAS would they ?) doesn't mean they are in any way associated. In fact I will repeat for the fourth time, they are DISSOCIATED. That was the whole point of the AAS development boom in the 60's and 70's : The DISSOCIATION of anabolic and androgenic effects. The fact that they have both, and both are mediated by the same receptor does not mean, they are "associated".
And ... this development has been a failure, because they are in fact associated. Anabolism and androgenicty are not in fact very different, both refers to tissue's growth. If it is the male genital apparatus, we say androgenicty, if it is skeletal muscles, we say anabolism ...
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Not all SARMS are AAS, but some AAS are SARMS. In fact, nandrolone is the typical SARM, as it mediates tissue specific effects where it causes less effect in androgenic target tissues, and more effect in muscle for a given dose.
No it is not true, nandrolone is not a SARM. The term selective androgen receptor modulators describes a group of pharmaceuticals that function as androgen receptor agonists in some tissues but that oppose androgen action in others. It causes less effect in androgenic target tissues because its 5-a reduced metabolite is less potent. Give nandrolone with a potent 5-a reductase inhibitor or to a guy with 5-a reductace deficiency and the things will be different. The compound by itself is not a selective androgen receptor modulator. For example with a true selective receptor modulator (ER) like raloxifene I can obtain estrogenic effect in bone tissues and anti-estrogenic effects in breast tissues. With nandrolone you will have both androgenic effects on the seminal vesicles (for example) and the skeletal muscles.
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The reason the latest wave of SARMS are not AAS is simply because they do not fit the third criterium : they are not steroids.
True. (but remenber we speak about AAS)
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Of course it is. It was you who said that to be an AAS it had to have a 3-keto and a 17b-hydroxy group, not me.
Yes sometimes a chemical structure modification can play the role of another ...
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I say that to be an AAS it has to be
Anabolic
Androgenic
Steroid
Yes ... but in my opinion not enough. Because many compounds never classified as AAS could come in this definition. I think we must refer to the main activity of the compound.
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So is estradiol. It is derived from testosterone. In fact it is more literarally derived from testosterone, since this conversion occurs in vivo as well.
Yes we all know that. And you can say the same thing for all the natural steroids because they are all derivatives from the others. Because the aromatisation of the A-ring, estrogens have a different target receptor ... it is not the case of the others T derivatives refered as AAS. We must distinguish between small and big chemical structure modifications.
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I contest that because of its pyrazol ring, stanozolol is a very different compound from testosterone.
Please quote references because despite my biochemistry education, I do not really see a so huge difference between stanozolol and DHT despite the additionnal pyrazol ring to replace and act as the 3 keto-group.
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I also contest that progesterone is very similar in structure to testosterone and exerts its effect via a different receptor as well, same for cortisol.
well, that's mean that they are in fact very different ... to say if a compound is very similar or not, it is not just a draw. Again we must distinguish between minor and strong chemical structural modifications.
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I contest that 19-Nor-4,9-androstadiene-3-one-17b-ol is IN FACT a stronger progestin than progesterone, and a much weaker androgen than testosterone, this despite the fact that is classified in all sources as an AAS and structurally not even you can denie it since it is one double bond removed from both nandrolone and trenbolone,both typical AAS.
All modifications have to be taken into account, maybe we could have not well estimate this one ...
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Correction, the "arbitrary" definition of "some" authors.
Absolutely. But like I have said before, not "just me".
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Most definitely not. Look up the definition of anabolic, you will find it has nothing to do with muscles.
Here again each author seems to have its own definition for anabolism ...
08/12/2018 8:01 pm
And ... this development has been a failure, because they are in fact associated. Anabolism and androgenicty are not in fact very different, both refers to tissue's growth. If it is the male genital apparatus, we say androgenicty, if it is skeletal muscles, we say anabolism ...
