Originally Posted by Nathangarlike

What exactly is the difference?? I know dosage is slightly different i believe?? I can only get my hands on Tamoxifen Citrate for PCT and i was wondering what the difference is between the two?

Originally Posted by Nathangarlike

right but arent the two substances slightly different when it comes to dosages? That is what i was inquiring about

Originally Posted by Trouble

Translation: structure is weird as hell; Its spacey..space filling and the rings approximately span the cholesterol backbone of the ER (estrogen receptor) binding site... The quanternary amine happens to be the key, along with the phenyl ring substituted planar alkene. It blocks the binding of the portion of steroid structure that differentiates testosterone from estrogen.

I wondered, hmmm. Where else does it fit in to (what we call binding sites)? You gotta understand QSAR (qualitative structure function relationships) - structure correlated to function... So I went looking, and yeah, very recent article..and in the background section, second paragraph it sez...

"Based on the stimulation of AA release by several known cancer preventive agents, e.g., tamoxifen, 9-cis-retinoic acid, vitamin D3 , statins, anti-oxidants found in green tea and red wine, and peroxisome proliferator-activated receptor ligands, I have proposed that AA release by cells is associated with cancer prevention "

See? Those are nuclear receptor ligands. My conjecture was correct, intuition based on good gander at the structure.
(Psychem, he knows his line of logic using QSARs, he's a chemist, too.)

AA is necessary for hypertrophy, we talked about this elsewhere, with Phosphate Bond in a couple theads here and over at Avant.

This is really the bottom line in that paper I mentioned:

"I have suggested that inhibition of COX is a mechanism of action of NSAIDs. By inhibiting COX, more AA is made available as substrate for sphingomyelin to ceramide conversion. I have proposed that the release of AA is associated with cancer prevention. The AA release was observed from rat liver, human colon cancer (HT-29) and rat glioma (C-6) cells.

Growth of COX negative and COX positive cells is inhibited and their progression to apoptosis is increased by NSAIDs. In cells different than those cited above, others have demonstrated COX independence for NSAID actions."

There was also a hemolytic activity in red blood cells, which released AA and presumably stopped LOX type inflammation.

"The hemolysis suggests a mechanism proposed much earlier for the effects of NSAIDs (and tamoxiphen) on a variety of biological pathways, namely, perturbation of the cell membranes and disruption of normal signaling pathways. The deesterification of phospholipids (eg., cleaving fatty acids right off the glycerol backbone) could lead to altered signaling."

(aside - understatement of the century..can we say ' destroys membranes'? in concentrates in...we get to that in a minute)

See? You got these fuckchop reactions going on for a drug that is supposedly very specific in its actions.

And its doesn't get discussed much. This here paper, its novel shit, and I thought I'd bring it up for the AI user community to cogitate on.

---------- In a Nutshell ------------------------------------------------

It blocks hypertrophy and it promotes the turn over of cells we don't want to turn over.

Sure, it blocks pain. Who the fuck is taking tami for pain, eh?

If it's used for pct, and its causing loss of the growth you just juiced for in your cycle. A+B=?

Plus its hemolytic (causes membrane breakdown and cell lysis)----> the article mentions right out front just what I said, its very fat soluble and its gets sucked into membranes. Red blood cell membranes.

Y'all get my drift here?

Originally Posted by Trouble

Translation: structure is weird as hell; Its spacey..space filling and the rings approximately span the cholesterol backbone of the ER (estrogen receptor) binding site... The quanternary amine happens to be the key, along with the phenyl ring substituted planar alkene. It blocks the binding of the portion of steroid structure that differentiates testosterone from estrogen.

I wondered, hmmm. Where else does it fit in to (what we call binding sites)? You gotta understand QSAR (qualitative structure function relationships) - structure correlated to function... So I went looking, and yeah, very recent article..and in the background section, second paragraph it sez...

