Zero sex drive post sustanon cycle:<

e.g If you get your blood test results back and you have low testosterone and low LH & FSH,then you know all you need is more time and a bit more pct to get these levels going again.
But if you get your results back and you have normal LH & FSH but low testosterone this means you have issues with your testicles.
 
Blood tests should be done after completion of pct so yes best to come clean before getting the bloods.
Anymore improvements downstairs?
You have made a positive improvement with your latest pct stack,keep going with that for a couple of weeks before trying anything else

Got it. thanks for your informative replies bro :)
regarding the department downstairs, its definitely better than before,, my erections are getting stronger & I got morning erections the past few days which didn't occur in many weeks. What bothers me is this dull testicular ache, am gonna give it some more time, maybe it will resolve on itself.

e.g If you get your blood test results back and you have low testosterone and low LH & FSH,then you know all you need is more time and a bit more pct to get these levels going again.
But if you get your results back and you have normal LH & FSH but low testosterone this means you have issues with your testicles.

yes this will help me to identify the source of the problem, I think you are referring to primary & secondary hypogonadism & how to differ between the two via hormons test. nice approach, I really need to know how the boys are doing after those crazy HCG injections. In case everything is fine (I hope so), LH, FSH & T are ok then I will look into estrogens, prolactin, progestrone & TSH.......

I wish to thank everyone, you are really helping me thru these rough times my friends ...
 
OK this is a real 4-way pissing contest so Im still in.....

BBC3 said Conciliator, I Think we are all on the same page. I am simply trying to get the presentation details accurate for the learnees out there, and tell me if I am wrong. But here are some more thoughts answered withing your post.


What do you mean the pituitary is not directly involved? Of course it is. You say "nolva competes for the receptor 'Site', where ever that may be." Apparently, you don't know where the estrogen receptors are that you're trying to block. I'll tell you. They're in the pituitry. So you can bet your sweet ass that the pituitary is directly involved.

BBC3 Said While the pituitary itself (yes the tiny little gland so powerful deep in the base of out brains) is in charge of everything, I am pointing out that I believe you may be misinterpreting the action. I do believe the serms have some "direct action on the pituitary", and that this is why some can start you faster than others. BUT the estrogen receptors that are actually affected actually reside in the breast tissue, in the bicept, in the nipple, and most importantly in the prostate. The protective blocking action actually goes on right in the tittie!!! Some tissues are richer with estrogen receptors that others, hence they are hurt of helped more by the direct action of the serm at the actual tissue. The pituitary is actually getting reports from around the body letting it know what is going on hormone-wise and responding same....

Second, it's not the "HTPA", it's the HPTA. The "P" in there stands for pituitary... which is directly involved in the recovery of your H-P-T Axis.

BBC3 said Agreed on spelling of acronym...

Thrid, when you say "At 40mgs (even 20mgs) you have pretty much a max effective dose" you're talking about maximal saturation. That has nothing to do with "peak plasma concentrations", which can go much higher with higher doses.

BBC3 Said Ok, Peak plasma concentrations required to be effecting in the cancellation of the action of the excess estrogen. A higher dose would indeed create a high peak plasma concentration, you are correct.

Fourth, you don't need to explain to me in kindergarten terms what the difference is between a SERM and an AI. I know how they work, and judging from your comments about the pituitary, you're a little confused about it..

BBC3 Said Again, the methods that they work by are probably more "Indirect that direct" on the Pituitary. You make is sound like it is the presence of the Nolva or the Adex in the bloodstream that acting on the pituitary by "contact or exposure". I don't think this is the case. The more I think about it, the pituitary is probably behind the blood-brain barrier and I am not even sure it those drugs penetrate. As for the kidigarder explaination, this is for everyone else here as well, especially the new ones or watchers out there learning from this endless argument of symantics. As the others involved here mentioned, we are really only concerned with the overall result. HOWEVER, I do believe the difference of the action of a serm and an AI are very important.