Not really, androgenic effects are much wider than that, they comprise some anabolic events, like in prostate for instance, but also remoddeling (virilizing), supporting proper reproductive function and much more. Likewise, anabolism by AAS is mostly mediated by the AR, but the effects the AR elicits can also be elicited by other compounds and/or effects.
And the development was not a failure, we now have a whole arsenal of drugs that are less androgenic than anabolic. Which is the whole point. They are dissociated, or you wouldn't have AAS, you would just have weaker versions of testosterone if they weren't dissociated ...
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No it is not true, nandrolone is not a SARM. The term selective androgen receptor modulators describes a group of pharmaceuticals that function as androgen receptor agonists in some tissues but that oppose androgen action in others.
We know that definition to no longer be exactly true. SRM's of all categories have been shown to be agonistic above a certain threshold, they are in fact agonists, but because of selective recruitment of co-factors they repress the action of stronger acting products with a lower RBA. Which is a good argument for our RBA debate as well, since SRM's invariably are agonists, and have a higher RBA than natural ligands, yet exert considerably less activity.
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It causes less effect in androgenic target tissues because its 5-a reduced metabolite is less potent. Give nandrolone with a potent 5-a reductase inhibitor or to a guy with 5-a reductace deficiency and the things will be different. The compound by itself is not a selective androgen receptor modulator. For example with a true selective receptor modulator (ER) like raloxifene I can obtain estrogenic effect in bone tissues and anti-estrogenic effects in breast tissues.
Anti-estrogenic opposite estradiol. It is in fact still a very weak agonist. Same story for DHN opposite DHT.
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True. (but remenber we speak about AAS)
That was my point
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Yes sometimes a chemical structure modification can play the role of another ...
Indeed, as you need to take into account chemical as well as spatial factors of the groups. Which is why there are no strict structural demands attached to the definition of AAS, except that it has to be a steroid ...
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Yes ... but in my opinion not enough. Because many compounds never classified as AAS could come in this definition. I think we must refer to the main activity of the compound.
Yes, but that is your opinion
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Yes we all know that. And you can say the same thing for all the natural steroids because they are all derivatives from the others. Because the aromatisation of the A-ring, estrogens have a different target receptor ... it is not the case of the others T derivatives refered as AAS. We must distinguish between small and big chemical structure modifications.
Well, let's see, if I add a 2-carboxaldehyde group, an 11alpha-hydroxy group, and a 1,2 double bond, you are saying that is a smaller modification than the reactive splitting of the C-19 off of the androgen androstenediol ?
Or are you suggesting that small structure modifications means they are no androgens, but with big modifications they are androgens ?
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Please quote references because despite my biochemistry education, I do not really see a so huge difference between stanozolol and DHT despite the additionnal pyrazol ring to replace and act as the 3 keto-group.
Why do you need a reference ? Surely you can see that the modification made to obtain stanozolol is bigger and more profound than the modification to obtain estradiol ? A small child can see that when comparing both structures ...
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well, that's mean that they are in fact very different ... to say if a compound is very similar or not, it is not just a draw. Again we must distinguish between minor and strong chemical structural modifications.
Don't roll your eyes at me ! that was my point !
Progesterone, estradiol, cortisol = minor chemical and structural modification
Many AAS = string chemical and structural modification
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All modifications have to be taken into account, maybe we could have not well estimate this one ...
That IS the ONLY modification. It has one extra double bond than nandrolone, one less than trenbolone.
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Absolutely. But like I have said before, not "just me".
Well if I publish a textbook that says AAS are candy, and somebody says its candy, refers to my book and says "not just me that's saying it", then it is still arbitrary ...
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Here again each author seems to have its own definition for anabolism ...
No you will find that the definition of anabolism generally means the consumption of energy to build protein.
Metabolism, anabolism and catabolism are fairly well defined terms.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
08/12/2018 8:40 pm
Not really, androgenic effects are much wider than that, they comprise some anabolic events, like in prostate for instance, but also remoddeling (virilizing), supporting proper reproductive function and much more. Likewise, anabolism by AAS is mostly mediated by the AR, but the effects the AR elicits can also be elicited by other compounds and/or effects.
