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28/09/2018 1:00 pm
Most likely it is due to its affinity for the progesterone receptor, which gives it progestin like effects on the body. That would include a higher rate of negative feedback inhibition on test production.
28/09/2018 1:50 pm
Also, Often forgotten is that test is usually cyp or enth, whereas deca is decanoate, so longer time in the body, and deca does have the peculiar quality of re-esterifying quite easily.
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.
28/09/2018 2:25 pm
and deca does have the peculiar quality of re-esterifying quite easily.
Really? That is quite interesting actually.
28/09/2018 3:24 pm
The problem with deca, tren, THG and Anadrol is that they all raise prolactin levels, it's the increase in prolactin that causes the problems. Deca has affinity for the prolactin receptor so does progesterone. Deca, Tren, THg and anadrol also greatly lower cortisol which further increases prolactin.
liftsiron is a fictional character and should be taken as such.
28/09/2018 4:02 pm
The problem with deca, tren, THG and anadrol is that they all raise prolactin levels, it's the increase in prolactin that causes the problems. Deca has affinity for the prolactin receptor so does progesterone. Deca, Tren, THg and anadrol also greatly lower cortisol which further increases prolactin.
Not sure with anadrol (oxymetholone).
I assume that the 4-ene-double bound is needed to enhance progestogenic activity. Metabolites like DHN have very low to no progestogenic activity.
The AR affinity is another point of interest. Because 19-Nor can bind very strongly to the AR.
So : progestogenic activity + great AR affinity + long ester chain ...
Research about male contraception use a 19-Nor derived called MENT (7 alpha-methyl-19-nortestosterone).
28/09/2018 4:52 pm
Great stuff MENT, personally feel its even better than tren, but almost impossible to get a hold of. Wonder why ? It's under full examination for several uses, and its not that difficult to make (compared to some other more available steroids).
You are right on the anadrol by the way, it has less progestagenic binding than even testosterone, and likely the same holds true for prolactin.
Liftsiron, bro, you really need to get with the times on this stuff and start reading studies instead of outdated websites and 1980's steroid manuals. Actually, though, I think the study that shows drol has no progestagenic affinity is like really old as well, you'd have to check my steroid profiles.
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.
28/09/2018 5:31 pm
Well BC, bro explain why Anadrol has caused more cases of GALACTORRHEA than even deca or tren in the real world. Anadrol can and does cause both progestrone gyno (galactorrhea) as well as estrogen gyno. I believe than anadrol while not a true progestin like deca, Tren And THG, may work by another mechanism to induce both estrogen and progesterone side effects. Also anadrol gyno is not appropiately treated by nolva alone, in most cases it will continue to proliferate. Proper treatment of gyno from anadrol includes bromo or another similiar anti-prolactin, as well as a strong anti-e. Studies are cool, but don't always apply. As for your profiles, I have read most of the profiles attributed to you, enough said there.
liftsiron is a fictional character and should be taken as such.
28/09/2018 6:28 pm
I believe than anadrol while not a true progestin like deca, tren and THG, may work by another mechanism to induce both estrogen and progesterone side effects.
Maybe by influencing before dopamine levels :
Increased dopaminergic and 5-hydroxytryptaminergic activities in male rat brain following long-term treatment with anabolic androgenic steroids.
Thiblin I, Finn A, Ross SB, Stenfors C.
Department of Forensic Medicine, Karolinska Institute, Stockholm, Sweden.