Fifth, you say "With Nolva, your blood is still packed with heavy estrogens." Packed with heavy estrogens? First of all, WTF is a "heavy estrogen"? Second, estrogen is formed when testosterone aromatizes. When you don't have much testosterone, you won't have much estrogen either (hint: after a cycle). Your blood is NOT packed with estrogens when you take Nolva during PCT. Quite the contrary. So when you ask "Am I right??" The answer is, no, you are not right. There is not an excess of "heavy estrogens" (watever the hell that's supposed to mean) during recovery.

BBC3 said "Heavy estrogens" would be those that are nice and perdectily formed, and really pissed off that they can't stick (serm). "light estrogens" would be the bitchy little half mutated ones that could barely form during an incredibly hindered aromitaze process due to an AI. THis is called "fun with terms"... Have a little. And probably yes, you are constantly packed with estrogens. Contrary to belief, testosterone and its derivatives remain pretty damn high in the body for 6-8 weeks post cycle. Expecially a heavy one that also included Deca. etc....
THENNNNN
Nolva = Block = more test = more estrogen. The goal of NOlva is mostly to block, bad stimulator in my and others opinions.
Clomid = same but better restart effect = still equals estrogen.
Arimidex = NO aromitization = NO estrogen in blood = i really doubt this one is any good for proper restart. Seems like it would encourage aromatization to what the body whats, E & E2.
The bottom line is that from the last pin you pull on a cycle Estrogen is the problem. It will always predominate in a way it did not prior to discontinuation, the proportions will remain warped until you are truely returned to normal, WHICH NO ONE EVER DOES ANYWAY SO IT REMAINS A SERIOUS PROBLEM, ALWAYS..... Cicrculating high levels of test both during and post cycle remain a magical, serious problem that unfortunately does not subside as one would/might think.....


Surprisingly, I agree with you at the end when you talk about all the "processes in your body that require estrogen." That's why I've been repeating that SERMS have an advantage over AIs. They act like estrogen in several tissues where you want estrogen. In contrast, AI's are much more "all or nothing", you're right. They don't have a dual effect like SERMS do (antiestrogens in some tissues and pro-estrogens in others).

BBC3 Said Again with the SERMS "acting like estrogen" I believe this misnomer once confused my terminology as well. This is a VERY loose interpretation. The SERM is acting like nothing other, than A SERM. It is not an estrogen, its not a testosterone, it is NOLVADEX ((Z)2-[4-(1,2-diphenyl-1-butenyl) phenoxy]-N, N-dimethylethanamine 2 hydroxy-1,2,3- propanetricarboxylate (1:1), and its filling up parking spots in titties so that estrogen cant. It is still present in blood to whatever extent it would have been, and it just so happens that cholesterol is OK with that. They still get to swim together so all remains good on that side. Hence the benefit we have been talking about with serms over AIs. AI's like Arimidex or (It is chemically described as 1,3-Benzenediacetonitrile, ?, ?, ?', ?'-tetramethyl-5-(1H-1,2,4-triazol-1-ylmethyl). Its molecular formula is C17H19N5 and its structural formula is). I cant help but think that this one is the funkier of the two. I mean, Nolva may keep estrogen from sticking, BUT this bad boy keeps estrogen from ever forming by disrupting the action of the cytochromes P450 1A2, 2C8/9, and 3A4 EVER ACTUALLY AROMATIZING ( being broken down from test to E and E2) ....... NOW THAT IS SOME SERIOUS SHIT............ You really have to wonder what the odds are of the possibility of any long term effect on this process. I mean where does it even happen. Is this drug telling the Testosterone that it can no long break down. Is it making it morph of by products we dont know about? does it make test last longer in the body? If test can breakdown in to the metabolites E & E2, is it now living longer as itself? Is it breaking down into three times as much Progesterone. What are the other products of the termination of the life of a testosterone molecule and how are they affected. Do we even know what all of them are??
ONE FINAL, is the reason that clomid is proported to work as a better restart mechanism because it has a direct effect on the ledigs (in the physical nuts). I belive I have heard this is BODY STEP IN ON THIS POINT PLEASE. Chew on some of that for a while conciliator.......
Conciliator, I consider your work here honorable to say the least. Simply put, there are not very many here that give a shit about this. They are just going to temp alter their body in a way that gets an initial result they are looking for with no refard for efficiency, maximum safety, and best practice. You are welcome to refute anything I have stated here. You really have earned this effort an interest from me and I really appreciate a good arguer, right or wrong...:D
 
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That dull testicular ache is your balls comming back on line. Optimally you want a painful nasty ache that last no more that a day. That is a good restart. That pain is your body on the right track. Enjoy it.... You just made it back...!