Never said the contrary. But because AAS are AR agonists, and because both anabolism and androgenicity are at least in some extent AR-mediated effects, the two effects are linked.
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And the development was not a failure, we now have a whole arsenal of drugs that are less androgenic than anabolic. Which is the whole point. They are dissociated, or you wouldn't have AAS, you would just have weaker versions of testosterone if they weren't dissociated ...
Again in the opinion of many authors it is. We have searched for a pure anabolic compound and never find it. Because AAS effects are AR-mediated, they will act and promote AR-mediated effects in all tissues were these receptors are present. No T derivative is both anabolic and free of androgenicity.
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We know that definition to no longer be exactly true. SRM's of all categories have been shown to be agonistic above a certain threshold, they are in fact agonists, but because of selective recruitment of co-factors they repress the action of stronger acting products with a lower RBA. Which is a good argument for our RBA debate as well, since SRM's invariably are agonists, and have a higher RBA than natural ligands, yet exert considerably less activity.
Your answer mean you have not understood my reasonning in our previous debate. I have nerver said that RBA alone was always the relevant information to compare compounds. But like you in your "Superdrol writeup", I suggest that it is sometimes the good point to compare two AAS.
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Anti-estrogenic opposite estradiol. It is in fact still a very weak agonist. Same story for DHN opposite DHT.
Good point. But nandrolone is able to promote virilization in women, raloxifene is not able to promote feminization in men. Raloxifene can be used as a SRM to elicit a specific answer and not another, for example to prevent osteoporosis without breast stimulation, nandrolone cannot. With the use of nandrolone you must accept both anabolic and androgenic effects.
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Indeed, as you need to take into account chemical as well as spatial factors of the groups.
Absolutely, and that was my statement.
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Which is why there are no strict structural demands attached to the definition of AAS, except that it has to be a steroid ...
Yes you can replace the 3-keto and 17-OH groups by other chemical modifications able to act as and to make the steroid a potent AR-agonist.
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Well, let's see, if I add a 2-carboxaldehyde group, an 11alpha-hydroxy group, and a 1,2 double bond, you are saying that is a smaller modification than the reactive splitting of the C-19 off of the androgen androstenediol ?
In terms of biological activity it is.
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Or are you suggesting that small structure modifications means they are no androgens, but with big modifications they are androgens ?
No. I mean that all modifications are not equal in term of biological activity repercussions. More chemical modifications can lead to less biological differences in activity. We must take into spirit each steroid receptor specific requirements.
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Why do you need a reference ? Surely you can see that the modification made to obtain stanozolol is bigger and more profound than the modification to obtain estradiol ? A small child can see that when comparing both structures ...
No sorry to add a methyl group in the 17-a position and to replace the 3 keto-group by an additionnal pyrazole ring is in fact a less profound modification than the modifications to make estradiol from T, because these modifications are the requirement to bind to a different receptor.
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Progesterone, estradiol, cortisol = minor chemical and structural modification
Many AAS = string chemical and structural modification
I think we have not the same definition to say what is a minor or major structural modification ...
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That IS the ONLY modification. It has one extra double bond than nandrolone, one less than trenbolone.
If its main action is to act as a progestin, it must be classified as a progestin and not as an AAS.
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Well if I publish a textbook that says AAS are candy, and somebody says its candy, refers to my book and says "not just me that's saying it", then it is still arbitrary ...
Let's return to the earth, we are internet contributors, not scientific researchers or renowned scientific authors. To refer to university books and authors/teachers is not to refer to unreliable datas.
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No you will find that the definition of anabolism generally means the consumption of energy to build protein.
Metabolism, anabolism and catabolism are fairly well defined terms.
Anabolism is often refered to the constructive metabolism. It is not a very informative definition. And more important are the method retained to estimate anabolism.