"Based on the stimulation of AA release by several known cancer preventive agents, e.g., tamoxifen, 9-cis-retinoic acid, vitamin D3 , statins, anti-oxidants found in green tea and red wine, and peroxisome proliferator-activated receptor ligands, I have proposed that AA release by cells is associated with cancer prevention "

See? Those are nuclear receptor ligands. My conjecture was correct, intuition based on good gander at the structure.
(Psychem, he knows his line of logic using QSARs, he's a chemist, too.)

AA is necessary for hypertrophy, we talked about this elsewhere, with Phosphate Bond in a couple theads here and over at Avant.

This is really the bottom line in that paper I mentioned:

"I have suggested that inhibition of COX is a mechanism of action of NSAIDs. By inhibiting COX, more AA is made available as substrate for sphingomyelin to ceramide conversion. I have proposed that the release of AA is associated with cancer prevention. The AA release was observed from rat liver, human colon cancer (HT-29) and rat glioma (C-6) cells.

Growth of COX negative and COX positive cells is inhibited and their progression to apoptosis is increased by NSAIDs. In cells different than those cited above, others have demonstrated COX independence for NSAID actions."

There was also a hemolytic activity in red blood cells, which released AA and presumably stopped LOX type inflammation.

"The hemolysis suggests a mechanism proposed much earlier for the effects of NSAIDs (and tamoxiphen) on a variety of biological pathways, namely, perturbation of the cell membranes and disruption of normal signaling pathways. The deesterification of phospholipids (eg., cleaving fatty acids right off the glycerol backbone) could lead to altered signaling."

(aside - understatement of the century..can we say ' destroys membranes'? in concentrates in...we get to that in a minute)

See? You got these fuckchop reactions going on for a drug that is supposedly very specific in its actions.

And its doesn't get discussed much. This here paper, its novel shit, and I thought I'd bring it up for the AI user community to cogitate on.

---------- In a Nutshell ------------------------------------------------

It blocks hypertrophy and it promotes the turn over of cells we don't want to turn over.

Sure, it blocks pain. Who the fuck is taking tami for pain, eh?

If it's used for pct, and its causing loss of the growth you just juiced for in your cycle. A+B=?

Plus its hemolytic (causes membrane breakdown and cell lysis)----> the article mentions right out front just what I said, its very fat soluble and its gets sucked into membranes. Red blood cell membranes.

Y'all get my drift here?

Originally Posted by redflash

Trouble - what are you on!?!? Do you think that 1% of the audience on this forum is going to understand a word you say?

I don't know whether you're trying to set yourself up as some sort of guru with your long words and pseudo-scientific shit but get real, man...

If you can't follow up on your geek stuff with a translation into WHAT IT MEANS PRACTICALLY (like for training, for dosages, for drug choice), this is all just intellectual masturbation and, as such, probably best conducted in the dark in private or on another forum where your unique contributions will be better appreciated....

Originally Posted by redflash

Trouble - what are you on!?!? Do you think that 1% of the audience on this forum is going to understand a word you say?

I don't know whether you're trying to set yourself up as some sort of guru with your long words and pseudo-scientific shit but get real, man...

If you can't follow up on your geek stuff with a translation into WHAT IT MEANS PRACTICALLY (like for training, for dosages, for drug choice), this is all just intellectual masturbation and, as such, probably best conducted in the dark in private or on another forum where your unique contributions will be better appreciated....

Originally Posted by ForemanRules

Trouble always posts great stuff, if you don't understand it them ask her nicely to explain it to you son.

Originally Posted by ForemanRules

Trouble always posts great stuff, if you don't understand it them ask her nicely to explain it to you son.

Originally Posted by redflash

But here goes....

Dear Ms Trouble,

I found your recent post on Tamoxifen and Tamoxifen Citrate most interesting, although I confess to not having understood a number of scientific terms used therein.

I would be extremely grateful if you would explain to me and other interested forum members what the practical implications of this might be. For example, in terms of what products/formulations to use and to avoid; what dosages to take, when and for how long; or any other relevant practical information.

I thank you in anticipation of your assistance in this matter.

Yours sincerely,

Mr Flash