1. The effects of treating groups of rats with four different anabolic androgenic steroids (AAS) (testosterone, nandrolone, methandrostenolone, and oxymetholone) on 5-hydroxytryptamine (5-HT) and dopamine (DA) neurones in different brain regions were examined. The AAS was injected six times with 1 week's interval and the rats were sacrificed 2 days after the final injection. 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured. The effect on DA and 5-HT synthesis rate was analysed as the accumulation of 3,4-dihydroxyphenyl-alanine (DOPA) and 5-hydroxytryptophan (5-HTP), respectively, after inhibition of the amino acid decarboxylase with NSD-1015 (3-hydroxy-benzylhydrazine dihydrochloride). Additionally, the monoamine oxidase (MAO) activity was analysed in the hypothalamus. 2. The DOPAC + HVA/DA ratio was increased in the striatum in all treatment groups. However, the synthesis rate of DA was significantly increased only in the methandrostenolone treated group. 3. The 5-HIAA/5-HT ratio was increased in all treatment groups in the hippocampus, in the frontal cortex in the methandrostenolone-treated animals and in the hypothalamus in the testosterone- and oxymetholone-treated rats, while the 5-HT synthesis rate was not affected by the AAS-treatments. 4. The MAO-A activity was increased in the oxymetholone-treated rats while the other treatment groups were unaffected. The MAO-B activity was not changed. 5. The results indicate that relatively high doses of AAS increase dopaminergic and 5-hydroxytryptaminergic metabolism in male rat brain, probably due to enhanced turnover in these monaminergic systems.
28/09/2018 7:28 pm
Maybe by enhancing before dopamine levels :Increased dopaminergic and 5-hydroxytryptaminergic activities in male rat brain following long-term treatment with anabolic androgenic steroids.
Thiblin I, Finn A, Ross SB, Stenfors C.
Department of Forensic Medicine, Karolinska Institute, Stockholm, Sweden.
1. The effects of treating groups of rats with four different anabolic androgenic steroids (AAS) (testosterone, nandrolone, methandrostenolone, and oxymetholone) on 5-hydroxytryptamine (5-HT) and dopamine (DA) neurones in different brain regions were examined. The AAS was injected six times with 1 week's interval and the rats were sacrificed 2 days after the final injection. 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured. The effect on DA and 5-HT synthesis rate was analysed as the accumulation of 3,4-dihydroxyphenyl-alanine (DOPA) and 5-hydroxytryptophan (5-HTP), respectively, after inhibition of the amino acid decarboxylase with NSD-1015 (3-hydroxy-benzylhydrazine dihydrochloride). Additionally, the monoamine oxidase (MAO) activity was analysed in the hypothalamus. 2. The DOPAC + HVA/DA ratio was increased in the striatum in all treatment groups. However, the synthesis rate of DA was significantly increased only in the methandrostenolone treated group. 3. The 5-HIAA/5-HT ratio was increased in all treatment groups in the hippocampus, in the frontal cortex in the methandrostenolone-treated animals and in the hypothalamus in the testosterone- and oxymetholone-treated rats, while the 5-HT synthesis rate was not affected by the AAS-treatments. 4. The MAO-A activity was increased in the oxymetholone-treated rats while the other treatment groups were unaffected. The MAO-B activity was not changed. 5. The results indicate that relatively high doses of AAS increase dopaminergic and 5-hydroxytryptaminergic metabolism in male rat brain, probably due to enhanced turnover in these monaminergic systems.
I recently read this study, it's interesting no doubt.
liftsiron is a fictional character and should be taken as such.
28/09/2018 8:14 pm
Funny, I read this abstract right after I read this post.
You did a search for "oxymetholone AND dopamine" too?
If it lowers dopamine it could also explain why some feel like crap on a anadrol cycle.
28/09/2018 9:12 pm
Well BC, bro explain why Anadrol has caused more cases of GALACTORRHEA than even deca or tren in the real world. Anadrol can and does cause both progestrone gyno (galactorrhea) as well as estrogen gyno. I believe than anadrol while not a true progestin like deca, tren and THG, may work by another mechanism to induce both estrogen and progesterone side effects. Also anadrol gyno is not appropiately treated by nolva alone, in most cases it will continue to proliferate. Proper treatment of gyno from anadrol includes bromo or another similiar anti-prolactin, as well as a strong anti-e. Studies are cool, but don't always apply. As for your profiles, I have read most of the profiles attributed to you, enough said there.