08/12/2018 9:16 pm
[B]Never said the contrary. But because AAS are AR agonists, and because both anabolism and androgenicity are at least in some extent AR-mediated effects, the two effects are linked.
To some extent, definitely.
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Again in the opinion of many authors it is. We have searched for a pure anabolic compound and never find it. Because AAS effects are AR-mediated, they will act and promote AR-mediated effects in all tissues were these receptors are present. No T derivative is both anabolic and free of androgenicity.
The fact that there never was a 100% dissociation does not make the development a failure. The fact that we have dissociation to such an extent means greater anabolic efficacy attached to the same risk compared to testosterone. That is a medical breakthrough no matter how you look at it.
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Your answer mean you have not understood my reasonning in our previous debate. I have nerver said that RBA alone was always the relevant information to compare compounds. But like you in your "Superdrol writeup", I suggest that it is sometimes the good point to compare two AAS.
One of the points, yes
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Good point. But nandrolone is able to promote virilization in women, raloxifene is not able to promote feminization in men. Raloxifene can be used as a SRM to elicit a specific answer and not another, for example to prevent osteoporosis without breast stimulation, nandrolone cannot. With the use of nandrolone you must accept both anabolic and androgenic effects.
But nandrolone can be dosed so that the androgenic effects are weaker than test, and the anabolic effects greater. Granted, the dissociation is not as great as with SERMS of course, but its only a matter of quantity of effect.
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Yes you can replace the 3-keto and 17-OH groups by other chemical modifications able to act as and to make the steroid a potent AR-agonist.
Possibly other elements activating different functions resulting in similar conformations could do so as well, not necessarily replacing functions. On top of that, the ones that do act replacing have a wide variety, as even estradiol is a potential AR agonist.
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In terms of biological activity it is.
Then the 4,9,11 double bond structure of trenbolone is much more significant as it drastically increases affinity for all 5 classical nuclear receptors ....
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No. I mean that all modifications are not equal in term of biological activity repercussions. More chemical modifications can lead to less biological differences in activity. We must take into spirit each steroid receptor specific requirements.
If you are going to rank each steroid by which receptor it stimulates most, so you can classify estradiol differently, then you would have to classify a lot of AAS as progestins primarily, more than as AAS. So again, you are importing very arbitrary definitions.
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No sorry to add a methyl group in the 17-a position and to replace the 3 keto-group by an additionnal pyrazole ring is in fact a less profound modification than the modifications to make estradiol from T, because these modifications are the requirement to bind to a different receptor.
Then the modification of adding a 9-double bond is far more profound, since it increases progesterone binding to a much larger degree than an aromatic A-ring does affinity for the ER ...
For every example you try to give to prove your point I do have a counter-example showing the exact opposite. This demonstrates my point that any additional criteria are very arbitrary. The only true criteria are that they anabolic, androgenic and a steroid.
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I think we have not the same definition to say what is a minor or major structural modification ...
I doubt we do. My definition of major structural modification has two criteria. It ha to be MAJOR and it has to be STRUCTURAL. Major, being opposed to minor, in a comparison, indicates the greater change. Structural means difference in structure from the starting compound. hence the major structural modification is that which differs most in structure from the original ...
What is you definition ?
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If its main action is to act as a progestin, it must be classified as a progestin and not as an AAS.
Ok, according to ojasoo and raynaud, 4,9,11-triene steroids are more progestagenic than androgenic, does that make trenbolone a progestin as well ?
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Let's return to the earth, we are internet contributors, not scientific researchers or renowned scientific authors. To refer to university books and authors/teachers is not to refer to unreliable datas.
No, but it is arbitrary. It is based on personal criteria and does not hold any value as an absolute reference in any case. That was my point. I'm sure 95% of what is in that book is very reliable and absolute data. Their definition of AAS, however is not, since it is uncontestedly different in other publications.
And for the record, I am a scientific researcher ...