Got it. thanks for your informative replies bro :)
regarding the department downstairs, its definitely better than before,, my erections are getting stronger & I got morning erections the past few days which didn't occur in many weeks. What bothers me is this dull testicular ache, am gonna give it some more time, maybe it will resolve on itself.



yes this will help me to identify the source of the problem, I think you are referring to primary & secondary hypogonadism & how to differ between the two via hormons test. nice approach, I really need to know how the boys are doing after those crazy HCG injections. In case everything is fine (I hope so), LH, FSH & T are ok then I will look into estrogens, prolactin, progestrone & TSH.......

I wish to thank everyone, you are really helping me thru these rough times my friends ...
 
BBC3 Said Again with the SERMS "acting like estrogen" I believe this misnomer once confused my terminology as well. This is a VERY loose interpretation. The SERM is acting like nothing other, than A SERM. It is not an estrogen, its not a testosterone, it is NOLVADEX ((Z)2-[4-(1,2-diphenyl-1-butenyl) phenoxy]-N, N-dimethylethanamine 2 hydroxy-1,2,3- propanetricarboxylate (1:1), and its filling up parking spots in titties so that estrogen cant.
I honestly don't think you understand what nolvadex does. When I say that it acts like estrogen in some tissues, it does exactly that, it ACTS as though estrogen were there. Let me put it into kindergarten terms: nolva fills up parking spots. In some spots, all it does is block the space so estrogen can't park and product an effect. In other spaces, not only does it occupy the space, but it produces the same effect that estrogen does. This is why the S in SERMS stands for selective and the M stands for modulator. Nolvadex has selective effects, depending on the tissue, and it moduates the estrogen receptor by being anti-estrogenic in some tissues (an antagonist) and pro-estrogenic in other tissues (an agonist). Depending on the estrogen receptor, nolvadex can either do nothing in the receptor (blocking it), or ACT like estrogen (activating it). If you think that the only thing nolva does is block receptors, you're mistaken. It also activates receptors, depending on the receptor subtype.
It is still present in blood to whatever extent it would have been, and it just so happens that cholesterol is OK with that. They still get to swim together so all remains good on that side. Hence the benefit we have been talking about with serms over AIs. AI's like Arimidex or (It is chemically described as 1,3-Benzenediacetonitrile, ?, ?, ?', ?'-tetramethyl-5-(1H-1,2,4-triazol-1-ylmethyl). Its molecular formula is C17H19N5 and its structural formula is). I cant help but think that this one is the funkier of the two. I mean, Nolva may keep estrogen from sticking, BUT this bad boy keeps estrogen from ever forming by disrupting the action of the cytochromes P450 1A2, 2C8/9, and 3A4 EVER ACTUALLY AROMATIZING ( being broken down from test to E and E2) ....... NOW THAT IS SOME SERIOUS SHIT............
Randomly cutting and pasting the chemical names doesn't make you sound any smarter. And again, nolva does more than just "keep estrogen from sticking." It can also act like estrogen, activating the receptor, and producing an estrogenic effect depending on the tissue (e.g. in the liver, in bone, etc).
ONE FINAL, is the reason that clomid is proported to work as a better restart mechanism because it has a direct effect on the ledigs (in the physical nuts). I belive I have heard this is BODY STEP IN ON THIS POINT PLEASE. Chew on some of that for a while conciliator.......
What do you mean clomid has a direct effect on leydig cells?
 