Actually anadrol gyno IS treated properly with Nolva (possibly in rare cases I would assume not, but then estrogen gyno isn't always treated properly with Nolva alone, usually they will employ anti-aromatase for longer treatments), there is NO SUCH THING as progesterone gyno, and if it induces progesterone side-effects I'd love to hear your explanation on how, as well as a list, with proof, of what you deem to be progestagenic side-effects. Seriously. Because if you are going to say shit like that last line, you best be coming in with a whole lot of proof.
Anadrol produces ESTROGENIC side-effects because anadrol is an ESTROGEN. It's acidic A-ring has an affinity for the estradiol receptor. Nuff said.
If you want to know why people experience problems AFTER Anadrol, then I would read up on the effects of 17AA on cortisol receptor number, and the effects of estrogens on progesterone receptor number.
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.
28/09/2018 9:52 pm
Actually anadrol is a drivative of dht, but exhibits both estrogen and progestin side effects by a method other than direct conversion. Galactorrhea is commonly referred to as progesterone gyno, and is frequently caused by anadrol, deca and tren of course estrogen is also required for glactorrhea to really become a problem. B6 at 300mgs twice per day eliminates the progestin activity in most users of anadrol, deca and tren.
liftsiron is a fictional character and should be taken as such.
29/09/2018 7:26 am
Galactorrhea has nothing to do with gyno, it is inappropriate lactation. It requires, and I quote, the presence of estrogen, progesterone and most importantly prolactin. If either of these is not present, galactorrhea does not occur, hence a proper course of anti-estrogens will suffice to treat it if it should occur. Likewise it establishes that estrogen is one of the causative factors of galactorrhea with permissive levels of A prolactin.
So where exactly this horsecrap is coming from I don't know.
A French study was conducted showing no progestagenic activity or binding during the use of oxymetholone. Which means at that time there was no activation of the progesterone receptors. So how exactly do you propose it acts progestagenic ?
Oxymetholone is one of the drugs I have worked with most extensively because of its very unique properties, and I've never seen galactorrhea, not even in women. Pubmed shows no case studies linking the two either. If it does, then dopamine supression as baccara suggested (and provided some base of likelihood for) seems a lot more likely.
Further more galactorrhead is mostly seen with amenhorrea, whilst patients with amenorrhea show REDUCED progesterone levels (Radojcic et al, 1997) and another study (Kidd et al, 1982) showed that acute and chronic administration of B6 at 600 mg had no effect on prolactin or significant effect on galactorrhea ...
Just so you are aware of what you are recommending to people.
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.
29/09/2018 8:01 am
Galactorrhea has nothing to do with gyno, it is inappropriate lactation. It requires, and I quote, the presence of estrogen, progesterone and most importantly prolactin. If either of these is not present, galactorrhea does not occur, hence a proper course of anti-estrogens will suffice to treat it if it should occur. Likewise it establishes that estrogen is one of the causative factors of galactorrhea with permissive levels of A prolactin.So where exactly this horsecrap is coming from I don't know.
A French study was conducted showing no progestagenic activity or binding during the use of oxymetholone. Which means at that time there was no activation of the progesterone receptors. So how exactly do you propose it acts progestagenic ?
Oxymetholone is one of the drugs I have worked with most extensively because of its very unique properties, and I've never seen galactorrhea, not even in women. Pubmed shows no case studies linking the two either. If it does, then dopamine supression as baccara suggested (and provided some base of likelihood for) seems a lot more likely.
Further more galactorrhead is mostly seen with amenhorrea, whilst patients with amenorrhea show REDUCED progesterone levels (Radojcic et al, 1997) and another study (Kidd et al, 1982) showed that acute and chronic administration of B6 at 600 mg had no effect on prolactin or significant effect on galactorrhea ...
Just so you are aware of what you are recommending to people.
You put women on Anadrol? I'm not going to debate you on any issue, your one of those people who think that they have all the answers. It's amazing at how much you think know about aas cycles considering the fact that by your own admission you have never done a cycle.
liftsiron is a fictional character and should be taken as such.
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