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Anabolism is often refered to the constructive metabolism. It is not a very informative definition. And more important are the method retained to estimate anabolism.
True enough, but that just confirms my stance that anabolism is not related to muscle growth per se.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
08/12/2018 10:00 pm
But nandrolone can be dosed so that the androgenic effects are weaker than test, and the anabolic effects greater. Granted, the dissociation is not as great as with SERMS of course, but its only a matter of quantity of effect.
It sounds like nandrolone could be more anabolic than T ...
Yes its a matter of quantity of effect but it is a very important point, with a SRM you can achieve a specific goal and only it. AAS are different, when you use them you must accept both androgenic and anabolic effects. So you cannot assimilate AAS to SARM.
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Possibly other elements activating different functions resulting in similar conformations could do so as well, not necessarily replacing functions. On top of that, the ones that do act replacing have a wide variety, as even estradiol is a potential AR agonist.
Steroids are often potential agonists of different steroid's receptors. But we must take care about real in-vivo agonistic activity.
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Then the 4,9,11 double bond structure of trenbolone is much more significant as it drastically increases affinity for all 5 classical nuclear receptors ....
Again which is its receptor of predilection ?
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If you are going to rank each steroid by which receptor it stimulates most, so you can classify estradiol differently, then you would have to classify a lot of AAS as progestins primarily, more than as AAS. So again, you are importing very arbitrary definitions.
Give examples please.
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Then the modification of adding a 9-double bond is far more profound, since it increases progesterone binding to a much larger degree than an aromatic A-ring does affinity for the ER ...
I disagree. Trenbolone is a very potent AR agonist, even if it has also PR affinity, E2 is not only T with an aromatic A-ring and it is only a virtually AR agonist and in the other hand a potent ER agonist.
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For every example you try to give to prove your point I do have a counter-example showing the exact opposite. This demonstrates my point that any additional criteria are very arbitrary. The only true criteria are that they anabolic, androgenic and a steroid.
Maybe you can but here your counter-examples are not very pertinent in my opinion.
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I doubt we do. My definition of major structural modification has two criteria. It ha to be MAJOR and it has to be STRUCTURAL. Major, being opposed to minor, in a comparison, indicates the greater change. Structural means difference in structure from the starting compound. hence the major structural modification is that which differs most in structure from the original ...
What is you definition ?
I mean that you cannot only count the number of structural modifications and say if compounds are good analogs or not. Some structural modifications are really more important than others.
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Ok, according to ojasoo and raynaud, 4,9,11-triene steroids are more progestagenic than androgenic, does that make trenbolone a progestin as well ?
Please quote because I do not remember to have read something like that. I'm pretty sure that trenbolone is far more androgenic than progestogenic.
08/12/2018 10:31 pm
[B]It sounds like nandrolone could be more anabolic than T ...
Yes its a matter of quantity of effect but it is a very important point, with a SRM you can achieve a specific goal and only it. AAS are different, when you use them you must accept both androgenic and anabolic effects. So you cannot assimilate AAS to SARM.
Nandrolone can be dosed such that it is more anabolic and still less androgenic than test, this does not imply a difference in strength mg for mg.
And yes you can assimilate AAS to SARMs, just because it is far cruder than the current line of SERMS, does not mean it is not so. If the goal is to achieve a reduction in androgenic effect for the prostate opposite the normal environment, while maintaining same level of anabolism, nandrolone can be dosed as such to do that. its no different from what tamoxifen does, though tamoxifens estrogenic effect is even weaker in some tissues than the effect of DHN. That being the only difference. In the end, the result for both is a reduction in specific activity in some tissues opposite normal, while maintaining specific activity in others.
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Steroids are often potential agonists of different steroid's receptors. But we must take care about real in-vivo agonistic activity.
The in vivo agonist activity has often not been determined, its only now becoming apparent that ligands previously thought not to be in vivo effectors are in fact effectors in some tissues.
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Again which is its receptor of predilection ?
Progesterone receptor
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Give examples please.