OK Conciliator, we are starting to argue more and more the same point to a foolish degree. the only I am only pointing out that the only thing about nolva resembling an estrogen is the fact that when it parks there it triggers the receptor sure, BUT NOTHING LIKE AN ESTROGEN OR ELSE YOU WOULD CONTINUE GROWING TITTIES!!!!!!

And I meant a better and more direct effect on the ledigs in the nuts..
 
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Regarding the action and location of receptors. I guess you are now in agreement with me that they are no where near the pituitary? At least 99.9% of them....?

FURTHER, it is not acting like an estrogen anywhere. The "Agonism" comes from the fact that the estrogen remains free to circulate throughout the body still playing its role where is is NOT RECEPTOR DEPENDENT. For example its role in cholesterol levels..... It is not some function that the Nolva is doing by itself. It is the result of the estrogen that remains aromatized and unchecked. The agonism is a RESULT. The ANTAGONISM IS A RESULT. They are results of the action of the chemical compositions that I have copied and pasted above!!

Come on Conciliator. I think its time you bow down and beg for oblivion. Havent you had enough? I promise I will send you there quickly, gracfully, and with as much honor and still remains. :p:eek: The only thing I see here is you neglecting the fact that I have whitled you down to nothing and you are starting to sound more and more like me. Just let that last little incorrect premise go, turn to the BBC3 Side and forever will I rule your attempts to discredit the righteous. There is hope for you yet...:D[:o)][:o)]

ON a final note. You obviously have not read the list of side effects of serms or ai's. It is a mile long and ugly as hell! If you had you would clearly understand that these chemical not only do not ACT like estrogens, THEY LOOK NOTHING LIKE THEM.!!!
 
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NAH NAH NAH NA> NA NA NA NAH. HEY HEY HEY HEY ... GOOD Bye. Go home conciliator. You have lost this battle. I must now proceed with a serious victory trash talking to you. Take your picture and go night night. Actually, the more I think about it. I am not even sure where you got that pic. You may actually be Arnold himself. If you are, no offense. No one ever said that you knew the details of what you were taking. We only expected you to keep on looking good.;) You still go it babe. Keep that hard work up over in Sacramento, try to get that pot legalized for us here. I sure could use a $50.00 oz of K.B. I am excited to say the least. It is obvious that you never lost that love of the gonja from back in your training days. I would only have to insist that you cut you smoking down to a minimum prior to forum time. You are starting to look as silly as Leu says you are. I do believe he did say that your only saving grace was that all he had to do to avoid your constand bullshit was to look away. He found his deafness to be quite a perk with regards to your relationship, did he not. Ok, i'll let you alone now. I am sure you are so stewed up that you are having to run right over to your custom gym you have installed in the masion. Just remember, dont stay up too late. Its a school night. And dont let this conversation get you too excited when pull your pin out tonight, you cant afford any more side effects from that heavy dosing. Sleep tight. "I have to let you go." Oh, and one more thing, "let off some steam". Good night matrix.:)
 
I am only pointing out that the only thing about nolva resembling an estrogen is the fact that when it parks there it triggers the receptor sure, BUT NOTHING LIKE AN ESTROGEN OR ELSE YOU WOULD CONTINUE GROWING TITTIES!!!!!!
You have no freaking clue what you're talking about, do you? In breast tissue, SERMS have minimal to no estrogenic effect. It has the effect of blocking estrogen there, by occupying the receptor, but not activating it. However, in some estrogen receptors, in some tissues, such as the liver, nolva acts LIKE AN ESTROGEN. It activates the estrogen receptor as though estrogen was there.
And I meant a better and more direct effect on the ledigs in the nuts..
So first you say clomid has a direct effect on leydig cells. I ask what that's supposed to mean, and now you say "a better and more direct effect on the ledigs." That's even more vague than the first thing you said. Unbelievable.
 
That dull testicular ache is your balls comming back on line. Optimally you want a painful nasty ache that last no more that a day. That is a good restart. That pain is your body on the right track. Enjoy it.... You just made it back...!

I just awoke, seemingly the ache is subsiding right now, I really need the boys to go online ASAP, coz I'm having good luck with sexy ladies :p guys I was wondering if its ok if I throw in some Proviron ? does it affect pct ? I used it before during the cycle & it was a great stuff for sky rocketing sex drive..
 
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Regarding the action and location of receptors. I guess you are now in agreement with me that they are no where near the pituitary? At least 99.9% of them....?
What the hell are you talking about? Of course there are estrogen receptors in the pituitary. They're also in the hypothalamus. When you take SERMS for PCT, you're taking them to block estrogen in the pituitary and in the hypothalamus. That's where estrogen exerts negative feedback on GnRH release and LH release. There are estrogen receptors in all sorts of other tissues as well.
FURTHER, it is not acting like an estrogen anywhere. The "Agonism" comes from the fact that the estrogen remains free to circulate throughout the body still playing its role where is is NOT RECEPTOR DEPENDENT. For example its role in cholesterol levels..... It is not some function that the Nolva is doing by itself. It is the result of the estrogen that remains aromatized and unchecked. The agonism is a RESULT. The ANTAGONISM IS A RESULT. They are results of the action of the chemical compositions that I have copied and pasted above!!
Wrong, wrong, and completely wrong. You need to research SERMs because you don't even understand their basic function. They DO act like an estrogen in some itssues, which is why they're called SELECTIVE MODULATORS of the estrogen receptor. The agonism does NOT come from estrogen that "remains free to circulate throughout the body." You just proved here that you are ignorant about how SERMS work. The agonism (in tissues like the liver) comes from the SERMs themselves acting like estrogen in the estrogen receptor. SERMS are NOT pure estrogen receptor antagonists, like the drug fulvestrant. They can have DIRECT estrogenic effects, depending on the tissue. They can also have direct anti-estrogenic effects, again, depending on the tissue (and the SERM). The point you need to comprehend, though, is that in some tissues SERMS ACT LIKE ESTROGEN, as agonists of the receptor.
Come on Conciliator. I think its time you bow down and beg for oblivion. Havent you had enough? I promise I will send you there quickly, gracfully, and with as much honor and still remains. :p:eek: The only thing I see here is you neglecting the fact that I have whitled you down to nothing and you are starting to sound more and more like me. Just let that last little incorrect premise go, turn to the BBC3 Side and forever will I rule your attempts to discredit the righteous. There is hope for you yet...:D[:o)][:o)]
After demonstrating your gross ignorance about SERMS and estrogen receptor agonism, you should be embarassed for posting arrogant bullshit like this.
ON a final note. You obviously have not read the list of side effects of serms or ai's. It is a mile long and ugly as hell! If you had you would clearly understand that these chemical not only do not ACT like estrogens, THEY LOOK NOTHING LIKE THEM.!!!
I'm getting sick of how fucking clueless you are. SERMS DO ACT LIKE ESTROGENS. Do some basic research dipshit.
 