Look over the list of androgens (designated with the letter B) in the study i sent you by ojasoo and raynaud, and look how many are more potent agonists of another receptor than the AR ...
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I disagree. Trenbolone is a very potent AR agonist, even if it has also PR affinity, E2 is not only T with an aromatic A-ring and it is only a virtually AR agonist and in the other hand a potent ER agonist.
The passage you quoted didn't mention trenbolone, though I believe trenbolone is also a more potent PR agonist. It made reference to 19-nor-4,9-androstadiene-3-one,17b-ol, which is actually A LOT more progestagenic than androgenic.
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Maybe you can but here your counter-examples are not very pertinent in my opinion.
That's because you refuse to see them, even though I'm offering examples by standards you set. Which is rather ridiculous, since you keep making up criteria, and I keep showing you examples that don't match your criteria and then you just call them not pertinent. That's a tad hypocritical in my opinion.
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I mean that you cannot only count the number of structural modifications and say if compounds are good analogs or not. Some structural modifications are really more important than others.
No they are not. You are they one that says an aromatic A-ring is most important. Why ? Several 11b-modified estrogens show more affinity for other receptors than for the ER. Its no more important than any other modification. You are the one that keeps talking about profound structural and chemical changes, while i've show you that drugs with far more profound structural and chemical changes do in fact belong to the same class. Your criteria hold no ground, and your argument is as leaky as a poorly fastened diaper.
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Please quote because I do not remember to have read something like that. I'm pretty sure that trenbolone is far more androgenic than progestogenic.
I sent you both studies, one of them has a nice little graph showing relative affinity of 4,9,11-trienes ...
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
08/12/2018 11:23 pm
If the goal is to achieve a reduction in androgenic effect for the prostate opposite the normal environment, while maintaining same level of anabolism, nandrolone can be dosed as such to do that. [...] That being the only difference. In the end, the result for both is a reduction in specific activity in some tissues opposite normal, while maintaining specific activity in others.
tamoxifen can be used by a woman with a breast cancer history, its even the treatment of choice, you cannot say the same thing with nandrolone in a man with prostate cancer.
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Progesterone receptor
Trenbolone binds 3 times more strongly to the AR than T and in the other hand it binds half that progesterone does to the PR. But you are true, trenbolone is not a very selective compound. If we look at the in-vivo biological effects of the compounds, its main activity is to act as T, I mean androgenic/anabolic activity.
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Look over the list of androgens (designated with the letter B) in the study i sent you by ojasoo and raynaud, and look how many are more potent agonists of another receptor than the AR ...
Yes, but remember that the introduction of a third double bond (4,9,11 trienes) displaces the compound toward AR.
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The passage you quoted didn't mention trenbolone, though I believe trenbolone is also a more potent PR agonist. It made reference to 19-nor-4,9-androstadiene-3-one,17b-ol, which is actually A LOT more progestagenic than androgenic.
Trenbolone is a potent PR agonist, but its a very potent AR agonist too.
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No they are not. You are they one that says an aromatic A-ring is most important. Why ?
Quoted from the study : only steroids without an aromatic A-ring are located firmly within the AR zone.
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Several 11b-modified estrogens show more affinity for other receptors than for the ER. Its no more important than any other modification. You are the one that keeps talking about profound structural and chemical changes, while i've show you that drugs with far more profound structural and chemical changes do in fact belong to the same class. Your criteria hold no ground, and your argument is as leaky as a poorly fastened diaper.
You can turn it over and over but actually, AAS are steroids derivatived from the natural androgen T with androgenic and anabolic properties and in some extent because the opposite action of the androgenic to estrogenic activity in many (but not all) tissues : they are anti-estrogenic too. That what I say that they are anti-e "by nature".
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I sent you both studies, one of them has a nice little graph showing relative affinity of 4,9,11-trienes ...
Yes and we can see that 4,9,11-trienes are not very specific compounds ... something else ?