Here's are several quotes from William Llewewllyn's recently released book Anabolics 9th Edition. Try to learn something:
Raloxifene hydrochloride is a second-generation Selective Estrogen Receptor Modulator (SERM) of the benzothiophene family. This drug is similar in effect to tamoxifen, exhibiting estrogen receptor antagonist (blocking) properties in some tissues while acting as an estrogen receptor agonist (activator) in others.
...
While raloxifene hydrochloride is a strong antiestrogen in breast and uterine tissues, it appears to be estrogenic in bone. This allows it to protect bone density, mimicking the beneficial effects of endogenous estradiol.
...
Raloxifene hydrochloride is classified a selective estrogen receptor modulator, with both agonist and antagonist properties.
...
Toremifene citrate is an anti-estrogenic drug, specifically classified as a Selective Estrogen-Receptor Modulator (SERM) with mixed agonist and antagonist properties.
...
The triphenylethylene compounds (toremifene citrate, tamoxifen citrate, clomiphene citrate) tend to be somewhat intrinsically estrogenic in the liver. This means that while they can block estrogenic activity in some areas of the body, they can actually act as estrogens in this other key area.
...
Cyclofenil is a non-steroidal anti-estrogen that is used in the treatment of menstrual disturbances and anovualtory infertility (an inability to ovulate). It is very similar in structure to Clomid and Nolvadex, and also works in the body as a mixed estrogen agonist/antagonist.
...
Cyclofenil is classified as a selective estrogen receptor modulator, with both agonist and antagonist properties.
...
Tamoxifen citrate is a non-steroidal anti-estrogenic drug, used widely in clinical medicine. It is specifically a Selective Estrogen-Receptor Modulator (SERM) of the triphenylethylene family, and possesses both estrogen agonist and antagonist properties. As such, it may act as an estrogen in some tissues while blocking the action of estrogen in others.
...
Note that like some other triphenylethylene compounds, tamoxifen citrate can act as an estrogen in the liver. Estrogenic action in the liver is important in the regulation of serum cholesterol, and tends to support HDL (good) cholesterol synthesis and LDL (bad) cholesterol reductions. Since steroid-using bodybuilders are already dealing with the negative cardiovascular effects of these drugs, compounding the issue with aromatase inhibitors (which will lower total serum estrogen levels) may not always be the best option. Using a drug that blocks gynecomastia, for example, while at the same time supporting improved cholesterol values, might be much more ideal.
...
Tamoxifen citrate is classified as a selective estrogen receptor modulator, with both agonist and antagonist properties (also known as an estrogen agonist/angagonist).
Good luck trash talking after getting an intelectual ass whooping that makes you look like the clueless moron you are.
 


I just awoke, seemingly the ache is subsiding right now, I really need the boys to go online ASAP, coz I'm having good luck with sexy ladies :p guys I was wondering if its ok if I throw in some Proviron ? does it affect pct ? I used it before during the cycle & it was a great stuff for sky rocketing sex drive..

That is a tough one. It has been shown to not show negative effects on a healthy HPTA, but no real studies show if it allows one to recover post cycle. But at the same time, it does free bound test and will help with libido and overall good feelings. If your test and estrodial levels along with all other levels are fine, then I would say a small dose 25-50mgs will not be bad as your body could just be binding test as its natural levels rise.
 
AHHHHHHHH, you are missing the god damn point. The SERMS is not "signaling the bone" per say. is is the fact that the estrogens are still circulating in the blood thus still allowed to have an effect. The reason they can still have an affect is because that particular chemical compound just so happens to have a minimal ability to park in the bone receptors because that chemical DONT LIKE IT THERE>>>... What, are you telling me nolva stunts bone health?? I know it is a huge side of Arimidex as ADEX completely removes estrogen from the body, but not novla....

YOU ARE MISSING THE WHOLE CHICKEN/EGG ARGUMENT!!! tHE WHOLE description of acting as an estrogen is a verbal misnomer designed for laymen.. The agonism, or ant-agonism is an ACT!!!! and a measured result of what the remained estrogen is allowed to do in the face of the particular drug. Llewelen is simply putting in terms for children like you. WHat you did not think Bady builders were smart did you?? Look in the mirror Conciliator, and dont try to make anymore movies. You are washed up. SO just admit it you sellout. I mean, who marries a fucking Kennedy and then goes on the be the GUUvoner of a conservative state. California is one giant retardation of idiots. You found your home...:eek::D[:o)]
 
By the way. NOw that I am sure you are the real Scwarzeneggaer, CAN I HAVE YOUR AUTOGRAPH???

AHHHHHHHH, you are missing the god damn point. The SERMS is not "signaling the bone" per say. is is the fact that the estrogens are still circulating in the blood thus still allowed to have an effect. The reason they can still have an affect is because that particular chemical compound just so happens to have a minimal ability to park in the bone receptors because that chemical DONT LIKE IT THERE>>>... What, are you telling me nolva stunts bone health?? I know it is a huge side of Arimidex as ADEX completely removes estrogen from the body, but not novla....

YOU ARE MISSING THE WHOLE CHICKEN/EGG ARGUMENT!!! tHE WHOLE description of acting as an estrogen is a verbal misnomer designed for laymen.. The agonism, or ant-agonism is an ACT!!!! and a measured result of what the remained estrogen is allowed to do in the face of the particular drug. Llewelen is simply putting in terms for children like you. WHat you did not think Bady builders were smart did you?? Look in the mirror Conciliator, and dont try to make anymore movies. You are washed up. SO just admit it you sellout. I mean, who marries a fucking Kennedy and then goes on the be the GUUvoner of a conservative state. California is one giant retardation of idiots. You found your home...:eek::D[:o)]
 
AHHHHHHHH, you are missing the god damn point. The SERMS is not "signaling the bone" per say. is is the fact that the estrogens are still circulating in the blood thus still allowed to have an effect. The reason they can still have an affect is because that particular chemical compound just so happens to have a minimal ability to park in the bone receptors because that chemical DONT LIKE IT THERE>>>... What, are you telling me nolva stunts bone health?? I know it is a huge side of Arimidex as ADEX completely removes estrogen from the body, but not novla....

YOU ARE MISSING THE WHOLE CHICKEN/EGG ARGUMENT!!! tHE WHOLE description of acting as an estrogen is a verbal misnomer designed for laymen.. The agonism, or ant-agonism is an ACT!!!! and a measured result of what the remained estrogen is allowed to do in the face of the particular drug. Llewelen is simply putting in terms for children like you. WHat you did not think Bady builders were smart did you?? Look in the mirror Conciliator, and dont try to make anymore movies. You are washed up. SO just admit it you sellout. I mean, who marries a fucking Kennedy and then goes on the be the GUUvoner of a conservative state. California is one giant retardation of idiots. You found your home...:eek::D[:o)]
Wrong again moron. That is not how SERMs work. Raloxifene, for example, IS "signaling the bone per se." The raloxifene molecule acts like an estrogen in bone. It is an agonist itself and activates the estrogen receptor in bone. This is why it's marketed as preventing osteoporosis. Nolva, on the other hand, is different. Nolva is antiestrogenic in both breast and bone. Most SERMs, however, are DIRECTLY estrogenic in the liver, which has positive effects on lipid values.

I'm not missing anything. You're the asswipe who's putting things in kindergarten terms. Llewewlyn is not. He means exactly what he says. Seriously, do some basic research on SERMs and learn how they work. You're an embarassment to this site when you go around spouting off garbage that's incorrect. SERMS are SELECTIVE. They have mixed antagonist/agonist properties, and that's from DIRECT action of the SERM itself. Try to open that small brain of yours and learn something.
 
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you are correct about nolva blocking receptors at the bones. i must have omitted due to the long list of side effects,,, asshole..

group during treatment or within 14 days of the end of treatment are presented in the following table.

Adverse events occurring with an incidence of at least 5% in either treatment group during treatment, or within 14 days of the end of treatment


Body system and adverse event by COSTART-preferred term* Anastrozole 1 mg
(N = 3092) NOLVADEX 20 mg
(N = 3094)
Body as a whole
Asthenia 575 (19) 544 (18)
Pain 533 (17) 485 (16)
Back pain 321 (10) 309 (10)
Headache 314 (10) 249 (8)
Abdominal pain 271 (9) 276 (9)
Infection 285 (9) 276 (9)
Accidental injury 311 (10) 303 (10)
Flu syndrome 175 (6) 195 (6)
Chest pain 200 (7) 150 (5)
Neoplasm 162 (5) 144 (5)
Cyst 138 (5) 162 (5)
Cardiovascular
Vasodilatation 1104 (36) 1264 (41)
Hypertension 402 (13) 349 (11)
Digestive
Nausea 343 (11) 335 (11)
Constipation 249 (8) 252 (8)
Diarrhea 265 (9) 216 (7)
Dyspepsia 206 (7) 169 (6)
Gastrointestinal disorder 210 (7) 158 (5)
Hemic and lymphatic
Lymphoedema 304 (10) 341 (11)
Anemia 113 (4) 159 (5)
Metabolic and nutritional
Peripheral edema 311 (10) 343 (11)
Weight gain 285 (9) 274 (9)
Hypercholesterolemia 278 (9) 108 (3.5)
Musculoskeletal
Arthritis 512 (17) 445 (14)
Arthralgia 467 (15) 344 (11)
Osteoporosis 325 (11) 226 (7)
Fracture 315 (10) 209 (7)
Bone pain 201 (7) 185 (6)
Arthrosis 207 (7) 156 (5)
Joint Disorder 184 (6) 160 (5)
Myalgia 179 (6) 160 (5)
Nervous system
Depression 413 (13) 382 (12)
Insomnia 309 (10) 281 (9)
Dizziness 236 (8) 234 (8)
Anxiety 195 (6) 180 (6)
Paraesthesia 215 (7) 145 (5)
Respiratory
Pharyngitis 443 (14) 422 (14)
Cough increased 261 (8) 287 (9)
Dyspnea 234 (8) 237 (8)
Sinusitis 184 (6) 159 (5)
Bronchitis 167 (5) 153 (5)
Skin and appendages
Rash 333 (11) 387 (13)
Sweating 145 (5) 177 (6)
Special Senses
Cataract Specified 182 (6) 213 (7)
Urogenital
Leukorrhea 86 (3) 286 (9)
Urinary tract infection 244 (8) 313 (10)
Breast pain 251 (8) 169 (6)
Breast Neoplasm 164 (5) 139 (5)
Vulvovaginitis 194 (6) 150 (5)
Vaginal Hemorrhage 122 (4) 180 (6)
Vaginitis 125 (4) 158 (5)
COSTART Coding Symbols for Thesaurus of Adverse Reaction Terms.
N = Number of patients receiving the treatment.
*A patient may have had more than 1 adverse event, including more than 1 adverse event in the same body system. Vaginal Hemorrhage without further diagnosis.
** The combination arm was discontinued due to lack of efficacy benefit at 33 months of follow-up.


Certain adverse events and combinations of adverse events were prospectively specified for analysis, based on the known pharmacologic properties and side effect profiles of the two

left numbers are sides, right numbers placebo.... boy thats some healthy stuff!:D
 
Okay, boys, time to let the gentleman have his thread back. Conciliator, you've been most patient but it still takes two to keep a shouting match going. Time to go back behind your lines.

Solo

(Now izzat conciliatory or what?:rolleyes:)
 
Here's another quote from a review paper in The Journal of Pharmacology and Experimental Therapeutics called "Molecular Mechanisms of Selective Estrogen Receptor Modulator (SERM) Action:" Molecular Mechanisms of Selective Estrogen Receptor Modulator (SERM) Action -- Dutertre and Smith 295 (2): 431 -- Journal of Pharmacology And Experimental Therapeutics

Selective estrogen receptor modulators (SERMs) are ER ligands that in some tissues act like estrogens, but block estrogen action in others. Thus, SERMs may exhibit an agonistic or antagonistic biocharacter depending on the context in which their activity is examined. For example, the SERMs tamoxifen and raloxifene both exhibit ER antagonist activity in breast and agonist activity in bone, but only tamoxifen manifests agonist activity in the uterus.
...
More recently, another SERM, raloxifene, is being used for the prevention of osteoporosis (Fig. 1; Cosman and Lindsay, 1999). Like tamoxifen, raloxifene is an ER antagonist in breast and an agonist in bone. However, it does not exert ER agonist properties in the uterus (Mitlak and Cohen, 1997; Cosman and Lindsay, 1999). Both tamoxifen and raloxifene also have beneficial, estrogen-like effects in the liver with respect to lipid metabolism (Mitlak and Cohen, 1997; Cosman and Lindsay, 1999).
The whole paper is how SERMs are selective, how they can ACT LIKE ESTROGEN some of the time (as an agonist) and block estrogen other times (as an antagonist). That's how SERMs work...
 
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